Amy J. McMichael, MD

Hidradenitis suppurativa (HS)—a chronic, relapsing, inflammatory disorder involving terminal hair follicles in apocrine gland–rich skin—manifests as tender inflamed nodules that transform into abscesses, sinus tracts, and scarring.^1,2 The etiology of HS is multifactorial, encompassing lifestyle, microbiota, hormonal status, and genetic and environmental factors. These factors activate the immune system around the terminal hair follicles and lead to hyperkeratosis of the infundibulum of the hair follicles in intertriginous regions. This progresses to follicular occlusion, stasis, and eventual rupture. Bacterial multiplication within the plugged pilosebaceous units further boosts immune activation. Resident and migrated cells of the innate and adaptive immune system then release proinflammatory cytokines such as tumor necrosis factor, IL-1β, and IL-17, which further enhance immune cell influx and inflammation.^3,4 This aberrant immune response propagates the production of deep-seated inflammatory nodules and abscesses.^3-8

The estimated prevalence of HS is 1% worldwide.⁹ It is more prevalent in female and Black patients (0.30%) than White patients (0.09%) and is intermediate in prevalence in the biracial population (0.22%).¹⁰ Hidradenitis suppurativa is thought to be associated with lower socioeconomic status (SES). In a retrospective analysis of HS patients (N=375), approximately one-third of patients were Black, had advanced disease, and had a notably lower SES.¹¹ Furthermore, HS has been reported to be associated with systemic inflammation and comorbidities such as morbid obesity (38.3%) and hypertension (39.6%) as well as other metabolic syndrome–related disorders and depression (48.1%).¹

Hidradenitis suppurativa may contribute to the risk for depression through its substantial impact on health-related quality of life, which culminates in social withdrawal, unemployment, and suicidal thoughts.¹² The high prevalence of depression in individuals with HS¹ and its association with systemic inflammation¹³ increases the likelihood that a common genetic predisposition also may exist between both conditions. Because depression frequently has been discovered as a concomitant diagnosis in patients with HS, we hypothesize that a shared genetic susceptibility also may exist between the 2 disorders. Our study sought to explore data on the co-occurrence of depression with HS, including its demographics and racial data.

Methods

We conducted a PubMed search of articles indexed for MEDLINE as well as Google Scholar using the terms depression and hidradenitis suppurativa to obtain all research articles published from 2000 to 2022. Articles were selected based on relevance to the topic of exploration. English-language articles that directly addressed the epidemiology, etiology, pathophysiology, and co-occurrence of both depression and HS with numerical data were included. Articles were excluded if they did not explore the information of interest on these 2 disorders or did not contain clear statistical data of patients with the 2 concurrent medical conditions.

Results

Twenty-two cross-sectional, prospective, and retrospective studies that fit the search criteria were identified and included in the analysis (eTable).^1,14-34 Sixteen (72.7%) studies were cross-sectional, 5 (22.7%) were retrospective, and only 1 (4.5%) was a prospective study. Only 6 of the studies provided racial data,^{1,14,17,26,28,32} and of them, 4 had predominately White patients,^1,14,26,32 whereas the other 2 had predominantly Black patients.^17,28

Hidradenitis suppurativa was found to coexist with depression in all the studies, with a prevalence of 1.2% to 48.1%. There also was a higher prevalence of depression in HS patients than in the control patients without HS. Furthermore, a recent study by Wright and colleagues¹⁴ stratified the depression prevalence data by age and found a higher prevalence of depression in adults vs children with HS (30% vs 12%).

Comment

Major depression—a chronic and debilitating illness—is the chief cause of disability globally and in the United States alone and has a global lifetime prevalence of 17%.³⁵ In a study of 388 patients diagnosed with depression and 404 community-matched controls who were observed for 10 years, depressed patients had a two-thirds higher likelihood of developing a serious physical illness than controls. The depression-associated elevated risk for serious physical illness persisted after controlling for confounding variables such as alcohol abuse, smoking, and level of physical activity.³⁶ Studies also have demonstrated that HS is more prevalent in Black individuals¹⁰ and in individuals of low SES,³⁷ who are mostly the Black and Hispanic populations that experience the highest burden of racial microaggression³⁸ and disparities in health access and outcomes.^39,40 The severity and chronicity of major depressive disorder also is higher in Black patients compared with White patients (57% vs 39%).⁴¹ Because major depression and HS are most common among Black patients who experience the highest-burden negative financial and health disparities, there may be a shared genetic disposition to both medical conditions.

Moreover, the common detrimental lifestyle choices associated with patients with depression and HS also suggest the possibility of a collective genetic susceptibility. Patients with depression also report increased consumption of alcohol, tobacco, and illicit substances; sedentary lifestyle leading to obesity; and poor compliance with prescribed medical treatment.⁴² Smoking and obesity are known contributors to the pathogenesis of HS, and their modification also is known to positively impact the disease course. In a retrospective single-cohort study, 50% of obese HS patients (n=35) reported a substantial decrease in disease severity after a reduction of more than 15% in body mass index over 2 years following bariatric surgery (n=35).⁴³ Patients with HS also have reported disease remission following extensive weight loss.⁴⁴ In addition, evidence has supported smoking cessation in improving the disease course of HS.⁴³ Because these detrimental lifestyle choices are prevalent in both patients with HS and those with depression, a co-genetic susceptibility also may exist.

Furthermore, depression is characterized by a persistent inflammatory state,^13,45 similar to HS.⁴⁶ Elevated levels of a variety of inflammatory markers, such as C-reactive protein (CRP), IL-6, and soluble intercellular adhesion molecule 1, have been reported in patients with depression compared with healthy controls.^13,45 Further analysis found a positive correlation and a strong association between depression and these inflammatory markers.⁴⁷ Moreover, adipokines regulate inflammatory responses, and adipokines play a role in the pathogenesis of HS. Adipokine levels such as elevated omentin-1 (a recently identified adipokine) were found to be altered in patients with HS compared with controls.⁴⁸ Results from clinical studies and meta-analyses of patients with depression also have demonstrated that adipokines are dysregulated in this population,^49,50 which may be another potential genetic link between depression and HS.

In addition, genetic susceptibility to depression and HS may be shared because the inflammatory markers that have a strong association with depression also have been found to play an important role in HS treatment and disease severity prediction. In a retrospective cohort study of 404 patients, CRP or IL-6 levels were found to be reliable predictors of HS disease severity, which may explain why anti–tumor necrosis factor antibody regimens such as adalimumab and infliximab have clinically ameliorated disease activity in several cases of HS.⁵¹ In a study evaluating these drugs, high baseline levels of high-sensitivity CRP and IL-6 were predictive of patient response to infliximab.⁵² In a meta-analysis evaluating 20,791 participants, an association was found between concurrent depression and CRP. Furthermore, inflammation measured by high levels of CRP or IL-6 was observed to predict future depression.⁵³ If the same inflammatory markers—CRP and IL-6—both play a major role in the disease activity of depression and HS, then a concurrent genetic predisposition may exist.

Conclusion

Understanding the comorbidities, etiologies, and risk factors for the development and progression of HS is an important step toward improved disease management. Available studies on comorbid depression in HS largely involve White patients, and more studies are needed in patients with skin of color, particularly the Black population, who have the highest prevalence of HS.¹⁰ Given the evidence for an association between depression and HS, we suggest a large-scale investigation of this patient population that includes a complete medical history, onset of HS in comparison to the onset of depression, and specific measures of disease progress and lifetime management of depression, which may help to increase knowledge about the role of depression in HS and encourage more research in this area. If shared genetic susceptibility is established, aggressive management of depression in patients at risk for HS may reduce disease incidence and severity as well as the psychological burden on patients.

Hidradenitis suppurativa (HS)—a chronic, relapsing, inflammatory disorder involving terminal hair follicles in apocrine gland–rich skin—manifests as tender inflamed nodules that transform into abscesses, sinus tracts, and scarring.^1,2 The etiology of HS is multifactorial, encompassing lifestyle, microbiota, hormonal status, and genetic and environmental factors. These factors activate the immune system around the terminal hair follicles and lead to hyperkeratosis of the infundibulum of the hair follicles in intertriginous regions. This progresses to follicular occlusion, stasis, and eventual rupture. Bacterial multiplication within the plugged pilosebaceous units further boosts immune activation. Resident and migrated cells of the innate and adaptive immune system then release proinflammatory cytokines such as tumor necrosis factor, IL-1β, and IL-17, which further enhance immune cell influx and inflammation.^3,4 This aberrant immune response propagates the production of deep-seated inflammatory nodules and abscesses.^3-8

The estimated prevalence of HS is 1% worldwide.⁹ It is more prevalent in female and Black patients (0.30%) than White patients (0.09%) and is intermediate in prevalence in the biracial population (0.22%).¹⁰ Hidradenitis suppurativa is thought to be associated with lower socioeconomic status (SES). In a retrospective analysis of HS patients (N=375), approximately one-third of patients were Black, had advanced disease, and had a notably lower SES.¹¹ Furthermore, HS has been reported to be associated with systemic inflammation and comorbidities such as morbid obesity (38.3%) and hypertension (39.6%) as well as other metabolic syndrome–related disorders and depression (48.1%).¹

Hidradenitis suppurativa may contribute to the risk for depression through its substantial impact on health-related quality of life, which culminates in social withdrawal, unemployment, and suicidal thoughts.¹² The high prevalence of depression in individuals with HS¹ and its association with systemic inflammation¹³ increases the likelihood that a common genetic predisposition also may exist between both conditions. Because depression frequently has been discovered as a concomitant diagnosis in patients with HS, we hypothesize that a shared genetic susceptibility also may exist between the 2 disorders. Our study sought to explore data on the co-occurrence of depression with HS, including its demographics and racial data.

Methods

We conducted a PubMed search of articles indexed for MEDLINE as well as Google Scholar using the terms depression and hidradenitis suppurativa to obtain all research articles published from 2000 to 2022. Articles were selected based on relevance to the topic of exploration. English-language articles that directly addressed the epidemiology, etiology, pathophysiology, and co-occurrence of both depression and HS with numerical data were included. Articles were excluded if they did not explore the information of interest on these 2 disorders or did not contain clear statistical data of patients with the 2 concurrent medical conditions.

Results

Twenty-two cross-sectional, prospective, and retrospective studies that fit the search criteria were identified and included in the analysis (eTable).^1,14-34 Sixteen (72.7%) studies were cross-sectional, 5 (22.7%) were retrospective, and only 1 (4.5%) was a prospective study. Only 6 of the studies provided racial data,^{1,14,17,26,28,32} and of them, 4 had predominately White patients,^1,14,26,32 whereas the other 2 had predominantly Black patients.^17,28

Hidradenitis suppurativa was found to coexist with depression in all the studies, with a prevalence of 1.2% to 48.1%. There also was a higher prevalence of depression in HS patients than in the control patients without HS. Furthermore, a recent study by Wright and colleagues¹⁴ stratified the depression prevalence data by age and found a higher prevalence of depression in adults vs children with HS (30% vs 12%).

Comment

Major depression—a chronic and debilitating illness—is the chief cause of disability globally and in the United States alone and has a global lifetime prevalence of 17%.³⁵ In a study of 388 patients diagnosed with depression and 404 community-matched controls who were observed for 10 years, depressed patients had a two-thirds higher likelihood of developing a serious physical illness than controls. The depression-associated elevated risk for serious physical illness persisted after controlling for confounding variables such as alcohol abuse, smoking, and level of physical activity.³⁶ Studies also have demonstrated that HS is more prevalent in Black individuals¹⁰ and in individuals of low SES,³⁷ who are mostly the Black and Hispanic populations that experience the highest burden of racial microaggression³⁸ and disparities in health access and outcomes.^39,40 The severity and chronicity of major depressive disorder also is higher in Black patients compared with White patients (57% vs 39%).⁴¹ Because major depression and HS are most common among Black patients who experience the highest-burden negative financial and health disparities, there may be a shared genetic disposition to both medical conditions.

Moreover, the common detrimental lifestyle choices associated with patients with depression and HS also suggest the possibility of a collective genetic susceptibility. Patients with depression also report increased consumption of alcohol, tobacco, and illicit substances; sedentary lifestyle leading to obesity; and poor compliance with prescribed medical treatment.⁴² Smoking and obesity are known contributors to the pathogenesis of HS, and their modification also is known to positively impact the disease course. In a retrospective single-cohort study, 50% of obese HS patients (n=35) reported a substantial decrease in disease severity after a reduction of more than 15% in body mass index over 2 years following bariatric surgery (n=35).⁴³ Patients with HS also have reported disease remission following extensive weight loss.⁴⁴ In addition, evidence has supported smoking cessation in improving the disease course of HS.⁴³ Because these detrimental lifestyle choices are prevalent in both patients with HS and those with depression, a co-genetic susceptibility also may exist.

Furthermore, depression is characterized by a persistent inflammatory state,^13,45 similar to HS.⁴⁶ Elevated levels of a variety of inflammatory markers, such as C-reactive protein (CRP), IL-6, and soluble intercellular adhesion molecule 1, have been reported in patients with depression compared with healthy controls.^13,45 Further analysis found a positive correlation and a strong association between depression and these inflammatory markers.⁴⁷ Moreover, adipokines regulate inflammatory responses, and adipokines play a role in the pathogenesis of HS. Adipokine levels such as elevated omentin-1 (a recently identified adipokine) were found to be altered in patients with HS compared with controls.⁴⁸ Results from clinical studies and meta-analyses of patients with depression also have demonstrated that adipokines are dysregulated in this population,^49,50 which may be another potential genetic link between depression and HS.

In addition, genetic susceptibility to depression and HS may be shared because the inflammatory markers that have a strong association with depression also have been found to play an important role in HS treatment and disease severity prediction. In a retrospective cohort study of 404 patients, CRP or IL-6 levels were found to be reliable predictors of HS disease severity, which may explain why anti–tumor necrosis factor antibody regimens such as adalimumab and infliximab have clinically ameliorated disease activity in several cases of HS.⁵¹ In a study evaluating these drugs, high baseline levels of high-sensitivity CRP and IL-6 were predictive of patient response to infliximab.⁵² In a meta-analysis evaluating 20,791 participants, an association was found between concurrent depression and CRP. Furthermore, inflammation measured by high levels of CRP or IL-6 was observed to predict future depression.⁵³ If the same inflammatory markers—CRP and IL-6—both play a major role in the disease activity of depression and HS, then a concurrent genetic predisposition may exist.

Conclusion

Understanding the comorbidities, etiologies, and risk factors for the development and progression of HS is an important step toward improved disease management. Available studies on comorbid depression in HS largely involve White patients, and more studies are needed in patients with skin of color, particularly the Black population, who have the highest prevalence of HS.¹⁰ Given the evidence for an association between depression and HS, we suggest a large-scale investigation of this patient population that includes a complete medical history, onset of HS in comparison to the onset of depression, and specific measures of disease progress and lifetime management of depression, which may help to increase knowledge about the role of depression in HS and encourage more research in this area. If shared genetic susceptibility is established, aggressive management of depression in patients at risk for HS may reduce disease incidence and severity as well as the psychological burden on patients.

Hidradenitis suppurativa (HS)—a chronic, relapsing, inflammatory disorder involving terminal hair follicles in apocrine gland–rich skin—manifests as tender inflamed nodules that transform into abscesses, sinus tracts, and scarring.^1,2 The etiology of HS is multifactorial, encompassing lifestyle, microbiota, hormonal status, and genetic and environmental factors. These factors activate the immune system around the terminal hair follicles and lead to hyperkeratosis of the infundibulum of the hair follicles in intertriginous regions. This progresses to follicular occlusion, stasis, and eventual rupture. Bacterial multiplication within the plugged pilosebaceous units further boosts immune activation. Resident and migrated cells of the innate and adaptive immune system then release proinflammatory cytokines such as tumor necrosis factor, IL-1β, and IL-17, which further enhance immune cell influx and inflammation.^3,4 This aberrant immune response propagates the production of deep-seated inflammatory nodules and abscesses.^3-8

The estimated prevalence of HS is 1% worldwide.⁹ It is more prevalent in female and Black patients (0.30%) than White patients (0.09%) and is intermediate in prevalence in the biracial population (0.22%).¹⁰ Hidradenitis suppurativa is thought to be associated with lower socioeconomic status (SES). In a retrospective analysis of HS patients (N=375), approximately one-third of patients were Black, had advanced disease, and had a notably lower SES.¹¹ Furthermore, HS has been reported to be associated with systemic inflammation and comorbidities such as morbid obesity (38.3%) and hypertension (39.6%) as well as other metabolic syndrome–related disorders and depression (48.1%).¹

Hidradenitis suppurativa may contribute to the risk for depression through its substantial impact on health-related quality of life, which culminates in social withdrawal, unemployment, and suicidal thoughts.¹² The high prevalence of depression in individuals with HS¹ and its association with systemic inflammation¹³ increases the likelihood that a common genetic predisposition also may exist between both conditions. Because depression frequently has been discovered as a concomitant diagnosis in patients with HS, we hypothesize that a shared genetic susceptibility also may exist between the 2 disorders. Our study sought to explore data on the co-occurrence of depression with HS, including its demographics and racial data.

Methods

We conducted a PubMed search of articles indexed for MEDLINE as well as Google Scholar using the terms depression and hidradenitis suppurativa to obtain all research articles published from 2000 to 2022. Articles were selected based on relevance to the topic of exploration. English-language articles that directly addressed the epidemiology, etiology, pathophysiology, and co-occurrence of both depression and HS with numerical data were included. Articles were excluded if they did not explore the information of interest on these 2 disorders or did not contain clear statistical data of patients with the 2 concurrent medical conditions.

Results

Twenty-two cross-sectional, prospective, and retrospective studies that fit the search criteria were identified and included in the analysis (eTable).^1,14-34 Sixteen (72.7%) studies were cross-sectional, 5 (22.7%) were retrospective, and only 1 (4.5%) was a prospective study. Only 6 of the studies provided racial data,^{1,14,17,26,28,32} and of them, 4 had predominately White patients,^1,14,26,32 whereas the other 2 had predominantly Black patients.^17,28

Hidradenitis suppurativa was found to coexist with depression in all the studies, with a prevalence of 1.2% to 48.1%. There also was a higher prevalence of depression in HS patients than in the control patients without HS. Furthermore, a recent study by Wright and colleagues¹⁴ stratified the depression prevalence data by age and found a higher prevalence of depression in adults vs children with HS (30% vs 12%).

Comment

Major depression—a chronic and debilitating illness—is the chief cause of disability globally and in the United States alone and has a global lifetime prevalence of 17%.³⁵ In a study of 388 patients diagnosed with depression and 404 community-matched controls who were observed for 10 years, depressed patients had a two-thirds higher likelihood of developing a serious physical illness than controls. The depression-associated elevated risk for serious physical illness persisted after controlling for confounding variables such as alcohol abuse, smoking, and level of physical activity.³⁶ Studies also have demonstrated that HS is more prevalent in Black individuals¹⁰ and in individuals of low SES,³⁷ who are mostly the Black and Hispanic populations that experience the highest burden of racial microaggression³⁸ and disparities in health access and outcomes.^39,40 The severity and chronicity of major depressive disorder also is higher in Black patients compared with White patients (57% vs 39%).⁴¹ Because major depression and HS are most common among Black patients who experience the highest-burden negative financial and health disparities, there may be a shared genetic disposition to both medical conditions.

Moreover, the common detrimental lifestyle choices associated with patients with depression and HS also suggest the possibility of a collective genetic susceptibility. Patients with depression also report increased consumption of alcohol, tobacco, and illicit substances; sedentary lifestyle leading to obesity; and poor compliance with prescribed medical treatment.⁴² Smoking and obesity are known contributors to the pathogenesis of HS, and their modification also is known to positively impact the disease course. In a retrospective single-cohort study, 50% of obese HS patients (n=35) reported a substantial decrease in disease severity after a reduction of more than 15% in body mass index over 2 years following bariatric surgery (n=35).⁴³ Patients with HS also have reported disease remission following extensive weight loss.⁴⁴ In addition, evidence has supported smoking cessation in improving the disease course of HS.⁴³ Because these detrimental lifestyle choices are prevalent in both patients with HS and those with depression, a co-genetic susceptibility also may exist.

Furthermore, depression is characterized by a persistent inflammatory state,^13,45 similar to HS.⁴⁶ Elevated levels of a variety of inflammatory markers, such as C-reactive protein (CRP), IL-6, and soluble intercellular adhesion molecule 1, have been reported in patients with depression compared with healthy controls.^13,45 Further analysis found a positive correlation and a strong association between depression and these inflammatory markers.⁴⁷ Moreover, adipokines regulate inflammatory responses, and adipokines play a role in the pathogenesis of HS. Adipokine levels such as elevated omentin-1 (a recently identified adipokine) were found to be altered in patients with HS compared with controls.⁴⁸ Results from clinical studies and meta-analyses of patients with depression also have demonstrated that adipokines are dysregulated in this population,^49,50 which may be another potential genetic link between depression and HS.

In addition, genetic susceptibility to depression and HS may be shared because the inflammatory markers that have a strong association with depression also have been found to play an important role in HS treatment and disease severity prediction. In a retrospective cohort study of 404 patients, CRP or IL-6 levels were found to be reliable predictors of HS disease severity, which may explain why anti–tumor necrosis factor antibody regimens such as adalimumab and infliximab have clinically ameliorated disease activity in several cases of HS.⁵¹ In a study evaluating these drugs, high baseline levels of high-sensitivity CRP and IL-6 were predictive of patient response to infliximab.⁵² In a meta-analysis evaluating 20,791 participants, an association was found between concurrent depression and CRP. Furthermore, inflammation measured by high levels of CRP or IL-6 was observed to predict future depression.⁵³ If the same inflammatory markers—CRP and IL-6—both play a major role in the disease activity of depression and HS, then a concurrent genetic predisposition may exist.

Conclusion

Understanding the comorbidities, etiologies, and risk factors for the development and progression of HS is an important step toward improved disease management. Available studies on comorbid depression in HS largely involve White patients, and more studies are needed in patients with skin of color, particularly the Black population, who have the highest prevalence of HS.¹⁰ Given the evidence for an association between depression and HS, we suggest a large-scale investigation of this patient population that includes a complete medical history, onset of HS in comparison to the onset of depression, and specific measures of disease progress and lifetime management of depression, which may help to increase knowledge about the role of depression in HS and encourage more research in this area. If shared genetic susceptibility is established, aggressive management of depression in patients at risk for HS may reduce disease incidence and severity as well as the psychological burden on patients.

With the introduction of the first US Food and Drug Administration (FDA)–approved medication for alopecia areata (AA)—the Janus kinase (JAK) inhibitor, baricitinib—there is an important focus on this disease in the literature and for practicing dermatologists. Known by all as an autoimmune genetic disease that causes relapsing and remitting nonscarring hair loss, AA is a condition where the psychological burden has been less widely recognized. Patients with AA have reported lower health-related quality of life scores compared to patients with other skin conditions, including psoriasis or atopic dermatitis. In addition, a lesser amount of scalp coverage is negatively correlated to health-related quality of life scores.¹ Patients with AA also have a 39% lifetime prevalence of major depressive disorder and generalized anxiety disorder.² The treatment of AA has been a hodgepodge of topical, intralesional, and systemic agents, all with indirect immunosuppressive or anagen prolongation effects. Now that there is an approved therapy for AA with more treatments likely to be approved in the near future, there must be a focus on real-world outcomes. With the dawn of a new era in the treatment of AA as well as new information showcasing an altered prevalence of AA in skin of color, highlighting disparities among this population may help ease challenges dermatologic providers will face.

Efficacy of Baricitinib in Different Races and Ethnicities

How will patients of different races and ethnicities respond to this new treatment, and how will their emotional health be affected? The 2 phase 3 pivotal trials showing efficacy of baricitinib in AA included Black and Latino patients but not in a way that is representative of the US population.³ Until recently, the most commonly used prevalence of AA in the United States was from the NHANES I study completed between 1971 and 1974, which was between 0.1% and 0.2%⁴ with minimal focus on race and ethnicity. Recent studies suggest that there may be increased prevalence of this condition in Black patients in the United States. These new findings raise concern around access to care and treatment and the need to tailor psychosocial interventions for populations that may not currently have these supports.

A large cross-sectional study published in 2020 demonstrated that these data remained similar, with a lifetime prevalence of 0.21%.⁵ Of the 45,016 participants—representative of the US population based on the 2015 US Census—the average age of AA patients was 41.2 years, with 61.3% being White and not of Hispanic origin.⁵ In recent years, other studies have challenged the narrative that AA predominantly affects White patients.^6-8 A different cross-sectional study utilizing National Alopecia Areata Registry data from 2002 to 2016 suggested that Black patients have greater odds of developing AA.⁶ In this study of 2645 cases of AA, the odds ratios of developing the condition were 1.36 for Blacks, 0.53 for Asians, and 0.83 for Hispanics compared with the referent White population. These results were consistent through the varying subtypes of AA.⁶ In a reply to these findings, Gonzalez and Fleischer⁷ analyzed data from the 2007 to 2016 National Ambulatory Medical Care Survey database with a focus on racial and ethnic prevalence of AA. This study concluded that Latino and non-White individuals had an increased likelihood of clinician visits for AA compared with White individuals.⁷

More evidence of the Black predominance of AA was demonstrated in a study published in 2018. In this large-scale study, 63,960 women from the Nurses’ Health Study (NHS) and 88,368 women from the Nurses’ Health Study II (NHSII) were included to examine prevalence of disease among these US women.⁸ Analysis showed increased odds of AA based on self-reported race in Black and Hispanic women. Lifetime incidence of AA was greater in Black women, with 2.63 and 5.23 in NHS and NHSII, respectively. It was hypothesized that hairstyling practices in Black and Hispanic women may cause AA to be more noticeable,⁸ which may drive patients to seek medical evaluation.

Feaster and McMichael⁹ published information on the epidemiology of AA in a busy hair loss clinic. This retrospective single-institution study of 265 pediatric and adult Black patients with AA seen over a 5-year period showed that patients aged 18 to 34 years were most likely to present for care, which accounted for 35.8% of the study population, followed by patients aged 10 to 17 years, which accounted for 15.1%. This study also found that females were the larger segment of AA patients, with an increased distribution of disease in young patients. Most of these patients (68.2%) had patchy hair loss, and the ophiasis pattern was seen in 15.1%.⁹ Although the pathogenesis of AA is linked to autoimmunity,¹⁰ the leading cause for these epidemiologic findings of increased prevalence in Black patients is still uncertain.

Baricitinib for AA

In June 2022, the FDA announced the first biologic drug approved for the treatment of AA—baricitinib. Baricitinib is an oral, selective, reversible inhibitor of JAK1 and JAK2.³ The phase 3 trials for baricitinib—BRAVE-AA1 (N=654) and BRAVE-AA2 (N=546)—were conducted between March 2019 and May 2020. In these double-blind, parallel-group, randomized, placebo-controlled trials, 33% of the patient population receiving baricitinib accomplished 80% or more scalp coverage at 36 weeks. The Severity of Alopecia Tool (SALT) score also decreased to 20 or less in 36 weeks. The BRAVE-AA1 and BRAVE-AA2 trials consisted of a total of 1200 patients, with only 98 identifying as Black. Of these 98 patients, 33 were randomly selected to receive placebo.³ With studies now suggesting that Black individuals have greater odds of AA compared with White individuals⁶ and Black patients being more likely to seek medical care for AA,⁷ the BRAVE-AA1 and BRAVE-AA2 study population did not allow for significant comparative data for Black patients. These studies did not document Latino patient involvement.³ Future studies in AA must recruit a diversified group of study participants to better reflect the patients with an increased likelihood of presenting with AA.

Other Treatments on the Horizon

Baricitinib likely will remain alone in its class for only a short time. Phase 3 trials have been completed for ritlecitinib, brepocitinib, and deuruxolitinib for AA. Ritlecitinib, an irreversible inhibitor of JAK3 and the tyrosine kinase expressed in hepatocellular carcinoma (TEC) kinase family, has met all end points in a phase 2b/3 study.¹¹ Brepocitinib is an oral tyrosine kinase 2/JAK1 inhibitor,¹² and deuruxolitinib is an investigational JAK1/2 inhibitor for AA.¹³

Prior authorizations have been the initial step for many drugs in varying fields of medical practice. A study completed in 2016 suggested that insurance coverage for biologics used in the treatment of psoriasis was becoming increasingly difficult.¹⁴ Prior authorization requirement rates increased from 16% of patients in 2009 to 75% in 2014. The decision time also increased from 3.7 days in 2009 to 6.7 days in 2014. The most common reason for delay in decisions and denials was due to step therapy.¹⁴ Insurance companies wanted many patients to try less expensive treatment options prior to “stepping up” to more expensive treatments. Although this may be the case in the treatment of psoriasis, the role of step therapy is unclear for patients with AA because there is only 1 FDA-approved medication. This sets out an ambiguous future for our patients with AA and approval for baricitinib.

The time required for the correspondence between insurance companies, clinic staff, and patients for drug approval may delay treatments, and not all providers have enough staff to coordinate and perform this work. For Black patients, who may present more frequently and with more severe disease,⁷ this could lead to a health care disparity due to the likelihood of the increased need for biologic treatment. Because Black patients have an increased likelihood of being uninsured or underinsured,¹⁵ this further decreases the chances of the most severe AA patients receiving the most helpful medication for their condition.

Many pharmaceutical companies have drug cost assistance programs that aim to provide support covering expensive medications for patients unable to afford them. Although this is a good first step, treatment with any JAK inhibitor potentially can be lifelong. Regarding the social determinants of health, it is known that access to medications does not solely depend on cost. Transportation and access to qualified health professionals are among the issues that create barriers to health care. Instilling long-term practices to ensure equal access to JAK inhibitors and treatment of AA may be the cornerstone to treating AA with equity. Whether we require pharmaceutical companies to make sure all patients have equal access to medications or provide community resources to hairstylists and federally qualified health centers, raising awareness and advocating for and creating attainable access to treatment modalities is imperative to providing well-rounded care to a diverse population.

With the introduction of the first US Food and Drug Administration (FDA)–approved medication for alopecia areata (AA)—the Janus kinase (JAK) inhibitor, baricitinib—there is an important focus on this disease in the literature and for practicing dermatologists. Known by all as an autoimmune genetic disease that causes relapsing and remitting nonscarring hair loss, AA is a condition where the psychological burden has been less widely recognized. Patients with AA have reported lower health-related quality of life scores compared to patients with other skin conditions, including psoriasis or atopic dermatitis. In addition, a lesser amount of scalp coverage is negatively correlated to health-related quality of life scores.¹ Patients with AA also have a 39% lifetime prevalence of major depressive disorder and generalized anxiety disorder.² The treatment of AA has been a hodgepodge of topical, intralesional, and systemic agents, all with indirect immunosuppressive or anagen prolongation effects. Now that there is an approved therapy for AA with more treatments likely to be approved in the near future, there must be a focus on real-world outcomes. With the dawn of a new era in the treatment of AA as well as new information showcasing an altered prevalence of AA in skin of color, highlighting disparities among this population may help ease challenges dermatologic providers will face.

Efficacy of Baricitinib in Different Races and Ethnicities

How will patients of different races and ethnicities respond to this new treatment, and how will their emotional health be affected? The 2 phase 3 pivotal trials showing efficacy of baricitinib in AA included Black and Latino patients but not in a way that is representative of the US population.³ Until recently, the most commonly used prevalence of AA in the United States was from the NHANES I study completed between 1971 and 1974, which was between 0.1% and 0.2%⁴ with minimal focus on race and ethnicity. Recent studies suggest that there may be increased prevalence of this condition in Black patients in the United States. These new findings raise concern around access to care and treatment and the need to tailor psychosocial interventions for populations that may not currently have these supports.

A large cross-sectional study published in 2020 demonstrated that these data remained similar, with a lifetime prevalence of 0.21%.⁵ Of the 45,016 participants—representative of the US population based on the 2015 US Census—the average age of AA patients was 41.2 years, with 61.3% being White and not of Hispanic origin.⁵ In recent years, other studies have challenged the narrative that AA predominantly affects White patients.^6-8 A different cross-sectional study utilizing National Alopecia Areata Registry data from 2002 to 2016 suggested that Black patients have greater odds of developing AA.⁶ In this study of 2645 cases of AA, the odds ratios of developing the condition were 1.36 for Blacks, 0.53 for Asians, and 0.83 for Hispanics compared with the referent White population. These results were consistent through the varying subtypes of AA.⁶ In a reply to these findings, Gonzalez and Fleischer⁷ analyzed data from the 2007 to 2016 National Ambulatory Medical Care Survey database with a focus on racial and ethnic prevalence of AA. This study concluded that Latino and non-White individuals had an increased likelihood of clinician visits for AA compared with White individuals.⁷

More evidence of the Black predominance of AA was demonstrated in a study published in 2018. In this large-scale study, 63,960 women from the Nurses’ Health Study (NHS) and 88,368 women from the Nurses’ Health Study II (NHSII) were included to examine prevalence of disease among these US women.⁸ Analysis showed increased odds of AA based on self-reported race in Black and Hispanic women. Lifetime incidence of AA was greater in Black women, with 2.63 and 5.23 in NHS and NHSII, respectively. It was hypothesized that hairstyling practices in Black and Hispanic women may cause AA to be more noticeable,⁸ which may drive patients to seek medical evaluation.

Feaster and McMichael⁹ published information on the epidemiology of AA in a busy hair loss clinic. This retrospective single-institution study of 265 pediatric and adult Black patients with AA seen over a 5-year period showed that patients aged 18 to 34 years were most likely to present for care, which accounted for 35.8% of the study population, followed by patients aged 10 to 17 years, which accounted for 15.1%. This study also found that females were the larger segment of AA patients, with an increased distribution of disease in young patients. Most of these patients (68.2%) had patchy hair loss, and the ophiasis pattern was seen in 15.1%.⁹ Although the pathogenesis of AA is linked to autoimmunity,¹⁰ the leading cause for these epidemiologic findings of increased prevalence in Black patients is still uncertain.

Baricitinib for AA

In June 2022, the FDA announced the first biologic drug approved for the treatment of AA—baricitinib. Baricitinib is an oral, selective, reversible inhibitor of JAK1 and JAK2.³ The phase 3 trials for baricitinib—BRAVE-AA1 (N=654) and BRAVE-AA2 (N=546)—were conducted between March 2019 and May 2020. In these double-blind, parallel-group, randomized, placebo-controlled trials, 33% of the patient population receiving baricitinib accomplished 80% or more scalp coverage at 36 weeks. The Severity of Alopecia Tool (SALT) score also decreased to 20 or less in 36 weeks. The BRAVE-AA1 and BRAVE-AA2 trials consisted of a total of 1200 patients, with only 98 identifying as Black. Of these 98 patients, 33 were randomly selected to receive placebo.³ With studies now suggesting that Black individuals have greater odds of AA compared with White individuals⁶ and Black patients being more likely to seek medical care for AA,⁷ the BRAVE-AA1 and BRAVE-AA2 study population did not allow for significant comparative data for Black patients. These studies did not document Latino patient involvement.³ Future studies in AA must recruit a diversified group of study participants to better reflect the patients with an increased likelihood of presenting with AA.

Other Treatments on the Horizon

Baricitinib likely will remain alone in its class for only a short time. Phase 3 trials have been completed for ritlecitinib, brepocitinib, and deuruxolitinib for AA. Ritlecitinib, an irreversible inhibitor of JAK3 and the tyrosine kinase expressed in hepatocellular carcinoma (TEC) kinase family, has met all end points in a phase 2b/3 study.¹¹ Brepocitinib is an oral tyrosine kinase 2/JAK1 inhibitor,¹² and deuruxolitinib is an investigational JAK1/2 inhibitor for AA.¹³

Prior authorizations have been the initial step for many drugs in varying fields of medical practice. A study completed in 2016 suggested that insurance coverage for biologics used in the treatment of psoriasis was becoming increasingly difficult.¹⁴ Prior authorization requirement rates increased from 16% of patients in 2009 to 75% in 2014. The decision time also increased from 3.7 days in 2009 to 6.7 days in 2014. The most common reason for delay in decisions and denials was due to step therapy.¹⁴ Insurance companies wanted many patients to try less expensive treatment options prior to “stepping up” to more expensive treatments. Although this may be the case in the treatment of psoriasis, the role of step therapy is unclear for patients with AA because there is only 1 FDA-approved medication. This sets out an ambiguous future for our patients with AA and approval for baricitinib.

The time required for the correspondence between insurance companies, clinic staff, and patients for drug approval may delay treatments, and not all providers have enough staff to coordinate and perform this work. For Black patients, who may present more frequently and with more severe disease,⁷ this could lead to a health care disparity due to the likelihood of the increased need for biologic treatment. Because Black patients have an increased likelihood of being uninsured or underinsured,¹⁵ this further decreases the chances of the most severe AA patients receiving the most helpful medication for their condition.

Many pharmaceutical companies have drug cost assistance programs that aim to provide support covering expensive medications for patients unable to afford them. Although this is a good first step, treatment with any JAK inhibitor potentially can be lifelong. Regarding the social determinants of health, it is known that access to medications does not solely depend on cost. Transportation and access to qualified health professionals are among the issues that create barriers to health care. Instilling long-term practices to ensure equal access to JAK inhibitors and treatment of AA may be the cornerstone to treating AA with equity. Whether we require pharmaceutical companies to make sure all patients have equal access to medications or provide community resources to hairstylists and federally qualified health centers, raising awareness and advocating for and creating attainable access to treatment modalities is imperative to providing well-rounded care to a diverse population.

With the introduction of the first US Food and Drug Administration (FDA)–approved medication for alopecia areata (AA)—the Janus kinase (JAK) inhibitor, baricitinib—there is an important focus on this disease in the literature and for practicing dermatologists. Known by all as an autoimmune genetic disease that causes relapsing and remitting nonscarring hair loss, AA is a condition where the psychological burden has been less widely recognized. Patients with AA have reported lower health-related quality of life scores compared to patients with other skin conditions, including psoriasis or atopic dermatitis. In addition, a lesser amount of scalp coverage is negatively correlated to health-related quality of life scores.¹ Patients with AA also have a 39% lifetime prevalence of major depressive disorder and generalized anxiety disorder.² The treatment of AA has been a hodgepodge of topical, intralesional, and systemic agents, all with indirect immunosuppressive or anagen prolongation effects. Now that there is an approved therapy for AA with more treatments likely to be approved in the near future, there must be a focus on real-world outcomes. With the dawn of a new era in the treatment of AA as well as new information showcasing an altered prevalence of AA in skin of color, highlighting disparities among this population may help ease challenges dermatologic providers will face.

Efficacy of Baricitinib in Different Races and Ethnicities

How will patients of different races and ethnicities respond to this new treatment, and how will their emotional health be affected? The 2 phase 3 pivotal trials showing efficacy of baricitinib in AA included Black and Latino patients but not in a way that is representative of the US population.³ Until recently, the most commonly used prevalence of AA in the United States was from the NHANES I study completed between 1971 and 1974, which was between 0.1% and 0.2%⁴ with minimal focus on race and ethnicity. Recent studies suggest that there may be increased prevalence of this condition in Black patients in the United States. These new findings raise concern around access to care and treatment and the need to tailor psychosocial interventions for populations that may not currently have these supports.

A large cross-sectional study published in 2020 demonstrated that these data remained similar, with a lifetime prevalence of 0.21%.⁵ Of the 45,016 participants—representative of the US population based on the 2015 US Census—the average age of AA patients was 41.2 years, with 61.3% being White and not of Hispanic origin.⁵ In recent years, other studies have challenged the narrative that AA predominantly affects White patients.^6-8 A different cross-sectional study utilizing National Alopecia Areata Registry data from 2002 to 2016 suggested that Black patients have greater odds of developing AA.⁶ In this study of 2645 cases of AA, the odds ratios of developing the condition were 1.36 for Blacks, 0.53 for Asians, and 0.83 for Hispanics compared with the referent White population. These results were consistent through the varying subtypes of AA.⁶ In a reply to these findings, Gonzalez and Fleischer⁷ analyzed data from the 2007 to 2016 National Ambulatory Medical Care Survey database with a focus on racial and ethnic prevalence of AA. This study concluded that Latino and non-White individuals had an increased likelihood of clinician visits for AA compared with White individuals.⁷

More evidence of the Black predominance of AA was demonstrated in a study published in 2018. In this large-scale study, 63,960 women from the Nurses’ Health Study (NHS) and 88,368 women from the Nurses’ Health Study II (NHSII) were included to examine prevalence of disease among these US women.⁸ Analysis showed increased odds of AA based on self-reported race in Black and Hispanic women. Lifetime incidence of AA was greater in Black women, with 2.63 and 5.23 in NHS and NHSII, respectively. It was hypothesized that hairstyling practices in Black and Hispanic women may cause AA to be more noticeable,⁸ which may drive patients to seek medical evaluation.

Feaster and McMichael⁹ published information on the epidemiology of AA in a busy hair loss clinic. This retrospective single-institution study of 265 pediatric and adult Black patients with AA seen over a 5-year period showed that patients aged 18 to 34 years were most likely to present for care, which accounted for 35.8% of the study population, followed by patients aged 10 to 17 years, which accounted for 15.1%. This study also found that females were the larger segment of AA patients, with an increased distribution of disease in young patients. Most of these patients (68.2%) had patchy hair loss, and the ophiasis pattern was seen in 15.1%.⁹ Although the pathogenesis of AA is linked to autoimmunity,¹⁰ the leading cause for these epidemiologic findings of increased prevalence in Black patients is still uncertain.

Baricitinib for AA

In June 2022, the FDA announced the first biologic drug approved for the treatment of AA—baricitinib. Baricitinib is an oral, selective, reversible inhibitor of JAK1 and JAK2.³ The phase 3 trials for baricitinib—BRAVE-AA1 (N=654) and BRAVE-AA2 (N=546)—were conducted between March 2019 and May 2020. In these double-blind, parallel-group, randomized, placebo-controlled trials, 33% of the patient population receiving baricitinib accomplished 80% or more scalp coverage at 36 weeks. The Severity of Alopecia Tool (SALT) score also decreased to 20 or less in 36 weeks. The BRAVE-AA1 and BRAVE-AA2 trials consisted of a total of 1200 patients, with only 98 identifying as Black. Of these 98 patients, 33 were randomly selected to receive placebo.³ With studies now suggesting that Black individuals have greater odds of AA compared with White individuals⁶ and Black patients being more likely to seek medical care for AA,⁷ the BRAVE-AA1 and BRAVE-AA2 study population did not allow for significant comparative data for Black patients. These studies did not document Latino patient involvement.³ Future studies in AA must recruit a diversified group of study participants to better reflect the patients with an increased likelihood of presenting with AA.

Other Treatments on the Horizon

Baricitinib likely will remain alone in its class for only a short time. Phase 3 trials have been completed for ritlecitinib, brepocitinib, and deuruxolitinib for AA. Ritlecitinib, an irreversible inhibitor of JAK3 and the tyrosine kinase expressed in hepatocellular carcinoma (TEC) kinase family, has met all end points in a phase 2b/3 study.¹¹ Brepocitinib is an oral tyrosine kinase 2/JAK1 inhibitor,¹² and deuruxolitinib is an investigational JAK1/2 inhibitor for AA.¹³

Prior authorizations have been the initial step for many drugs in varying fields of medical practice. A study completed in 2016 suggested that insurance coverage for biologics used in the treatment of psoriasis was becoming increasingly difficult.¹⁴ Prior authorization requirement rates increased from 16% of patients in 2009 to 75% in 2014. The decision time also increased from 3.7 days in 2009 to 6.7 days in 2014. The most common reason for delay in decisions and denials was due to step therapy.¹⁴ Insurance companies wanted many patients to try less expensive treatment options prior to “stepping up” to more expensive treatments. Although this may be the case in the treatment of psoriasis, the role of step therapy is unclear for patients with AA because there is only 1 FDA-approved medication. This sets out an ambiguous future for our patients with AA and approval for baricitinib.

The time required for the correspondence between insurance companies, clinic staff, and patients for drug approval may delay treatments, and not all providers have enough staff to coordinate and perform this work. For Black patients, who may present more frequently and with more severe disease,⁷ this could lead to a health care disparity due to the likelihood of the increased need for biologic treatment. Because Black patients have an increased likelihood of being uninsured or underinsured,¹⁵ this further decreases the chances of the most severe AA patients receiving the most helpful medication for their condition.

Many pharmaceutical companies have drug cost assistance programs that aim to provide support covering expensive medications for patients unable to afford them. Although this is a good first step, treatment with any JAK inhibitor potentially can be lifelong. Regarding the social determinants of health, it is known that access to medications does not solely depend on cost. Transportation and access to qualified health professionals are among the issues that create barriers to health care. Instilling long-term practices to ensure equal access to JAK inhibitors and treatment of AA may be the cornerstone to treating AA with equity. Whether we require pharmaceutical companies to make sure all patients have equal access to medications or provide community resources to hairstylists and federally qualified health centers, raising awareness and advocating for and creating attainable access to treatment modalities is imperative to providing well-rounded care to a diverse population.

Airbags are lifesaving during motor vehicle accidents (MVAs), but their deployment has been associated with skin issues such as irritant dermatitis¹; lacerations²; abrasions³; and thermal, friction, and chemical burns.^4-6 Ocular issues such as alkaline chemical keratitis⁷ and ocular alkali injuries⁸ also have been described.

Airbag deployment is triggered by rapid deceleration and impact, which ignite a sodium azide cartridge, causing the woven nylon bag to inflate with hydrocarbon gases.⁸ This leads to release of sodium hydroxide, sodium bicarbonate, and metallic oxides in an aerosolized form. If a tear in the meshwork of the airbag occurs, exposure to an even larger amount of powder containing caustic alkali chemicals can occur.⁸

We describe a patient who developed a bullous reaction to airbag contents after he was involved in an MVA in which the airbag deployed.

Case Report

A 35-year-old man with a history of type 2 diabetes mellitus and chronic hepatitis B presented to the dermatology clinic for an evaluation of new-onset blisters. The rash occurred 1 day after the patient was involved in an MVA in which he was exposed to the airbag’s contents after it burst. He had been evaluated twice in the emergency department for the skin eruption before being referred to dermatology. He noted the lesions were pruritic and painful. Prior treatments included silver sulfadiazine cream 1% and clobetasol cream 0.05%, though he discontinued using the latter because of burning with application. Physical examination revealed tense vesicles and bullae on an erythematous base on the right lower flank, forearms, and legs, with the exception of the lower right leg where a cast had been from a prior injury (Figure 1).

Two punch biopsies of the left arm were performed and sent for hematoxylin and eosin staining and direct immunofluorescence to rule out bullous diseases, such as bullous pemphigoid, linear IgA, and bullous lupus. Hematoxylin and eosin staining revealed extensive spongiosis with blister formation and a dense perivascular infiltrate in the superficial and mid dermis composed of lymphocytes with numerous scattered eosinophils (Figures 2 and 3). Direct immunofluorescence studies were negative. Treatment with oral prednisone and oral antihistamines was initiated.

At 10-day follow-up, the patient had a few residual bullae; most lesions were demonstrating various stages of healing (Figure 4). The patient’s cast had been removed, and there were no lesions in this previously covered area. At 6-week follow-up he had continued healing of the bullae and erosions as well as postinflammatory hyperpigmentation (Figure 5).

Comment

With the advent of airbags for safety purposes, these potentially lifesaving devices also have been known to cause injury.⁹ In 1998, the most commonly reported airbag injuries were ocular injuries.¹⁰ Cutaneous manifestations of airbag injury are less well known.¹¹

Two cases of airbag deployment with skin blistering have been reported in the literature based on a PubMed search of articles indexed for MEDLINE using the terms airbag blistering or airbag bullae^12,13; however, the blistering was described in the context of a burn. One case of the effects of airbag deployment residue highlights a patient arriving to the emergency department with erythema and blisters on the hands within 48 hours of airbag deployment in an MVA, and the treatment was standard burn therapy.¹² Another case report described a patient with a second-degree burn with a 12-cm blister occurring on the radial side of the hand and distal forearm following an MVA and airbag deployment, which was treated conservatively.¹³ Cases of thermal burns, chemical burns, and irritant contact dermatitis after airbag deployment have been described in the literature.^{4-6,11,12,14,15} Our patient’s distal right lower leg was covered with a cast for osteomyelitis, and no blisters had developed in this area. It is likely that the transfer of airbag contents occurred during the process of unbuckling his seatbelt, which could explain the bullae that developed on the right flank. Per the Centers for Disease Control and Prevention, individuals should quickly remove clothing and wash their body with large amounts of soap and water following exposure to sodium azide.¹⁶

In 1989, the Federal Motor Vehicle Safety Standard No. 208 (occupant crash protection) became effective, stating all cars must have vehicle crash protection.¹² Prior to 1993, it was reported that there had been no associated chemical injuries with airbag deployment. Subsequently, a 6-month retrospective study in 1993 showed that dermal injuries were found in connection with the presence of sodium hydroxide in automobile airbags.¹² By 2004, it was known that airbags could cause chemical and thermal burns in addition to traumatic injuries from deployment.¹ Since 2007, all motor vehicles have been required to have advanced airbags, which are engineered to sense the presence of passengers and determine if the airbag will deploy, and if so, how much to deploy to minimize airbag-related injury.³

The brand of car that our patient drove during the MVA is one with known airbag recalls due to safety defects; however, the year and actual model of the vehicle are not known, so specific information about the airbag in question is not available. It has been noted that some defective airbag inflators that were exposed to excess moisture during the manufacturing process could explode during deployment, causing shrapnel and airbag rupture, which has been linked to nearly 300 injuries worldwide.¹⁷

Conclusion

It is evident that the use of airbag devices reduces morbidity and mortality due to MVAs.⁹ It also had been reported that up to 96% of airbag-related injuries are relatively minor, which many would argue justifies their use.¹⁸ Furthermore, it has been reported that 99.8% of skin injuries following airbag deployment are minor.¹⁹ In the United States, it is mandated that every vehicle have functional airbags installed.⁸

This case highlights the potential for substantial airbag-induced skin reactions, specifically a bullous reaction, following airbag deployment. The persistent pruritus and lasting postinflammatory hyperpigmentation seen in this case were certainly worrisome for our patient. We also present this case to remind dermatology providers of possible treatment approaches to these skin reactions. Immediate cleansing of the affected areas of skin may help avoid such reactions.

Airbags are lifesaving during motor vehicle accidents (MVAs), but their deployment has been associated with skin issues such as irritant dermatitis¹; lacerations²; abrasions³; and thermal, friction, and chemical burns.^4-6 Ocular issues such as alkaline chemical keratitis⁷ and ocular alkali injuries⁸ also have been described.

Airbag deployment is triggered by rapid deceleration and impact, which ignite a sodium azide cartridge, causing the woven nylon bag to inflate with hydrocarbon gases.⁸ This leads to release of sodium hydroxide, sodium bicarbonate, and metallic oxides in an aerosolized form. If a tear in the meshwork of the airbag occurs, exposure to an even larger amount of powder containing caustic alkali chemicals can occur.⁸

We describe a patient who developed a bullous reaction to airbag contents after he was involved in an MVA in which the airbag deployed.

Case Report

A 35-year-old man with a history of type 2 diabetes mellitus and chronic hepatitis B presented to the dermatology clinic for an evaluation of new-onset blisters. The rash occurred 1 day after the patient was involved in an MVA in which he was exposed to the airbag’s contents after it burst. He had been evaluated twice in the emergency department for the skin eruption before being referred to dermatology. He noted the lesions were pruritic and painful. Prior treatments included silver sulfadiazine cream 1% and clobetasol cream 0.05%, though he discontinued using the latter because of burning with application. Physical examination revealed tense vesicles and bullae on an erythematous base on the right lower flank, forearms, and legs, with the exception of the lower right leg where a cast had been from a prior injury (Figure 1).

Two punch biopsies of the left arm were performed and sent for hematoxylin and eosin staining and direct immunofluorescence to rule out bullous diseases, such as bullous pemphigoid, linear IgA, and bullous lupus. Hematoxylin and eosin staining revealed extensive spongiosis with blister formation and a dense perivascular infiltrate in the superficial and mid dermis composed of lymphocytes with numerous scattered eosinophils (Figures 2 and 3). Direct immunofluorescence studies were negative. Treatment with oral prednisone and oral antihistamines was initiated.

At 10-day follow-up, the patient had a few residual bullae; most lesions were demonstrating various stages of healing (Figure 4). The patient’s cast had been removed, and there were no lesions in this previously covered area. At 6-week follow-up he had continued healing of the bullae and erosions as well as postinflammatory hyperpigmentation (Figure 5).

Comment

With the advent of airbags for safety purposes, these potentially lifesaving devices also have been known to cause injury.⁹ In 1998, the most commonly reported airbag injuries were ocular injuries.¹⁰ Cutaneous manifestations of airbag injury are less well known.¹¹

Two cases of airbag deployment with skin blistering have been reported in the literature based on a PubMed search of articles indexed for MEDLINE using the terms airbag blistering or airbag bullae^12,13; however, the blistering was described in the context of a burn. One case of the effects of airbag deployment residue highlights a patient arriving to the emergency department with erythema and blisters on the hands within 48 hours of airbag deployment in an MVA, and the treatment was standard burn therapy.¹² Another case report described a patient with a second-degree burn with a 12-cm blister occurring on the radial side of the hand and distal forearm following an MVA and airbag deployment, which was treated conservatively.¹³ Cases of thermal burns, chemical burns, and irritant contact dermatitis after airbag deployment have been described in the literature.^{4-6,11,12,14,15} Our patient’s distal right lower leg was covered with a cast for osteomyelitis, and no blisters had developed in this area. It is likely that the transfer of airbag contents occurred during the process of unbuckling his seatbelt, which could explain the bullae that developed on the right flank. Per the Centers for Disease Control and Prevention, individuals should quickly remove clothing and wash their body with large amounts of soap and water following exposure to sodium azide.¹⁶

In 1989, the Federal Motor Vehicle Safety Standard No. 208 (occupant crash protection) became effective, stating all cars must have vehicle crash protection.¹² Prior to 1993, it was reported that there had been no associated chemical injuries with airbag deployment. Subsequently, a 6-month retrospective study in 1993 showed that dermal injuries were found in connection with the presence of sodium hydroxide in automobile airbags.¹² By 2004, it was known that airbags could cause chemical and thermal burns in addition to traumatic injuries from deployment.¹ Since 2007, all motor vehicles have been required to have advanced airbags, which are engineered to sense the presence of passengers and determine if the airbag will deploy, and if so, how much to deploy to minimize airbag-related injury.³

The brand of car that our patient drove during the MVA is one with known airbag recalls due to safety defects; however, the year and actual model of the vehicle are not known, so specific information about the airbag in question is not available. It has been noted that some defective airbag inflators that were exposed to excess moisture during the manufacturing process could explode during deployment, causing shrapnel and airbag rupture, which has been linked to nearly 300 injuries worldwide.¹⁷

Conclusion

It is evident that the use of airbag devices reduces morbidity and mortality due to MVAs.⁹ It also had been reported that up to 96% of airbag-related injuries are relatively minor, which many would argue justifies their use.¹⁸ Furthermore, it has been reported that 99.8% of skin injuries following airbag deployment are minor.¹⁹ In the United States, it is mandated that every vehicle have functional airbags installed.⁸

This case highlights the potential for substantial airbag-induced skin reactions, specifically a bullous reaction, following airbag deployment. The persistent pruritus and lasting postinflammatory hyperpigmentation seen in this case were certainly worrisome for our patient. We also present this case to remind dermatology providers of possible treatment approaches to these skin reactions. Immediate cleansing of the affected areas of skin may help avoid such reactions.

Airbags are lifesaving during motor vehicle accidents (MVAs), but their deployment has been associated with skin issues such as irritant dermatitis¹; lacerations²; abrasions³; and thermal, friction, and chemical burns.^4-6 Ocular issues such as alkaline chemical keratitis⁷ and ocular alkali injuries⁸ also have been described.

Airbag deployment is triggered by rapid deceleration and impact, which ignite a sodium azide cartridge, causing the woven nylon bag to inflate with hydrocarbon gases.⁸ This leads to release of sodium hydroxide, sodium bicarbonate, and metallic oxides in an aerosolized form. If a tear in the meshwork of the airbag occurs, exposure to an even larger amount of powder containing caustic alkali chemicals can occur.⁸

We describe a patient who developed a bullous reaction to airbag contents after he was involved in an MVA in which the airbag deployed.

Case Report

A 35-year-old man with a history of type 2 diabetes mellitus and chronic hepatitis B presented to the dermatology clinic for an evaluation of new-onset blisters. The rash occurred 1 day after the patient was involved in an MVA in which he was exposed to the airbag’s contents after it burst. He had been evaluated twice in the emergency department for the skin eruption before being referred to dermatology. He noted the lesions were pruritic and painful. Prior treatments included silver sulfadiazine cream 1% and clobetasol cream 0.05%, though he discontinued using the latter because of burning with application. Physical examination revealed tense vesicles and bullae on an erythematous base on the right lower flank, forearms, and legs, with the exception of the lower right leg where a cast had been from a prior injury (Figure 1).

Two punch biopsies of the left arm were performed and sent for hematoxylin and eosin staining and direct immunofluorescence to rule out bullous diseases, such as bullous pemphigoid, linear IgA, and bullous lupus. Hematoxylin and eosin staining revealed extensive spongiosis with blister formation and a dense perivascular infiltrate in the superficial and mid dermis composed of lymphocytes with numerous scattered eosinophils (Figures 2 and 3). Direct immunofluorescence studies were negative. Treatment with oral prednisone and oral antihistamines was initiated.

At 10-day follow-up, the patient had a few residual bullae; most lesions were demonstrating various stages of healing (Figure 4). The patient’s cast had been removed, and there were no lesions in this previously covered area. At 6-week follow-up he had continued healing of the bullae and erosions as well as postinflammatory hyperpigmentation (Figure 5).

Comment

With the advent of airbags for safety purposes, these potentially lifesaving devices also have been known to cause injury.⁹ In 1998, the most commonly reported airbag injuries were ocular injuries.¹⁰ Cutaneous manifestations of airbag injury are less well known.¹¹

Two cases of airbag deployment with skin blistering have been reported in the literature based on a PubMed search of articles indexed for MEDLINE using the terms airbag blistering or airbag bullae^12,13; however, the blistering was described in the context of a burn. One case of the effects of airbag deployment residue highlights a patient arriving to the emergency department with erythema and blisters on the hands within 48 hours of airbag deployment in an MVA, and the treatment was standard burn therapy.¹² Another case report described a patient with a second-degree burn with a 12-cm blister occurring on the radial side of the hand and distal forearm following an MVA and airbag deployment, which was treated conservatively.¹³ Cases of thermal burns, chemical burns, and irritant contact dermatitis after airbag deployment have been described in the literature.^{4-6,11,12,14,15} Our patient’s distal right lower leg was covered with a cast for osteomyelitis, and no blisters had developed in this area. It is likely that the transfer of airbag contents occurred during the process of unbuckling his seatbelt, which could explain the bullae that developed on the right flank. Per the Centers for Disease Control and Prevention, individuals should quickly remove clothing and wash their body with large amounts of soap and water following exposure to sodium azide.¹⁶

In 1989, the Federal Motor Vehicle Safety Standard No. 208 (occupant crash protection) became effective, stating all cars must have vehicle crash protection.¹² Prior to 1993, it was reported that there had been no associated chemical injuries with airbag deployment. Subsequently, a 6-month retrospective study in 1993 showed that dermal injuries were found in connection with the presence of sodium hydroxide in automobile airbags.¹² By 2004, it was known that airbags could cause chemical and thermal burns in addition to traumatic injuries from deployment.¹ Since 2007, all motor vehicles have been required to have advanced airbags, which are engineered to sense the presence of passengers and determine if the airbag will deploy, and if so, how much to deploy to minimize airbag-related injury.³

The brand of car that our patient drove during the MVA is one with known airbag recalls due to safety defects; however, the year and actual model of the vehicle are not known, so specific information about the airbag in question is not available. It has been noted that some defective airbag inflators that were exposed to excess moisture during the manufacturing process could explode during deployment, causing shrapnel and airbag rupture, which has been linked to nearly 300 injuries worldwide.¹⁷

Conclusion

It is evident that the use of airbag devices reduces morbidity and mortality due to MVAs.⁹ It also had been reported that up to 96% of airbag-related injuries are relatively minor, which many would argue justifies their use.¹⁸ Furthermore, it has been reported that 99.8% of skin injuries following airbag deployment are minor.¹⁹ In the United States, it is mandated that every vehicle have functional airbags installed.⁸

This case highlights the potential for substantial airbag-induced skin reactions, specifically a bullous reaction, following airbag deployment. The persistent pruritus and lasting postinflammatory hyperpigmentation seen in this case were certainly worrisome for our patient. We also present this case to remind dermatology providers of possible treatment approaches to these skin reactions. Immediate cleansing of the affected areas of skin may help avoid such reactions.

Vitiligo is a chronic dermatologic condition that negatively affects quality of life (QOL), with substantial burden on the psychosocial well-being of patients.¹ There is no cure, and current treatment modalities are aimed at controlling the chronic relapsing condition.^1-3 Despite topical and cosmetic treatments for stabilization and repigmentation, vitiligo remains unpredictable.³

All genders, races, ethnicities, and socioeconomic classes are equally affected.⁴ The underlying etiology of vitiligo remains unknown to a great extent and is more poorly understood by the general public compared with other skin diseases (eg, acne).⁵ Patients with vitiligo experience social withdrawal, decreased sense of self-esteem, anxiety, depression, and suicidal ideation.^5,6 Stigmatization has the greatest impact on QOL, with strong correlations between avoidance behaviors and lesion concealment.^6-8 Although the condition is especially disfiguring for darker skin types, lighter skin types also are substantially affected, with similar overall self-reported stress.^6,7

Individuals with chronic illnesses such as vitiligo turn to online communities for health information and social support, commiserating with others who have the same condition.^9,10 Online forums are platforms for asynchronous peer-to-peer exchange of disease-related information for better management of long-term disease.¹¹ Moreover, of all available internet resources, online forum posts are the most commonly accessed source of information (91%) for patients following visits with their doctors.¹²

Qualitative research involving chronic skin conditions and the information exchanged in online forums has been conducted for patients with acne, psoriasis, and atopic dermatitis, but not for patients with vitiligo.^13-16 Although online questionnaires have been administered to patients with vitiligo, the content within online forums is not well characterized.^2,17

The purpose of this qualitative study was to evaluate the online content exchanged by individuals with vitiligo to better understand the general attitudes and help-seeking behaviors in online forums.

Methods

Study Design—This qualitative study sought to investigate health beliefs and messages about vitiligo posted by users in US-based online discussion forums. An interpretive research paradigm was utilized so that all content collected in online forums were the views expressed by individuals.^18-20 An integrated approach was used in the development of the coding manual, with pre-established major themes and subthemes as a guiding framework.^16,21,22 We adhered to an inductive grounded method by means of de novo line-by-line coding, such that we had flexibility for new subthemes to emerge throughout the duration of the entire coding process.²³

Individual posts and subsequent replies embedded within public online forums were used as the collected data source. Google was utilized as the primary search engine to identify forums pertaining to vitiligo, as 80% of US adults with chronic disease report that their inquiries for health information start with Google, Bing, or Yahoo.²⁴ The institutional review board at the Wake Forest School of Medicine (Winston-Salem, North Carolina) granted approval of the study (IRB00063073). Online forums were considered “property” of the public domain and were accessible to all, eliminating the need for written informed consent.^24-26

Search Criteria—We conducted our forum search in February 2020 with a systematic approach using predetermined phrases—online forum vitiligo support, vitiligo online message board, and vitiligo forums—which yielded more than 358,171 total results (eTable 1). Threads were identified in chronological order (from newest to oldest) based on how they appeared during each internet search, and all Google results for the respective search phrases were reviewed. Dates of selected threads ranged from 2005 to 2020. Only sites with US domains were included. Posts that either included views and understandings of vitiligo or belonged to a thread that contained a vitiligo discussion were deemed relevant for inclusion. Forums were excluded if registration or means of payment was required to view posts, if there were fewer than 2 user replies to a thread, if threads contained patient photographs, or if no posts had been made in the last 2 years (rendering the thread inactive). No social media platforms, such as Facebook, or formal online platforms, such as MyVitiligoTeam, were included in the search. A no-fee-for-access was chosen for this study, as the majority of those with a chronic condition who encounter a required paywall find the information elsewhere.²⁵

Data Analysis—A total of 39 online forums were deemed relevant to the topic of vitiligo; 9 of them met inclusion criteria (eTable 2). The messages within the forums were copied verbatim into a password-encrypted text document, and usernames in the threads were de-identified, ensuring user confidentiality.

An inductive thematic analysis was utilized to explore the views and beliefs of online forum users discussing vitiligo. One author (M.B.G.) read the extracted message threads, developed an initial codebook, and established a finalized version with the agreement of another author (A.M.B.)(eTable 3). The forums were independently coded (M.B.G. and A.M.B.) in a line-by-line manner according to the codebook. Discrepancies were documented and resolved. Data saturation was adequately achieved, such that no new themes emerged during the iterative coding process. NVivo was used for qualitative analysis.

Results

Nine forums met inclusion criteria, comprising 105 pages of text. There were 61 total discussion threads, with 382 anonymous contributing users. Most users initiated a thread by posting either a question, an advice statement, or a request for help. The psychosocial impact of the disease permeated multiple domains,including personal relationships and daily life. Several threads discussed treatment, including effective camouflage and makeup, as well as peer validation of physician-prescribed treatments, along with threads dedicated to “cures” or homeopathy regimens. In several instances, commercial product endorsement, testimonials, and marketing links were reposted by the same user multiple times.

Inductive thematic analysis highlighted diverse themes and subthemes related to the beliefs and perspectives of users with vitiligo or with relatives or friends with vitiligo: psychosocial impact, disease management and camouflage/concealment, alternative medicine/homeopathy/cures, interactions with the public and health care providers, and skin tone and race. Quotes from individuals were included to demonstrate themes and subthemes.

Psychosocial Impact: QOL, Sources of Support, and Coping—There was a broad range of comments on how patients cope with and view their vitiligo. Some individuals felt vitiligo made them special, and others were at peace with and accepted their condition. In contrast, others reported the disease had devastated them and interfered with relationships. Individuals shared their stories of grief and hardships through childhood and adulthood and their concerns, especially on affected visible areas or the potential for disease progression. Users were vocal about how vitiligo affected their daily routines and lives, sharing how they felt uncomfortable outside the home, no longer engaged in swimming or exposing their legs, and preferred to stay inside instead. Some users adopted a “tough love” approach to coping, sharing how they have learned to either embrace their vitiligo or “live with it.” Some examples include:

“My best advice is go with the flow, vitiligo is not the worst thing that can happen.”

“I hate my life with vitiligo yet really I feel so selfish that there is much worse suffering in the world than a few white patches.”

Other advice was very practical:

“I hope it isn’t vanity that is tearing you apart because that is only skin deep. Make a fashion statement with hats.”

Some users acknowledged and adopted the mantra that vitiligo is not a somatic condition or “physical ailment,” while others emphasized its pervasive psychological burden:

“I still deal with this psychologically . . . You must keep a positive attitude and frame of mind . . . Vitiligo will not kill you, but you do need to stay strong and keep your head up emotionally.”

“I am just really thankful that I have a disease that will not kill me or that has [not] affected me physically at all. I consider myself lucky.”

Disease Management: Treatment, Vitiligo Course, Advice-Seeking, Camouflage—The range of information discussed for treatment was highly variable. There were many accounts in which users advised others to seek professional help, namely that of a dermatologist, for a formal assessment. Many expressed frustrations with treatments and their ineffectiveness, to which the majority of users said to consult with a professional and to remain patient and hopeful/optimistic:

“The best thing to do would be to take an appointment with a dermatologist and have the discoloration checked out. That’s the only way to know whether it is vitiligo or not.”

“My way of dealing with it is to gain control by camouflage.”

“The calming effect of being in control of my vitiligo, whether with concealers, self-tan or anything else, has stopped my feelings of despair.”

Beliefs on Alternative Medicine: Homeopathy and Alternative Regimens—Although some threads started with a post asking for the best treatments, others initiated a discussion by posting “best herbal treatments for cure” or “how to cure my vitiligo,” emphasizing the beliefs and wishes for a cure for vitiligo. Alternative therapies that users endorsed included apple cider vinegar, toothpaste, vitamins, and Ayurvedic treatment, among others. Dietary plans were popular, with users claiming success with dietary alterations in stopping and preventing lesion progression. For example, individuals felt that avoidance of sugar, meat, dairy, and citrus fruits or drinks and consumption of only filtered water were crucial to preventing further lesion spread and resulted in their “cure”:

“Don’t eat chocolate, wine (made of grapes), coffee, or tea if you don’t want to have vitiligo or let it get worse. Take Vitamin B, biotin, and nuts for Vitamin E.”

Other dangerous messages pitted treatments by health professionals against beliefs in homeopathy:

“I feel that vitiligo treatment is all in your diet and vitamins. All that medicine and UV lights is a no-no . . .w ith every medicine there is a side effect. The doctors could be healing your vitiligo and severely damaging you inside and out, and you won’t know until years later.”

There was a minor presence of users advising against homeopathy and the associated misinformation and inaccurate claims on curing vitiligo, though this group was small in comparison to the number of users posting outlandish claims on cure:

“There is no cure . . . It’s where your immune system attacks your skin cells causing loss of pigmentation. The skin that has lost the pigmentation can’t be reversed.”

Interactions With the Public and Health Care Providers—Those with vitiligo encounter unique situations in public and in their daily lives. Many of the accounts shared anecdotal stories on how patients have handled the stigma and discrimination faced:

“I have had to face discrimination at school, public places, college, functions, and every new person I have met has asked me this: ‘how did this happen?’”

Those with vitiligo even stated how they wished others would deal with their condition out in public, hoping that others would directly ask what the lesions were instead of the more hurtful staring. There were many stories in which users said others feel vitiligo was contagious or “dirty” and stressed that the condition is not infectious:

“I refer to myself as ‘camo-man’ and reassure people I come into contact with that it is not contagious.”

“Once I was eating at a restaurant . . . and a little girl said to her mom, ‘Look, Mom, that lady doesn’t wash her arms, look how dirty they are.’ That just broke my heart.”

Skin Tone and Implications—The belief that vitiligo lesions are less dramatic or less anxiety provoking for individuals with lighter skin was noted by users themselves and by health care providers in certain cases. Skin tone and its impact on QOL was confusing and contentious. Some users with fair skin stated their vitiligo was “less of an annoyance” or “less obvious” compared with individuals with darker complexions. Conversely, other accounts of self-reported White users vehemently stressed the anxieties felt by depigmented lesions, despite being “already white at baseline.”

“Was told by my dermatologist (upon diagnosis) that ‘You’re lucky you’re not African American—it shows up on them much worse. You’re so fair, it doesn’t really matter.’ ”

“You didn’t say what race you are. I could imagine it has a bigger impact if you are anything other than White.”

Comment

Patients Looking for Cures—The general attitude within the forums was uplifting and encouraging, with users detailing how they respond to others in public and sharing their personal perspectives. We found a mix of information regarding disease management and treatment of vitiligo. Overall, there was uncertainty about treatments, with individuals expressing concern that their treatments were ineffective or had failed or that better alternatives would be more suitable for their condition. We found many anecdotal endorsements of homeopathic remedies for vitiligo, with users boasting that their disease had not only been cured but had never returned. Some users completely denounced these statements, while other threads seemed to revolve completely around “cure” discussions with no dissenting voices. The number of discussions related to homeopathy was concerning. Furthermore, there often were no moderators within threads to remove cure-related content, whether commercially endorsed or anecdotal. It is plausible that supplements and vitamins recommended by some physicians may be incorrectly interpreted as a “cure” in online discussions. Our findings are consistent with prior reports that forums are a platform to express dissatisfaction with treatment and the need for additional treatment options.^15,22

Concern Expressed by Health Care Providers—Prior qualitative research has described how patients with chronic dermatologic conditions believe that health care providers minimize patients’ psychological distress.^27,28 We found several accounts in which an individual had explicitly stated their provider had “belittled” the extent and impact of vitiligo when comparing skin phototypes. This suggests either that physicians underestimate the impact of vitiligo on their patients or that physicians are not expressing enough empathic concern about the impact the condition has on those affected.

Cosmetic Aspects of Vitiligo—Few clinical trials have investigated QOL and cosmetic acceptability of treatments as outcome measures.²⁹ We found several instances in which users with vitiligo had reported being dismissed as having a “cosmetic disease,” consistent with other work demonstrating the negative impact on such dismissals.²² Moreover, concealment and camouflage techniques frequently were discussed, demonstrating the relevance of cosmetic management as an important research topic.

Trustworthy Sources of Health Information—Patients still view physicians as trustworthy and a key source of health care information and advice.^30-32 Patients with vitiligo who have been directed to reliable information sources often express gratitude²² and want health professionals to remain an important source in their health information-seeking.³¹ Given the range in information discussed online, it may be valuable to invite patients to share what information they have encountered online.

Our study highlights the conflicting health information and advice shared by users in online forums, complicating an already psychologically burdensome condition. Guiding patients to credible, moderated sites and resources that are accurate, understandable, and easy to access may help dispel the conflicting messages and stories discussed in the online community.

Study Strengths and Limitations—Limitations included reporting bias and reliance on self-reported information on the diagnosis and extent of individuals’ vitiligo. Excluding social media websites and platforms from the data collection is a limitation to comprehensively assessing the topic of internet users with vitiligo. Many social media platforms direct patients and their family members to support groups and therefore may have excluded these particular individuals. Social media platforms were excluded from our research owing to the prerequisite of creating user accounts or registering as an online member. Our inclusion criteria were specific to forums that did not require registering or creating an account and were therefore freely accessible to all internet viewers. There is an inherent lack of context present in online forums, preventing data collection on individuals’ demographics and socioeconomic backgrounds. However, anonymity may have allowed individuals to express their thoughts more freely.

An integrated approach, along with our sampling method of online forums not requiring registration, allows for greater transferability and understanding of the health needs of the general public with vitiligo.

Conclusion

Individuals with vitiligo continue to seek peer psychosocial support for the physical and emotional management of their disease. Counseling those with vitiligo about cosmetic concealment options, homeopathy, and treatment scams remains paramount. Directing patients to evidence-based resources, along with providing structured sources of support, may help to improve the psychosocial burden and QOL experienced by patients with vitiligo. Connecting patients with local and national support groups moderated by physicians, such as the Global Vitiligo Foundation (https://globalvitiligofoundation.org/), may provide benefit to patients with vitiligo.

Vitiligo is a chronic dermatologic condition that negatively affects quality of life (QOL), with substantial burden on the psychosocial well-being of patients.¹ There is no cure, and current treatment modalities are aimed at controlling the chronic relapsing condition.^1-3 Despite topical and cosmetic treatments for stabilization and repigmentation, vitiligo remains unpredictable.³

All genders, races, ethnicities, and socioeconomic classes are equally affected.⁴ The underlying etiology of vitiligo remains unknown to a great extent and is more poorly understood by the general public compared with other skin diseases (eg, acne).⁵ Patients with vitiligo experience social withdrawal, decreased sense of self-esteem, anxiety, depression, and suicidal ideation.^5,6 Stigmatization has the greatest impact on QOL, with strong correlations between avoidance behaviors and lesion concealment.^6-8 Although the condition is especially disfiguring for darker skin types, lighter skin types also are substantially affected, with similar overall self-reported stress.^6,7

Individuals with chronic illnesses such as vitiligo turn to online communities for health information and social support, commiserating with others who have the same condition.^9,10 Online forums are platforms for asynchronous peer-to-peer exchange of disease-related information for better management of long-term disease.¹¹ Moreover, of all available internet resources, online forum posts are the most commonly accessed source of information (91%) for patients following visits with their doctors.¹²

Qualitative research involving chronic skin conditions and the information exchanged in online forums has been conducted for patients with acne, psoriasis, and atopic dermatitis, but not for patients with vitiligo.^13-16 Although online questionnaires have been administered to patients with vitiligo, the content within online forums is not well characterized.^2,17

The purpose of this qualitative study was to evaluate the online content exchanged by individuals with vitiligo to better understand the general attitudes and help-seeking behaviors in online forums.

Methods

Study Design—This qualitative study sought to investigate health beliefs and messages about vitiligo posted by users in US-based online discussion forums. An interpretive research paradigm was utilized so that all content collected in online forums were the views expressed by individuals.^18-20 An integrated approach was used in the development of the coding manual, with pre-established major themes and subthemes as a guiding framework.^16,21,22 We adhered to an inductive grounded method by means of de novo line-by-line coding, such that we had flexibility for new subthemes to emerge throughout the duration of the entire coding process.²³

Individual posts and subsequent replies embedded within public online forums were used as the collected data source. Google was utilized as the primary search engine to identify forums pertaining to vitiligo, as 80% of US adults with chronic disease report that their inquiries for health information start with Google, Bing, or Yahoo.²⁴ The institutional review board at the Wake Forest School of Medicine (Winston-Salem, North Carolina) granted approval of the study (IRB00063073). Online forums were considered “property” of the public domain and were accessible to all, eliminating the need for written informed consent.^24-26

Search Criteria—We conducted our forum search in February 2020 with a systematic approach using predetermined phrases—online forum vitiligo support, vitiligo online message board, and vitiligo forums—which yielded more than 358,171 total results (eTable 1). Threads were identified in chronological order (from newest to oldest) based on how they appeared during each internet search, and all Google results for the respective search phrases were reviewed. Dates of selected threads ranged from 2005 to 2020. Only sites with US domains were included. Posts that either included views and understandings of vitiligo or belonged to a thread that contained a vitiligo discussion were deemed relevant for inclusion. Forums were excluded if registration or means of payment was required to view posts, if there were fewer than 2 user replies to a thread, if threads contained patient photographs, or if no posts had been made in the last 2 years (rendering the thread inactive). No social media platforms, such as Facebook, or formal online platforms, such as MyVitiligoTeam, were included in the search. A no-fee-for-access was chosen for this study, as the majority of those with a chronic condition who encounter a required paywall find the information elsewhere.²⁵

Data Analysis—A total of 39 online forums were deemed relevant to the topic of vitiligo; 9 of them met inclusion criteria (eTable 2). The messages within the forums were copied verbatim into a password-encrypted text document, and usernames in the threads were de-identified, ensuring user confidentiality.

An inductive thematic analysis was utilized to explore the views and beliefs of online forum users discussing vitiligo. One author (M.B.G.) read the extracted message threads, developed an initial codebook, and established a finalized version with the agreement of another author (A.M.B.)(eTable 3). The forums were independently coded (M.B.G. and A.M.B.) in a line-by-line manner according to the codebook. Discrepancies were documented and resolved. Data saturation was adequately achieved, such that no new themes emerged during the iterative coding process. NVivo was used for qualitative analysis.

Results

Nine forums met inclusion criteria, comprising 105 pages of text. There were 61 total discussion threads, with 382 anonymous contributing users. Most users initiated a thread by posting either a question, an advice statement, or a request for help. The psychosocial impact of the disease permeated multiple domains,including personal relationships and daily life. Several threads discussed treatment, including effective camouflage and makeup, as well as peer validation of physician-prescribed treatments, along with threads dedicated to “cures” or homeopathy regimens. In several instances, commercial product endorsement, testimonials, and marketing links were reposted by the same user multiple times.

Inductive thematic analysis highlighted diverse themes and subthemes related to the beliefs and perspectives of users with vitiligo or with relatives or friends with vitiligo: psychosocial impact, disease management and camouflage/concealment, alternative medicine/homeopathy/cures, interactions with the public and health care providers, and skin tone and race. Quotes from individuals were included to demonstrate themes and subthemes.

Psychosocial Impact: QOL, Sources of Support, and Coping—There was a broad range of comments on how patients cope with and view their vitiligo. Some individuals felt vitiligo made them special, and others were at peace with and accepted their condition. In contrast, others reported the disease had devastated them and interfered with relationships. Individuals shared their stories of grief and hardships through childhood and adulthood and their concerns, especially on affected visible areas or the potential for disease progression. Users were vocal about how vitiligo affected their daily routines and lives, sharing how they felt uncomfortable outside the home, no longer engaged in swimming or exposing their legs, and preferred to stay inside instead. Some users adopted a “tough love” approach to coping, sharing how they have learned to either embrace their vitiligo or “live with it.” Some examples include:

“My best advice is go with the flow, vitiligo is not the worst thing that can happen.”

“I hate my life with vitiligo yet really I feel so selfish that there is much worse suffering in the world than a few white patches.”

Other advice was very practical:

“I hope it isn’t vanity that is tearing you apart because that is only skin deep. Make a fashion statement with hats.”

Some users acknowledged and adopted the mantra that vitiligo is not a somatic condition or “physical ailment,” while others emphasized its pervasive psychological burden:

“I still deal with this psychologically . . . You must keep a positive attitude and frame of mind . . . Vitiligo will not kill you, but you do need to stay strong and keep your head up emotionally.”

“I am just really thankful that I have a disease that will not kill me or that has [not] affected me physically at all. I consider myself lucky.”

Disease Management: Treatment, Vitiligo Course, Advice-Seeking, Camouflage—The range of information discussed for treatment was highly variable. There were many accounts in which users advised others to seek professional help, namely that of a dermatologist, for a formal assessment. Many expressed frustrations with treatments and their ineffectiveness, to which the majority of users said to consult with a professional and to remain patient and hopeful/optimistic:

“The best thing to do would be to take an appointment with a dermatologist and have the discoloration checked out. That’s the only way to know whether it is vitiligo or not.”

“My way of dealing with it is to gain control by camouflage.”

“The calming effect of being in control of my vitiligo, whether with concealers, self-tan or anything else, has stopped my feelings of despair.”

Beliefs on Alternative Medicine: Homeopathy and Alternative Regimens—Although some threads started with a post asking for the best treatments, others initiated a discussion by posting “best herbal treatments for cure” or “how to cure my vitiligo,” emphasizing the beliefs and wishes for a cure for vitiligo. Alternative therapies that users endorsed included apple cider vinegar, toothpaste, vitamins, and Ayurvedic treatment, among others. Dietary plans were popular, with users claiming success with dietary alterations in stopping and preventing lesion progression. For example, individuals felt that avoidance of sugar, meat, dairy, and citrus fruits or drinks and consumption of only filtered water were crucial to preventing further lesion spread and resulted in their “cure”:

“Don’t eat chocolate, wine (made of grapes), coffee, or tea if you don’t want to have vitiligo or let it get worse. Take Vitamin B, biotin, and nuts for Vitamin E.”

Other dangerous messages pitted treatments by health professionals against beliefs in homeopathy:

“I feel that vitiligo treatment is all in your diet and vitamins. All that medicine and UV lights is a no-no . . .w ith every medicine there is a side effect. The doctors could be healing your vitiligo and severely damaging you inside and out, and you won’t know until years later.”

There was a minor presence of users advising against homeopathy and the associated misinformation and inaccurate claims on curing vitiligo, though this group was small in comparison to the number of users posting outlandish claims on cure:

“There is no cure . . . It’s where your immune system attacks your skin cells causing loss of pigmentation. The skin that has lost the pigmentation can’t be reversed.”

Interactions With the Public and Health Care Providers—Those with vitiligo encounter unique situations in public and in their daily lives. Many of the accounts shared anecdotal stories on how patients have handled the stigma and discrimination faced:

“I have had to face discrimination at school, public places, college, functions, and every new person I have met has asked me this: ‘how did this happen?’”

Those with vitiligo even stated how they wished others would deal with their condition out in public, hoping that others would directly ask what the lesions were instead of the more hurtful staring. There were many stories in which users said others feel vitiligo was contagious or “dirty” and stressed that the condition is not infectious:

“I refer to myself as ‘camo-man’ and reassure people I come into contact with that it is not contagious.”

“Once I was eating at a restaurant . . . and a little girl said to her mom, ‘Look, Mom, that lady doesn’t wash her arms, look how dirty they are.’ That just broke my heart.”

Skin Tone and Implications—The belief that vitiligo lesions are less dramatic or less anxiety provoking for individuals with lighter skin was noted by users themselves and by health care providers in certain cases. Skin tone and its impact on QOL was confusing and contentious. Some users with fair skin stated their vitiligo was “less of an annoyance” or “less obvious” compared with individuals with darker complexions. Conversely, other accounts of self-reported White users vehemently stressed the anxieties felt by depigmented lesions, despite being “already white at baseline.”

“Was told by my dermatologist (upon diagnosis) that ‘You’re lucky you’re not African American—it shows up on them much worse. You’re so fair, it doesn’t really matter.’ ”

“You didn’t say what race you are. I could imagine it has a bigger impact if you are anything other than White.”

Comment

Patients Looking for Cures—The general attitude within the forums was uplifting and encouraging, with users detailing how they respond to others in public and sharing their personal perspectives. We found a mix of information regarding disease management and treatment of vitiligo. Overall, there was uncertainty about treatments, with individuals expressing concern that their treatments were ineffective or had failed or that better alternatives would be more suitable for their condition. We found many anecdotal endorsements of homeopathic remedies for vitiligo, with users boasting that their disease had not only been cured but had never returned. Some users completely denounced these statements, while other threads seemed to revolve completely around “cure” discussions with no dissenting voices. The number of discussions related to homeopathy was concerning. Furthermore, there often were no moderators within threads to remove cure-related content, whether commercially endorsed or anecdotal. It is plausible that supplements and vitamins recommended by some physicians may be incorrectly interpreted as a “cure” in online discussions. Our findings are consistent with prior reports that forums are a platform to express dissatisfaction with treatment and the need for additional treatment options.^15,22

Concern Expressed by Health Care Providers—Prior qualitative research has described how patients with chronic dermatologic conditions believe that health care providers minimize patients’ psychological distress.^27,28 We found several accounts in which an individual had explicitly stated their provider had “belittled” the extent and impact of vitiligo when comparing skin phototypes. This suggests either that physicians underestimate the impact of vitiligo on their patients or that physicians are not expressing enough empathic concern about the impact the condition has on those affected.

Cosmetic Aspects of Vitiligo—Few clinical trials have investigated QOL and cosmetic acceptability of treatments as outcome measures.²⁹ We found several instances in which users with vitiligo had reported being dismissed as having a “cosmetic disease,” consistent with other work demonstrating the negative impact on such dismissals.²² Moreover, concealment and camouflage techniques frequently were discussed, demonstrating the relevance of cosmetic management as an important research topic.

Trustworthy Sources of Health Information—Patients still view physicians as trustworthy and a key source of health care information and advice.^30-32 Patients with vitiligo who have been directed to reliable information sources often express gratitude²² and want health professionals to remain an important source in their health information-seeking.³¹ Given the range in information discussed online, it may be valuable to invite patients to share what information they have encountered online.

Our study highlights the conflicting health information and advice shared by users in online forums, complicating an already psychologically burdensome condition. Guiding patients to credible, moderated sites and resources that are accurate, understandable, and easy to access may help dispel the conflicting messages and stories discussed in the online community.

Study Strengths and Limitations—Limitations included reporting bias and reliance on self-reported information on the diagnosis and extent of individuals’ vitiligo. Excluding social media websites and platforms from the data collection is a limitation to comprehensively assessing the topic of internet users with vitiligo. Many social media platforms direct patients and their family members to support groups and therefore may have excluded these particular individuals. Social media platforms were excluded from our research owing to the prerequisite of creating user accounts or registering as an online member. Our inclusion criteria were specific to forums that did not require registering or creating an account and were therefore freely accessible to all internet viewers. There is an inherent lack of context present in online forums, preventing data collection on individuals’ demographics and socioeconomic backgrounds. However, anonymity may have allowed individuals to express their thoughts more freely.

An integrated approach, along with our sampling method of online forums not requiring registration, allows for greater transferability and understanding of the health needs of the general public with vitiligo.

Conclusion

Individuals with vitiligo continue to seek peer psychosocial support for the physical and emotional management of their disease. Counseling those with vitiligo about cosmetic concealment options, homeopathy, and treatment scams remains paramount. Directing patients to evidence-based resources, along with providing structured sources of support, may help to improve the psychosocial burden and QOL experienced by patients with vitiligo. Connecting patients with local and national support groups moderated by physicians, such as the Global Vitiligo Foundation (https://globalvitiligofoundation.org/), may provide benefit to patients with vitiligo.

Vitiligo is a chronic dermatologic condition that negatively affects quality of life (QOL), with substantial burden on the psychosocial well-being of patients.¹ There is no cure, and current treatment modalities are aimed at controlling the chronic relapsing condition.^1-3 Despite topical and cosmetic treatments for stabilization and repigmentation, vitiligo remains unpredictable.³

All genders, races, ethnicities, and socioeconomic classes are equally affected.⁴ The underlying etiology of vitiligo remains unknown to a great extent and is more poorly understood by the general public compared with other skin diseases (eg, acne).⁵ Patients with vitiligo experience social withdrawal, decreased sense of self-esteem, anxiety, depression, and suicidal ideation.^5,6 Stigmatization has the greatest impact on QOL, with strong correlations between avoidance behaviors and lesion concealment.^6-8 Although the condition is especially disfiguring for darker skin types, lighter skin types also are substantially affected, with similar overall self-reported stress.^6,7

Individuals with chronic illnesses such as vitiligo turn to online communities for health information and social support, commiserating with others who have the same condition.^9,10 Online forums are platforms for asynchronous peer-to-peer exchange of disease-related information for better management of long-term disease.¹¹ Moreover, of all available internet resources, online forum posts are the most commonly accessed source of information (91%) for patients following visits with their doctors.¹²

Qualitative research involving chronic skin conditions and the information exchanged in online forums has been conducted for patients with acne, psoriasis, and atopic dermatitis, but not for patients with vitiligo.^13-16 Although online questionnaires have been administered to patients with vitiligo, the content within online forums is not well characterized.^2,17

The purpose of this qualitative study was to evaluate the online content exchanged by individuals with vitiligo to better understand the general attitudes and help-seeking behaviors in online forums.

Methods

Study Design—This qualitative study sought to investigate health beliefs and messages about vitiligo posted by users in US-based online discussion forums. An interpretive research paradigm was utilized so that all content collected in online forums were the views expressed by individuals.^18-20 An integrated approach was used in the development of the coding manual, with pre-established major themes and subthemes as a guiding framework.^16,21,22 We adhered to an inductive grounded method by means of de novo line-by-line coding, such that we had flexibility for new subthemes to emerge throughout the duration of the entire coding process.²³

Individual posts and subsequent replies embedded within public online forums were used as the collected data source. Google was utilized as the primary search engine to identify forums pertaining to vitiligo, as 80% of US adults with chronic disease report that their inquiries for health information start with Google, Bing, or Yahoo.²⁴ The institutional review board at the Wake Forest School of Medicine (Winston-Salem, North Carolina) granted approval of the study (IRB00063073). Online forums were considered “property” of the public domain and were accessible to all, eliminating the need for written informed consent.^24-26

Search Criteria—We conducted our forum search in February 2020 with a systematic approach using predetermined phrases—online forum vitiligo support, vitiligo online message board, and vitiligo forums—which yielded more than 358,171 total results (eTable 1). Threads were identified in chronological order (from newest to oldest) based on how they appeared during each internet search, and all Google results for the respective search phrases were reviewed. Dates of selected threads ranged from 2005 to 2020. Only sites with US domains were included. Posts that either included views and understandings of vitiligo or belonged to a thread that contained a vitiligo discussion were deemed relevant for inclusion. Forums were excluded if registration or means of payment was required to view posts, if there were fewer than 2 user replies to a thread, if threads contained patient photographs, or if no posts had been made in the last 2 years (rendering the thread inactive). No social media platforms, such as Facebook, or formal online platforms, such as MyVitiligoTeam, were included in the search. A no-fee-for-access was chosen for this study, as the majority of those with a chronic condition who encounter a required paywall find the information elsewhere.²⁵

Data Analysis—A total of 39 online forums were deemed relevant to the topic of vitiligo; 9 of them met inclusion criteria (eTable 2). The messages within the forums were copied verbatim into a password-encrypted text document, and usernames in the threads were de-identified, ensuring user confidentiality.

An inductive thematic analysis was utilized to explore the views and beliefs of online forum users discussing vitiligo. One author (M.B.G.) read the extracted message threads, developed an initial codebook, and established a finalized version with the agreement of another author (A.M.B.)(eTable 3). The forums were independently coded (M.B.G. and A.M.B.) in a line-by-line manner according to the codebook. Discrepancies were documented and resolved. Data saturation was adequately achieved, such that no new themes emerged during the iterative coding process. NVivo was used for qualitative analysis.

Results

Nine forums met inclusion criteria, comprising 105 pages of text. There were 61 total discussion threads, with 382 anonymous contributing users. Most users initiated a thread by posting either a question, an advice statement, or a request for help. The psychosocial impact of the disease permeated multiple domains,including personal relationships and daily life. Several threads discussed treatment, including effective camouflage and makeup, as well as peer validation of physician-prescribed treatments, along with threads dedicated to “cures” or homeopathy regimens. In several instances, commercial product endorsement, testimonials, and marketing links were reposted by the same user multiple times.

Inductive thematic analysis highlighted diverse themes and subthemes related to the beliefs and perspectives of users with vitiligo or with relatives or friends with vitiligo: psychosocial impact, disease management and camouflage/concealment, alternative medicine/homeopathy/cures, interactions with the public and health care providers, and skin tone and race. Quotes from individuals were included to demonstrate themes and subthemes.

Psychosocial Impact: QOL, Sources of Support, and Coping—There was a broad range of comments on how patients cope with and view their vitiligo. Some individuals felt vitiligo made them special, and others were at peace with and accepted their condition. In contrast, others reported the disease had devastated them and interfered with relationships. Individuals shared their stories of grief and hardships through childhood and adulthood and their concerns, especially on affected visible areas or the potential for disease progression. Users were vocal about how vitiligo affected their daily routines and lives, sharing how they felt uncomfortable outside the home, no longer engaged in swimming or exposing their legs, and preferred to stay inside instead. Some users adopted a “tough love” approach to coping, sharing how they have learned to either embrace their vitiligo or “live with it.” Some examples include:

“My best advice is go with the flow, vitiligo is not the worst thing that can happen.”

“I hate my life with vitiligo yet really I feel so selfish that there is much worse suffering in the world than a few white patches.”

Other advice was very practical:

“I hope it isn’t vanity that is tearing you apart because that is only skin deep. Make a fashion statement with hats.”

Some users acknowledged and adopted the mantra that vitiligo is not a somatic condition or “physical ailment,” while others emphasized its pervasive psychological burden:

“I still deal with this psychologically . . . You must keep a positive attitude and frame of mind . . . Vitiligo will not kill you, but you do need to stay strong and keep your head up emotionally.”

“I am just really thankful that I have a disease that will not kill me or that has [not] affected me physically at all. I consider myself lucky.”

Disease Management: Treatment, Vitiligo Course, Advice-Seeking, Camouflage—The range of information discussed for treatment was highly variable. There were many accounts in which users advised others to seek professional help, namely that of a dermatologist, for a formal assessment. Many expressed frustrations with treatments and their ineffectiveness, to which the majority of users said to consult with a professional and to remain patient and hopeful/optimistic:

“The best thing to do would be to take an appointment with a dermatologist and have the discoloration checked out. That’s the only way to know whether it is vitiligo or not.”

“My way of dealing with it is to gain control by camouflage.”

“The calming effect of being in control of my vitiligo, whether with concealers, self-tan or anything else, has stopped my feelings of despair.”

Beliefs on Alternative Medicine: Homeopathy and Alternative Regimens—Although some threads started with a post asking for the best treatments, others initiated a discussion by posting “best herbal treatments for cure” or “how to cure my vitiligo,” emphasizing the beliefs and wishes for a cure for vitiligo. Alternative therapies that users endorsed included apple cider vinegar, toothpaste, vitamins, and Ayurvedic treatment, among others. Dietary plans were popular, with users claiming success with dietary alterations in stopping and preventing lesion progression. For example, individuals felt that avoidance of sugar, meat, dairy, and citrus fruits or drinks and consumption of only filtered water were crucial to preventing further lesion spread and resulted in their “cure”:

“Don’t eat chocolate, wine (made of grapes), coffee, or tea if you don’t want to have vitiligo or let it get worse. Take Vitamin B, biotin, and nuts for Vitamin E.”

Other dangerous messages pitted treatments by health professionals against beliefs in homeopathy:

“I feel that vitiligo treatment is all in your diet and vitamins. All that medicine and UV lights is a no-no . . .w ith every medicine there is a side effect. The doctors could be healing your vitiligo and severely damaging you inside and out, and you won’t know until years later.”

There was a minor presence of users advising against homeopathy and the associated misinformation and inaccurate claims on curing vitiligo, though this group was small in comparison to the number of users posting outlandish claims on cure:

“There is no cure . . . It’s where your immune system attacks your skin cells causing loss of pigmentation. The skin that has lost the pigmentation can’t be reversed.”

Interactions With the Public and Health Care Providers—Those with vitiligo encounter unique situations in public and in their daily lives. Many of the accounts shared anecdotal stories on how patients have handled the stigma and discrimination faced:

“I have had to face discrimination at school, public places, college, functions, and every new person I have met has asked me this: ‘how did this happen?’”

Those with vitiligo even stated how they wished others would deal with their condition out in public, hoping that others would directly ask what the lesions were instead of the more hurtful staring. There were many stories in which users said others feel vitiligo was contagious or “dirty” and stressed that the condition is not infectious:

“I refer to myself as ‘camo-man’ and reassure people I come into contact with that it is not contagious.”

“Once I was eating at a restaurant . . . and a little girl said to her mom, ‘Look, Mom, that lady doesn’t wash her arms, look how dirty they are.’ That just broke my heart.”

Skin Tone and Implications—The belief that vitiligo lesions are less dramatic or less anxiety provoking for individuals with lighter skin was noted by users themselves and by health care providers in certain cases. Skin tone and its impact on QOL was confusing and contentious. Some users with fair skin stated their vitiligo was “less of an annoyance” or “less obvious” compared with individuals with darker complexions. Conversely, other accounts of self-reported White users vehemently stressed the anxieties felt by depigmented lesions, despite being “already white at baseline.”

“Was told by my dermatologist (upon diagnosis) that ‘You’re lucky you’re not African American—it shows up on them much worse. You’re so fair, it doesn’t really matter.’ ”

“You didn’t say what race you are. I could imagine it has a bigger impact if you are anything other than White.”

Comment

Patients Looking for Cures—The general attitude within the forums was uplifting and encouraging, with users detailing how they respond to others in public and sharing their personal perspectives. We found a mix of information regarding disease management and treatment of vitiligo. Overall, there was uncertainty about treatments, with individuals expressing concern that their treatments were ineffective or had failed or that better alternatives would be more suitable for their condition. We found many anecdotal endorsements of homeopathic remedies for vitiligo, with users boasting that their disease had not only been cured but had never returned. Some users completely denounced these statements, while other threads seemed to revolve completely around “cure” discussions with no dissenting voices. The number of discussions related to homeopathy was concerning. Furthermore, there often were no moderators within threads to remove cure-related content, whether commercially endorsed or anecdotal. It is plausible that supplements and vitamins recommended by some physicians may be incorrectly interpreted as a “cure” in online discussions. Our findings are consistent with prior reports that forums are a platform to express dissatisfaction with treatment and the need for additional treatment options.^15,22

Concern Expressed by Health Care Providers—Prior qualitative research has described how patients with chronic dermatologic conditions believe that health care providers minimize patients’ psychological distress.^27,28 We found several accounts in which an individual had explicitly stated their provider had “belittled” the extent and impact of vitiligo when comparing skin phototypes. This suggests either that physicians underestimate the impact of vitiligo on their patients or that physicians are not expressing enough empathic concern about the impact the condition has on those affected.

Cosmetic Aspects of Vitiligo—Few clinical trials have investigated QOL and cosmetic acceptability of treatments as outcome measures.²⁹ We found several instances in which users with vitiligo had reported being dismissed as having a “cosmetic disease,” consistent with other work demonstrating the negative impact on such dismissals.²² Moreover, concealment and camouflage techniques frequently were discussed, demonstrating the relevance of cosmetic management as an important research topic.

Trustworthy Sources of Health Information—Patients still view physicians as trustworthy and a key source of health care information and advice.^30-32 Patients with vitiligo who have been directed to reliable information sources often express gratitude²² and want health professionals to remain an important source in their health information-seeking.³¹ Given the range in information discussed online, it may be valuable to invite patients to share what information they have encountered online.

Our study highlights the conflicting health information and advice shared by users in online forums, complicating an already psychologically burdensome condition. Guiding patients to credible, moderated sites and resources that are accurate, understandable, and easy to access may help dispel the conflicting messages and stories discussed in the online community.

Study Strengths and Limitations—Limitations included reporting bias and reliance on self-reported information on the diagnosis and extent of individuals’ vitiligo. Excluding social media websites and platforms from the data collection is a limitation to comprehensively assessing the topic of internet users with vitiligo. Many social media platforms direct patients and their family members to support groups and therefore may have excluded these particular individuals. Social media platforms were excluded from our research owing to the prerequisite of creating user accounts or registering as an online member. Our inclusion criteria were specific to forums that did not require registering or creating an account and were therefore freely accessible to all internet viewers. There is an inherent lack of context present in online forums, preventing data collection on individuals’ demographics and socioeconomic backgrounds. However, anonymity may have allowed individuals to express their thoughts more freely.

An integrated approach, along with our sampling method of online forums not requiring registration, allows for greater transferability and understanding of the health needs of the general public with vitiligo.

Conclusion

Individuals with vitiligo continue to seek peer psychosocial support for the physical and emotional management of their disease. Counseling those with vitiligo about cosmetic concealment options, homeopathy, and treatment scams remains paramount. Directing patients to evidence-based resources, along with providing structured sources of support, may help to improve the psychosocial burden and QOL experienced by patients with vitiligo. Connecting patients with local and national support groups moderated by physicians, such as the Global Vitiligo Foundation (https://globalvitiligofoundation.org/), may provide benefit to patients with vitiligo.

As manifestations of overt racism and macroaggressions have gained increased visibility, there is a need for discussion of another expression of racism: microaggressions. Although racism classically is viewed as blatant structural, attitudinal, and behavioral prejudice, experts pose that the face of racism has evolved into a more covert insidious form. This form of racism was originally coined racial microaggressions by psychiatrist Chester M. Pierce, MD, 50 years ago.^1,2 Since that time, microaggressions have further expanded to describe “brief and commonplace daily verbal, behavioral, and environmental indignities, whether intentional or unintentional, that communicate hostile, derogatory, or negative racial, gender, sexual-orientation, and religious slights and insults to the target person or group.” ³ This article aims to define and depict examples of microaggressions in medicine, discuss the resulting harmful effects, and offer strategies to minimize and counter these negative ramifications.

What are microaggressions?

Microaggressions are behaviors that stem from implicit bias and occur at an interpersonal level. Implicit bias refers to unconscious stereotypes, assumptions, and beliefs held about an individual’s identity. One of the earliest microaggressions—invisibility—was characterized by Ralph Ellison in his novel Invisible Man. Ellison states, “I am invisible, understand, simply because people refuse to see me . . . When they approach me they see only my surroundings, themselves, or figments of their imagination—indeed, everything and anything except me.”⁴ This concept of invisibility is a primary microaggression faced by people of color.

In medicine, microaggressions and implicit bias may be encountered throughout medical training and clinical practice in interactions with colleagues, superiors, patients, and patients’ families.^5,6 Examples of microaggressions in medicine include demeaning comments, nonverbal disrespect, generalizations of social identity, assumption of nonphysician status, role- or credential-questioning behavior, explicit epithets, rejection of care, questioning or inquiries of ethnic/racial origin, and sexual harassment.⁷

An example of microaggressions in medicine was fully displayed when physician Tamika Cross described her experience of being turned away from helping an unresponsive passenger during a flight emergency.

[T]he flight attendant yells “call overhead for a physician on board.” I raised my hand to grab her attention. She said to me “oh no sweetie put [your] hand down, we are looking for actual physicians or nurses or some type of medical personnel, we don’t have time to talk to you” . . . Another “seasoned” white male approaches the row and says he is a physician as well. She says to me “thanks for your help but he can help us, and he has his credentials.”⁸

What are the effects of microaggressions?

Although microaggressions may be unconscious and unintentional by the offender, the negative ramifications are notable. Recent studies report that women and underrepresented minority (URM) medical students, residents, and physicians experience microaggressions and implicit bias at a higher prevalence and frequency compared with their male and non-URM counterparts.^7,9 Repetitive microaggressions are harmful to the health and safety of women and URM medical students, residents, physicians, other providers, and patients. The Table provides example scenarios of microaggressions in medicine categorized according to Berk.¹⁰

Microaggressions negatively impact physical, mental, and emotional well-being. Current data support that medical students and residents who experience microaggressions are more likely to report associated symptoms of burnout, depression, and suicidal thoughts.^11,12 Subjection to persistent bias can lead to minority status stress and racial battle fatigue, creating feelings of invisibility, isolation, exclusion, and loneliness for those impacted.^13,14

In the book Black Man in a White Coat: A Doctor’s Reflections on Race and Medicine, Damon Tweedy, MD, reflects on race in medicine. Tweedy notes his experience as a medical student when a professor mistakenly assumed he was a maintenance worker in the classroom. Tweedy describes how he internalized the exchange and, despite his success throughout the course of his medical training, combatted feelings of anxiety, self-doubt, and implied inferiority.¹⁵

Although microaggressions are harmful to one’s health, they also undermine the learning and teaching experience for students, residents, and faculty, and they detract from the larger goal of providing care for patients.¹¹ Frequent devaluing and questioning of an individual’s contributions, qualifications, and credentials based on identity can lower productivity and problem-solving abilities. These behaviors cultivate an unwelcome and hostile work/learning environment that is stressful and polarizing for the recipient.

Despite the heavy burden of microaggressions, most students, residents, and faculty physicians do not report incidents to their institutions and feel that training, resources, and policies to respond to bias adequately are lacking.⁷ As a result of implicit bias and microaggressions, women and URM medical students and providers are unable to focus solely on the practice of medicine. They are tasked with the additional burden of shouldering the emotional and cognitive complexities that microaggressions produce.¹⁶

What are strategies to reduce microaggressions in medicine?

To minimize the harmful effects of microaggressions, intervention strategies must be implemented that reduce the likelihood of the occurrence of microaggressions and challenge the stereotypes that undergird implicit bias. These strategies include cultivating allies, followed by demanding structural accountability. Allies are members of the majority group who collectively collaborate with members of the nonmajority group to effect change through the promotion of diversity, equity, and inclusion efforts.¹⁷ Cultivating allies involves building a network of collaboration among these groups and emphasizes education. Education is critical for allies to address microaggressions at the interpersonal level. This process of education involves personal reflection and self-awareness in exploring one’s biases, fears, and assumptions. Integral to this step is broadening one’s acceptance of different cultures, racial/ethnic groups, and identities. There must be a willingness to engage in difficult or uncomfortable conversations and a readiness to actively listen to concerns rather than perpetuating further harm through avoidance and dismissive or defensive behavior.¹⁸

Demanding structural accountability facilitates deconstruction of bias and microaggression at the larger systemic level. This strategy involves implicit bias and antiracism training, development of retention plans, and identification of mentors for women and URM providers and students. Implicit bias and microaggression training and policies should be incorporated into medical education and resident curriculums. Similarly, educational resources and training must be made available to practicing physicians, faculty, and other providers through their institutions and places of employment. Equipping students and providers with the tools needed when microaggressions are witnessed or experienced demonstrates systemic-level accountability and communicates the importance of the issue. Furthermore, the development of retention plans and identification of mentors provide a support system and foster a culture of inclusion where recipients of microaggressions feel protected and valued. Increased feelings of inclusivity and belonging help bridge the gap created through microaggressions and implicit bias.

Final Thoughts

Despite an often covert nature, the detrimental effects of microaggressions are tangible and far reaching. As providers, we must strive to understand all categories of racism and expose the many ways prejudice manifests within medical training and clinical practice. It is our obligation to undertake the challenge of “making the ‘invisible’ visible” as we confront microaggressions and implicit bias to promote a safer and more inclusive medical community and workforce.¹⁹

As manifestations of overt racism and macroaggressions have gained increased visibility, there is a need for discussion of another expression of racism: microaggressions. Although racism classically is viewed as blatant structural, attitudinal, and behavioral prejudice, experts pose that the face of racism has evolved into a more covert insidious form. This form of racism was originally coined racial microaggressions by psychiatrist Chester M. Pierce, MD, 50 years ago.^1,2 Since that time, microaggressions have further expanded to describe “brief and commonplace daily verbal, behavioral, and environmental indignities, whether intentional or unintentional, that communicate hostile, derogatory, or negative racial, gender, sexual-orientation, and religious slights and insults to the target person or group.” ³ This article aims to define and depict examples of microaggressions in medicine, discuss the resulting harmful effects, and offer strategies to minimize and counter these negative ramifications.

What are microaggressions?

Microaggressions are behaviors that stem from implicit bias and occur at an interpersonal level. Implicit bias refers to unconscious stereotypes, assumptions, and beliefs held about an individual’s identity. One of the earliest microaggressions—invisibility—was characterized by Ralph Ellison in his novel Invisible Man. Ellison states, “I am invisible, understand, simply because people refuse to see me . . . When they approach me they see only my surroundings, themselves, or figments of their imagination—indeed, everything and anything except me.”⁴ This concept of invisibility is a primary microaggression faced by people of color.

In medicine, microaggressions and implicit bias may be encountered throughout medical training and clinical practice in interactions with colleagues, superiors, patients, and patients’ families.^5,6 Examples of microaggressions in medicine include demeaning comments, nonverbal disrespect, generalizations of social identity, assumption of nonphysician status, role- or credential-questioning behavior, explicit epithets, rejection of care, questioning or inquiries of ethnic/racial origin, and sexual harassment.⁷

An example of microaggressions in medicine was fully displayed when physician Tamika Cross described her experience of being turned away from helping an unresponsive passenger during a flight emergency.

[T]he flight attendant yells “call overhead for a physician on board.” I raised my hand to grab her attention. She said to me “oh no sweetie put [your] hand down, we are looking for actual physicians or nurses or some type of medical personnel, we don’t have time to talk to you” . . . Another “seasoned” white male approaches the row and says he is a physician as well. She says to me “thanks for your help but he can help us, and he has his credentials.”⁸

What are the effects of microaggressions?

Although microaggressions may be unconscious and unintentional by the offender, the negative ramifications are notable. Recent studies report that women and underrepresented minority (URM) medical students, residents, and physicians experience microaggressions and implicit bias at a higher prevalence and frequency compared with their male and non-URM counterparts.^7,9 Repetitive microaggressions are harmful to the health and safety of women and URM medical students, residents, physicians, other providers, and patients. The Table provides example scenarios of microaggressions in medicine categorized according to Berk.¹⁰

Microaggressions negatively impact physical, mental, and emotional well-being. Current data support that medical students and residents who experience microaggressions are more likely to report associated symptoms of burnout, depression, and suicidal thoughts.^11,12 Subjection to persistent bias can lead to minority status stress and racial battle fatigue, creating feelings of invisibility, isolation, exclusion, and loneliness for those impacted.^13,14

In the book Black Man in a White Coat: A Doctor’s Reflections on Race and Medicine, Damon Tweedy, MD, reflects on race in medicine. Tweedy notes his experience as a medical student when a professor mistakenly assumed he was a maintenance worker in the classroom. Tweedy describes how he internalized the exchange and, despite his success throughout the course of his medical training, combatted feelings of anxiety, self-doubt, and implied inferiority.¹⁵

Although microaggressions are harmful to one’s health, they also undermine the learning and teaching experience for students, residents, and faculty, and they detract from the larger goal of providing care for patients.¹¹ Frequent devaluing and questioning of an individual’s contributions, qualifications, and credentials based on identity can lower productivity and problem-solving abilities. These behaviors cultivate an unwelcome and hostile work/learning environment that is stressful and polarizing for the recipient.

Despite the heavy burden of microaggressions, most students, residents, and faculty physicians do not report incidents to their institutions and feel that training, resources, and policies to respond to bias adequately are lacking.⁷ As a result of implicit bias and microaggressions, women and URM medical students and providers are unable to focus solely on the practice of medicine. They are tasked with the additional burden of shouldering the emotional and cognitive complexities that microaggressions produce.¹⁶

What are strategies to reduce microaggressions in medicine?

To minimize the harmful effects of microaggressions, intervention strategies must be implemented that reduce the likelihood of the occurrence of microaggressions and challenge the stereotypes that undergird implicit bias. These strategies include cultivating allies, followed by demanding structural accountability. Allies are members of the majority group who collectively collaborate with members of the nonmajority group to effect change through the promotion of diversity, equity, and inclusion efforts.¹⁷ Cultivating allies involves building a network of collaboration among these groups and emphasizes education. Education is critical for allies to address microaggressions at the interpersonal level. This process of education involves personal reflection and self-awareness in exploring one’s biases, fears, and assumptions. Integral to this step is broadening one’s acceptance of different cultures, racial/ethnic groups, and identities. There must be a willingness to engage in difficult or uncomfortable conversations and a readiness to actively listen to concerns rather than perpetuating further harm through avoidance and dismissive or defensive behavior.¹⁸

Demanding structural accountability facilitates deconstruction of bias and microaggression at the larger systemic level. This strategy involves implicit bias and antiracism training, development of retention plans, and identification of mentors for women and URM providers and students. Implicit bias and microaggression training and policies should be incorporated into medical education and resident curriculums. Similarly, educational resources and training must be made available to practicing physicians, faculty, and other providers through their institutions and places of employment. Equipping students and providers with the tools needed when microaggressions are witnessed or experienced demonstrates systemic-level accountability and communicates the importance of the issue. Furthermore, the development of retention plans and identification of mentors provide a support system and foster a culture of inclusion where recipients of microaggressions feel protected and valued. Increased feelings of inclusivity and belonging help bridge the gap created through microaggressions and implicit bias.

Final Thoughts

Despite an often covert nature, the detrimental effects of microaggressions are tangible and far reaching. As providers, we must strive to understand all categories of racism and expose the many ways prejudice manifests within medical training and clinical practice. It is our obligation to undertake the challenge of “making the ‘invisible’ visible” as we confront microaggressions and implicit bias to promote a safer and more inclusive medical community and workforce.¹⁹

As manifestations of overt racism and macroaggressions have gained increased visibility, there is a need for discussion of another expression of racism: microaggressions. Although racism classically is viewed as blatant structural, attitudinal, and behavioral prejudice, experts pose that the face of racism has evolved into a more covert insidious form. This form of racism was originally coined racial microaggressions by psychiatrist Chester M. Pierce, MD, 50 years ago.^1,2 Since that time, microaggressions have further expanded to describe “brief and commonplace daily verbal, behavioral, and environmental indignities, whether intentional or unintentional, that communicate hostile, derogatory, or negative racial, gender, sexual-orientation, and religious slights and insults to the target person or group.” ³ This article aims to define and depict examples of microaggressions in medicine, discuss the resulting harmful effects, and offer strategies to minimize and counter these negative ramifications.

What are microaggressions?

Microaggressions are behaviors that stem from implicit bias and occur at an interpersonal level. Implicit bias refers to unconscious stereotypes, assumptions, and beliefs held about an individual’s identity. One of the earliest microaggressions—invisibility—was characterized by Ralph Ellison in his novel Invisible Man. Ellison states, “I am invisible, understand, simply because people refuse to see me . . . When they approach me they see only my surroundings, themselves, or figments of their imagination—indeed, everything and anything except me.”⁴ This concept of invisibility is a primary microaggression faced by people of color.

In medicine, microaggressions and implicit bias may be encountered throughout medical training and clinical practice in interactions with colleagues, superiors, patients, and patients’ families.^5,6 Examples of microaggressions in medicine include demeaning comments, nonverbal disrespect, generalizations of social identity, assumption of nonphysician status, role- or credential-questioning behavior, explicit epithets, rejection of care, questioning or inquiries of ethnic/racial origin, and sexual harassment.⁷

An example of microaggressions in medicine was fully displayed when physician Tamika Cross described her experience of being turned away from helping an unresponsive passenger during a flight emergency.

[T]he flight attendant yells “call overhead for a physician on board.” I raised my hand to grab her attention. She said to me “oh no sweetie put [your] hand down, we are looking for actual physicians or nurses or some type of medical personnel, we don’t have time to talk to you” . . . Another “seasoned” white male approaches the row and says he is a physician as well. She says to me “thanks for your help but he can help us, and he has his credentials.”⁸

What are the effects of microaggressions?

Although microaggressions may be unconscious and unintentional by the offender, the negative ramifications are notable. Recent studies report that women and underrepresented minority (URM) medical students, residents, and physicians experience microaggressions and implicit bias at a higher prevalence and frequency compared with their male and non-URM counterparts.^7,9 Repetitive microaggressions are harmful to the health and safety of women and URM medical students, residents, physicians, other providers, and patients. The Table provides example scenarios of microaggressions in medicine categorized according to Berk.¹⁰

Microaggressions negatively impact physical, mental, and emotional well-being. Current data support that medical students and residents who experience microaggressions are more likely to report associated symptoms of burnout, depression, and suicidal thoughts.^11,12 Subjection to persistent bias can lead to minority status stress and racial battle fatigue, creating feelings of invisibility, isolation, exclusion, and loneliness for those impacted.^13,14

In the book Black Man in a White Coat: A Doctor’s Reflections on Race and Medicine, Damon Tweedy, MD, reflects on race in medicine. Tweedy notes his experience as a medical student when a professor mistakenly assumed he was a maintenance worker in the classroom. Tweedy describes how he internalized the exchange and, despite his success throughout the course of his medical training, combatted feelings of anxiety, self-doubt, and implied inferiority.¹⁵

Although microaggressions are harmful to one’s health, they also undermine the learning and teaching experience for students, residents, and faculty, and they detract from the larger goal of providing care for patients.¹¹ Frequent devaluing and questioning of an individual’s contributions, qualifications, and credentials based on identity can lower productivity and problem-solving abilities. These behaviors cultivate an unwelcome and hostile work/learning environment that is stressful and polarizing for the recipient.

Despite the heavy burden of microaggressions, most students, residents, and faculty physicians do not report incidents to their institutions and feel that training, resources, and policies to respond to bias adequately are lacking.⁷ As a result of implicit bias and microaggressions, women and URM medical students and providers are unable to focus solely on the practice of medicine. They are tasked with the additional burden of shouldering the emotional and cognitive complexities that microaggressions produce.¹⁶

What are strategies to reduce microaggressions in medicine?

To minimize the harmful effects of microaggressions, intervention strategies must be implemented that reduce the likelihood of the occurrence of microaggressions and challenge the stereotypes that undergird implicit bias. These strategies include cultivating allies, followed by demanding structural accountability. Allies are members of the majority group who collectively collaborate with members of the nonmajority group to effect change through the promotion of diversity, equity, and inclusion efforts.¹⁷ Cultivating allies involves building a network of collaboration among these groups and emphasizes education. Education is critical for allies to address microaggressions at the interpersonal level. This process of education involves personal reflection and self-awareness in exploring one’s biases, fears, and assumptions. Integral to this step is broadening one’s acceptance of different cultures, racial/ethnic groups, and identities. There must be a willingness to engage in difficult or uncomfortable conversations and a readiness to actively listen to concerns rather than perpetuating further harm through avoidance and dismissive or defensive behavior.¹⁸

Demanding structural accountability facilitates deconstruction of bias and microaggression at the larger systemic level. This strategy involves implicit bias and antiracism training, development of retention plans, and identification of mentors for women and URM providers and students. Implicit bias and microaggression training and policies should be incorporated into medical education and resident curriculums. Similarly, educational resources and training must be made available to practicing physicians, faculty, and other providers through their institutions and places of employment. Equipping students and providers with the tools needed when microaggressions are witnessed or experienced demonstrates systemic-level accountability and communicates the importance of the issue. Furthermore, the development of retention plans and identification of mentors provide a support system and foster a culture of inclusion where recipients of microaggressions feel protected and valued. Increased feelings of inclusivity and belonging help bridge the gap created through microaggressions and implicit bias.

Final Thoughts

Despite an often covert nature, the detrimental effects of microaggressions are tangible and far reaching. As providers, we must strive to understand all categories of racism and expose the many ways prejudice manifests within medical training and clinical practice. It is our obligation to undertake the challenge of “making the ‘invisible’ visible” as we confront microaggressions and implicit bias to promote a safer and more inclusive medical community and workforce.¹⁹

Dermatologic treatment of patients with skin of color offers specific challenges. Studies have reported structural, morphologic, and physiologic distinctions among different ethnic groups,¹ which may account for distinct clinical presentations of skin disease seen in patients with skin of color. Patients with skin of color are at increased risk for specific dermatologic conditions, such as postinflammatory hyperpigmentation, keloid development, and central centrifugal cicatricial alopecia.^2,3 Furthermore, although skin cancer is less prevalent in patients with skin of color, it often presents at a more advanced stage and with a worse prognosis compared to white patients.⁴

Individuals with skin of color make up the majority of the world’s population and a rapidly expanding portion of the US population. By the year 2044, more than half of all Americans are projected to belong to an ethnic group that is currently a minority. By 2060, the population of citizens identifying with 2 or more races will increase by 226%, the Asian population is projected to grow by 128%, the Hispanic population will increase by 115%, and the black population will increase by 42%.⁵ The racial and ethnic composition of the United States is evolving, and dermatologic care must evolve accordingly to address patients’ unique concerns. It is essential for future dermatologists to be knowledgeable about dermatologic conditions presenting in patients of various ethnic backgrounds.

Prior studies have demonstrated the need for increased exposure, education, and training in diseases pertaining to skin of color in US dermatology residency programs.^6-8 The aim of this study was to assess if dermatologists in-training feel that their residency curriculum sufficiently educates them on the needs of patients with skin of color.

Methods

A 10-question anonymous survey was emailed to 109 dermatology residency programs to evaluate the attitudes of dermatology residents about their exposure to patients with skin of color and their skin-of-color curriculum. The study included individuals 18 years or older who were current residents in a dermatology program accredited by the Accreditation Council for Graduate Medical Education. Responses were measured on a 1 to 3 Likert scale, ranging from agree, neutral, and disagree. Data were analyzed using the Fisher exact test, and the statistical significance was set at P<.05.

Results

Forty-three dermatology residents completed the survey. Respondents self-selected their regions, with 8 (19%) from the Northeast (NE), 7 (16%) from the Southeast (SE), 12 (28%) from the Midwest (MW), 8 (19%) from the Southwest (SW), and 8 (18%) from the Northwest (NW)(Table 1). Overall, 31 (72%) respondents agreed that their practice treats a diverse patient population. Respondents who agreed most often were from the NE, SE, and SW. Less than two-thirds of respondents from the MW agreed, and only half of respondents from the NW agreed (Table 2). Although 37% of all respondents agreed that a dedicated multiethnic skin clinic is important for residents, 5 (63%) NE residents disagreed with this statement compared to 5 (42%) MW residents and 5 (63%) NW residents who agreed (P<.005). Overall, 39 (91%) respondents agreed that dedicated lectures on skin conditions in skin of color patients are important to gain competence in treating patients. Only 4 respondents were neutral to this question, 2 (17%) MW residents and 2 (25%) SW residents. When asked if reading textbook chapters on multiethnic skin is important to gain competence, 36 (83%) respondents agreed. Two respondents disagreed, 1 (13%) from the NE and 1 (8%) from the MW. Overall, 23% of respondents agreed that a rotation dedicated to skin of color is important to build competency. There was a significant difference in responses between the NE and MW (P=.032) and between the NE and NW (P=.019). Furthermore, 19 (44%) respondents agreed that having a faculty member or departmental expert is important for residents to gain competence in treating conditions affecting skin of color. Again, there was a significant difference in responses between the NE and MW (P=.003) and between the SE and MW (P=.009).

When asked the number of hours of lecture per month necessary to gain competence in conditions affecting patients with skin of color, 67% agreed that 1 to 5 hours was sufficient (Table 3). There were significant differences in the responses between the NE and SE (P=.024) and the SE and MW (P=.007). Of all respondents, 53% reported 1 to 5 months of clinical training are needed to gain competence in treating conditions affecting patients with skin of color, with significant differences in responses between the NE and MW (P<.001), the NE and SW (P=.019), and the SE and MW (P=.015)(Table 4).

Comment

Responses varied by practicing region. Less ethnically diverse regions, such as the MW and NW, were more likely to agree that dedicated clinics and rotations are important to gain competence compared to more ethnically diverse regions such as the NE, SE, and SW. Overall, more residents reported that dedicated lectures and textbook chapters were important to gain competency compared to dedicated clinics or rotations.

Although interactive lectures and textbook readings are important for obtaining a foundational understanding of dermatologic disease, they cannot substitute for clinical interactions and hands-on experience treating patients with skin of color.⁹ Not only do clinical interactions encourage independent reading and the study of encountered diagnoses, but intercommunication with patients may have a more profound and lasting impact on residents’ education.

Different regions of the United States have varying distributions of patients with skin of color, and dermatology residency program training reflects these disparities.⁶ In areas of less diversity, dermatology residents examine, diagnose, and treat substantially fewer patients with skin of color. The desire for more diverse training supports the prior findings of Nijhawan et al⁶ and is reflected in the responses we received in our study, whereby residents from the less ethnically diversified regions of the MW and NW were more likely to agree that clinics and rotations were necessary for training in preparation to sufficiently address the needs of patients with skin of color.

One way to compensate for the lack of ethnic diversity encountered in areas such as the MW and NW would be to develop educational programs featuring experts on skin of color.⁶ These specialists would not only train dermatology residents in areas of the country currently lacking ethnic diversity but also expand the expertise for treating patients with skin of color. Additionally, dedicated multiethnic skin clinics and externships devoted solely to treating patients with skin of color could be encouraged for residency training.⁶ Finally, community outreach through volunteer clinics may provide residents exposure to patients with skin of color seeking dermatologic care.¹⁰

This study was limited by the small number of respondents, but we were able to extract important trends and data from the collected responses. It is possible that respondents felt strongly about topics involving patients with skin of color, and the results were skewed to reflect individual bias. Additional limitations included not asking respondents for program names and population density (eg, urban, suburban, rural). Future studies should be directed toward analyzing how the diversity of the local population influences training in patients with skin of color, comparing program directors’ perceptions with residents’ perceptions on training in skin of color, and assessing patient perception of residents’ training in skin of color.

Conclusion

In the last decade it has become increasingly apparent that the US population is diversifying and that patients with skin of color will comprise a substantial proportion of the future population,^8,11 which emphasizes the need for dermatology residency programs to ensure that residents receive adequate training and exposure to patients with skin of color as well as the distinct skin diseases seen more commonly in these populations.¹²

Dermatologic treatment of patients with skin of color offers specific challenges. Studies have reported structural, morphologic, and physiologic distinctions among different ethnic groups,¹ which may account for distinct clinical presentations of skin disease seen in patients with skin of color. Patients with skin of color are at increased risk for specific dermatologic conditions, such as postinflammatory hyperpigmentation, keloid development, and central centrifugal cicatricial alopecia.^2,3 Furthermore, although skin cancer is less prevalent in patients with skin of color, it often presents at a more advanced stage and with a worse prognosis compared to white patients.⁴

Individuals with skin of color make up the majority of the world’s population and a rapidly expanding portion of the US population. By the year 2044, more than half of all Americans are projected to belong to an ethnic group that is currently a minority. By 2060, the population of citizens identifying with 2 or more races will increase by 226%, the Asian population is projected to grow by 128%, the Hispanic population will increase by 115%, and the black population will increase by 42%.⁵ The racial and ethnic composition of the United States is evolving, and dermatologic care must evolve accordingly to address patients’ unique concerns. It is essential for future dermatologists to be knowledgeable about dermatologic conditions presenting in patients of various ethnic backgrounds.

Prior studies have demonstrated the need for increased exposure, education, and training in diseases pertaining to skin of color in US dermatology residency programs.^6-8 The aim of this study was to assess if dermatologists in-training feel that their residency curriculum sufficiently educates them on the needs of patients with skin of color.

Methods

A 10-question anonymous survey was emailed to 109 dermatology residency programs to evaluate the attitudes of dermatology residents about their exposure to patients with skin of color and their skin-of-color curriculum. The study included individuals 18 years or older who were current residents in a dermatology program accredited by the Accreditation Council for Graduate Medical Education. Responses were measured on a 1 to 3 Likert scale, ranging from agree, neutral, and disagree. Data were analyzed using the Fisher exact test, and the statistical significance was set at P<.05.

Results

Forty-three dermatology residents completed the survey. Respondents self-selected their regions, with 8 (19%) from the Northeast (NE), 7 (16%) from the Southeast (SE), 12 (28%) from the Midwest (MW), 8 (19%) from the Southwest (SW), and 8 (18%) from the Northwest (NW)(Table 1). Overall, 31 (72%) respondents agreed that their practice treats a diverse patient population. Respondents who agreed most often were from the NE, SE, and SW. Less than two-thirds of respondents from the MW agreed, and only half of respondents from the NW agreed (Table 2). Although 37% of all respondents agreed that a dedicated multiethnic skin clinic is important for residents, 5 (63%) NE residents disagreed with this statement compared to 5 (42%) MW residents and 5 (63%) NW residents who agreed (P<.005). Overall, 39 (91%) respondents agreed that dedicated lectures on skin conditions in skin of color patients are important to gain competence in treating patients. Only 4 respondents were neutral to this question, 2 (17%) MW residents and 2 (25%) SW residents. When asked if reading textbook chapters on multiethnic skin is important to gain competence, 36 (83%) respondents agreed. Two respondents disagreed, 1 (13%) from the NE and 1 (8%) from the MW. Overall, 23% of respondents agreed that a rotation dedicated to skin of color is important to build competency. There was a significant difference in responses between the NE and MW (P=.032) and between the NE and NW (P=.019). Furthermore, 19 (44%) respondents agreed that having a faculty member or departmental expert is important for residents to gain competence in treating conditions affecting skin of color. Again, there was a significant difference in responses between the NE and MW (P=.003) and between the SE and MW (P=.009).

When asked the number of hours of lecture per month necessary to gain competence in conditions affecting patients with skin of color, 67% agreed that 1 to 5 hours was sufficient (Table 3). There were significant differences in the responses between the NE and SE (P=.024) and the SE and MW (P=.007). Of all respondents, 53% reported 1 to 5 months of clinical training are needed to gain competence in treating conditions affecting patients with skin of color, with significant differences in responses between the NE and MW (P<.001), the NE and SW (P=.019), and the SE and MW (P=.015)(Table 4).

Comment

Responses varied by practicing region. Less ethnically diverse regions, such as the MW and NW, were more likely to agree that dedicated clinics and rotations are important to gain competence compared to more ethnically diverse regions such as the NE, SE, and SW. Overall, more residents reported that dedicated lectures and textbook chapters were important to gain competency compared to dedicated clinics or rotations.

Although interactive lectures and textbook readings are important for obtaining a foundational understanding of dermatologic disease, they cannot substitute for clinical interactions and hands-on experience treating patients with skin of color.⁹ Not only do clinical interactions encourage independent reading and the study of encountered diagnoses, but intercommunication with patients may have a more profound and lasting impact on residents’ education.

Different regions of the United States have varying distributions of patients with skin of color, and dermatology residency program training reflects these disparities.⁶ In areas of less diversity, dermatology residents examine, diagnose, and treat substantially fewer patients with skin of color. The desire for more diverse training supports the prior findings of Nijhawan et al⁶ and is reflected in the responses we received in our study, whereby residents from the less ethnically diversified regions of the MW and NW were more likely to agree that clinics and rotations were necessary for training in preparation to sufficiently address the needs of patients with skin of color.

One way to compensate for the lack of ethnic diversity encountered in areas such as the MW and NW would be to develop educational programs featuring experts on skin of color.⁶ These specialists would not only train dermatology residents in areas of the country currently lacking ethnic diversity but also expand the expertise for treating patients with skin of color. Additionally, dedicated multiethnic skin clinics and externships devoted solely to treating patients with skin of color could be encouraged for residency training.⁶ Finally, community outreach through volunteer clinics may provide residents exposure to patients with skin of color seeking dermatologic care.¹⁰

This study was limited by the small number of respondents, but we were able to extract important trends and data from the collected responses. It is possible that respondents felt strongly about topics involving patients with skin of color, and the results were skewed to reflect individual bias. Additional limitations included not asking respondents for program names and population density (eg, urban, suburban, rural). Future studies should be directed toward analyzing how the diversity of the local population influences training in patients with skin of color, comparing program directors’ perceptions with residents’ perceptions on training in skin of color, and assessing patient perception of residents’ training in skin of color.

Conclusion

In the last decade it has become increasingly apparent that the US population is diversifying and that patients with skin of color will comprise a substantial proportion of the future population,^8,11 which emphasizes the need for dermatology residency programs to ensure that residents receive adequate training and exposure to patients with skin of color as well as the distinct skin diseases seen more commonly in these populations.¹²

Dermatologic treatment of patients with skin of color offers specific challenges. Studies have reported structural, morphologic, and physiologic distinctions among different ethnic groups,¹ which may account for distinct clinical presentations of skin disease seen in patients with skin of color. Patients with skin of color are at increased risk for specific dermatologic conditions, such as postinflammatory hyperpigmentation, keloid development, and central centrifugal cicatricial alopecia.^2,3 Furthermore, although skin cancer is less prevalent in patients with skin of color, it often presents at a more advanced stage and with a worse prognosis compared to white patients.⁴

Individuals with skin of color make up the majority of the world’s population and a rapidly expanding portion of the US population. By the year 2044, more than half of all Americans are projected to belong to an ethnic group that is currently a minority. By 2060, the population of citizens identifying with 2 or more races will increase by 226%, the Asian population is projected to grow by 128%, the Hispanic population will increase by 115%, and the black population will increase by 42%.⁵ The racial and ethnic composition of the United States is evolving, and dermatologic care must evolve accordingly to address patients’ unique concerns. It is essential for future dermatologists to be knowledgeable about dermatologic conditions presenting in patients of various ethnic backgrounds.

Prior studies have demonstrated the need for increased exposure, education, and training in diseases pertaining to skin of color in US dermatology residency programs.^6-8 The aim of this study was to assess if dermatologists in-training feel that their residency curriculum sufficiently educates them on the needs of patients with skin of color.

Methods

A 10-question anonymous survey was emailed to 109 dermatology residency programs to evaluate the attitudes of dermatology residents about their exposure to patients with skin of color and their skin-of-color curriculum. The study included individuals 18 years or older who were current residents in a dermatology program accredited by the Accreditation Council for Graduate Medical Education. Responses were measured on a 1 to 3 Likert scale, ranging from agree, neutral, and disagree. Data were analyzed using the Fisher exact test, and the statistical significance was set at P<.05.

Results

Forty-three dermatology residents completed the survey. Respondents self-selected their regions, with 8 (19%) from the Northeast (NE), 7 (16%) from the Southeast (SE), 12 (28%) from the Midwest (MW), 8 (19%) from the Southwest (SW), and 8 (18%) from the Northwest (NW)(Table 1). Overall, 31 (72%) respondents agreed that their practice treats a diverse patient population. Respondents who agreed most often were from the NE, SE, and SW. Less than two-thirds of respondents from the MW agreed, and only half of respondents from the NW agreed (Table 2). Although 37% of all respondents agreed that a dedicated multiethnic skin clinic is important for residents, 5 (63%) NE residents disagreed with this statement compared to 5 (42%) MW residents and 5 (63%) NW residents who agreed (P<.005). Overall, 39 (91%) respondents agreed that dedicated lectures on skin conditions in skin of color patients are important to gain competence in treating patients. Only 4 respondents were neutral to this question, 2 (17%) MW residents and 2 (25%) SW residents. When asked if reading textbook chapters on multiethnic skin is important to gain competence, 36 (83%) respondents agreed. Two respondents disagreed, 1 (13%) from the NE and 1 (8%) from the MW. Overall, 23% of respondents agreed that a rotation dedicated to skin of color is important to build competency. There was a significant difference in responses between the NE and MW (P=.032) and between the NE and NW (P=.019). Furthermore, 19 (44%) respondents agreed that having a faculty member or departmental expert is important for residents to gain competence in treating conditions affecting skin of color. Again, there was a significant difference in responses between the NE and MW (P=.003) and between the SE and MW (P=.009).

When asked the number of hours of lecture per month necessary to gain competence in conditions affecting patients with skin of color, 67% agreed that 1 to 5 hours was sufficient (Table 3). There were significant differences in the responses between the NE and SE (P=.024) and the SE and MW (P=.007). Of all respondents, 53% reported 1 to 5 months of clinical training are needed to gain competence in treating conditions affecting patients with skin of color, with significant differences in responses between the NE and MW (P<.001), the NE and SW (P=.019), and the SE and MW (P=.015)(Table 4).

Comment

Responses varied by practicing region. Less ethnically diverse regions, such as the MW and NW, were more likely to agree that dedicated clinics and rotations are important to gain competence compared to more ethnically diverse regions such as the NE, SE, and SW. Overall, more residents reported that dedicated lectures and textbook chapters were important to gain competency compared to dedicated clinics or rotations.

Although interactive lectures and textbook readings are important for obtaining a foundational understanding of dermatologic disease, they cannot substitute for clinical interactions and hands-on experience treating patients with skin of color.⁹ Not only do clinical interactions encourage independent reading and the study of encountered diagnoses, but intercommunication with patients may have a more profound and lasting impact on residents’ education.

Different regions of the United States have varying distributions of patients with skin of color, and dermatology residency program training reflects these disparities.⁶ In areas of less diversity, dermatology residents examine, diagnose, and treat substantially fewer patients with skin of color. The desire for more diverse training supports the prior findings of Nijhawan et al⁶ and is reflected in the responses we received in our study, whereby residents from the less ethnically diversified regions of the MW and NW were more likely to agree that clinics and rotations were necessary for training in preparation to sufficiently address the needs of patients with skin of color.

One way to compensate for the lack of ethnic diversity encountered in areas such as the MW and NW would be to develop educational programs featuring experts on skin of color.⁶ These specialists would not only train dermatology residents in areas of the country currently lacking ethnic diversity but also expand the expertise for treating patients with skin of color. Additionally, dedicated multiethnic skin clinics and externships devoted solely to treating patients with skin of color could be encouraged for residency training.⁶ Finally, community outreach through volunteer clinics may provide residents exposure to patients with skin of color seeking dermatologic care.¹⁰

This study was limited by the small number of respondents, but we were able to extract important trends and data from the collected responses. It is possible that respondents felt strongly about topics involving patients with skin of color, and the results were skewed to reflect individual bias. Additional limitations included not asking respondents for program names and population density (eg, urban, suburban, rural). Future studies should be directed toward analyzing how the diversity of the local population influences training in patients with skin of color, comparing program directors’ perceptions with residents’ perceptions on training in skin of color, and assessing patient perception of residents’ training in skin of color.

Conclusion

In the last decade it has become increasingly apparent that the US population is diversifying and that patients with skin of color will comprise a substantial proportion of the future population,^8,11 which emphasizes the need for dermatology residency programs to ensure that residents receive adequate training and exposure to patients with skin of color as well as the distinct skin diseases seen more commonly in these populations.¹²

Data are limited on the management of atopic dermatitis (AD) in adolescents, particularly in patients with skin of color, making it important to identify factors that may improve AD management in this population. Comorbid conditions (eg, acne, postinflammatory hyperpigmentation [PIH]), extracurricular activities (eg, athletics), and experimentation with cosmetics in adolescents, all of which can undermine treatment efficacy and medication adherence, make it particularly challenging to devise a therapeutic regimen in this patient population. We review the management of AD in black adolescents, with special consideration of concomitant treatment of acne vulgaris (AV) as well as lifestyle and social choices (Table).

Prevalence and Epidemiology

Atopic dermatitis affects 13% to 25% of children and 2% to 10% of adults.^1,2 Population‐based studies in the United States show a higher prevalence of AD in black children (19.3%) compared to European American (EA) children (16.1%).^3,4

AD in Black Adolescents

Atopic dermatitis is a common skin condition that is defined as a chronic, pruritic, inflammatory dermatosis with recurrent scaling, papules, and plaques (Figure) that usually develop during infancy and early childhood.³ Although AD severity improves for some patients in adolescence, it can be a lifelong issue affecting performance in academic and occupational settings.⁵ One US study of 8015 children found that there are racial and ethnic disparities in school absences among children (age range, 2–17 years) with AD, with children with skin of color being absent more often than white children.⁶ The same study noted that black children had a 1.5-fold higher chance of being absent 6 days over a 6-month school period compared to white children. It is postulated that AD has a greater impact on quality of life (QOL) in children with skin of color, resulting in the increased number of school absences in this population.⁶

The origin of AD currently is thought to be complex and can involve skin barrier dysfunction, environmental factors, microbiome effects, genetic predisposition, and immune dysregulation.^1,4 Atopic dermatitis is a heterogeneous disease with variations in the prevalence, genetic background, and immune activation patterns across racial groups.⁴ It is now understood to be an immune-mediated disease with multiple inflammatory pathways, with type 2–associated inflammation being a primary pathway. Patients with AD have strong helper T cell (T_H2) activation, and black patients with AD have higher IgE serum levels as well as absent T_H17/T_H1 activation.⁴

Atopic dermatitis currently is seen as a defect of the epidermal barrier, with variable clinical manifestations and expressivity.⁷ Filaggrin is an epidermal barrier protein, encoded by the FLG gene, and plays a major role in barrier function by regulating pH and promoting hydration of the skin.⁴ Loss of function of the FLG gene is the most well-studied genetic risk factor for developing AD, and this mutation is seen in patients with more severe and persistent AD in addition to patients with more skin infections and allergic sensitizations.^3,4 However, in the skin of color population, FLG mutations are 6 times less common than in the EA population, despite the fact that AD is more prevalent in patients of African descent.⁴ Therefore, the role of the FLG loss-of-function mutation and AD is not as well defined in black patients, and some researchers have found no association.³ The FLG loss-of-function mutation seems to play a smaller role in black patients than in EA patients, and other genes may be involved in skin barrier dysfunction.^3,4 In a small study of patients with mild AD compared to nonaffected patients, those with AD had lower total ceramide levels in the stratum corneum of affected sites than normal skin sites in healthy individuals.⁸

Particular disturbances in the gut microbiome have the possibility of impacting the development of AD.⁹ Additionally, the development of AD may be influenced by the skin microbiome, which can change depending on body site, with fungal organisms thought to make up a large proportion of the microbiome of patients with AD. In patients with AD, there is a lack of microbial diversity and an overgrowth of Staphylococcus aureus.⁹

Diagnosis

Clinicians diagnose AD based on clinical characteristics, and the lack of objective criteria can hinder diagnosis.¹ Thus, diagnosing AD in children with dark skin can pose a particular challenge given the varied clinical presentation of AD across skin types. Severe cases of AD may not be diagnosed or treated adequately in deeply pigmented children because erythema, a defining characteristic of AD, may be hard to identify in darker skin types.¹⁰ Furthermore, clinical erythema scores among black children may be “strongly” underestimated using scoring systems such as Eczema Area and Severity Index and SCORing Atopic Dermatitis.⁴ It is estimated that the risk for severe AD may be 6 times higher in black children compared to white children.¹⁰ Additionally, patients with skin of color can present with more treatment-resistant AD.⁴

Treatment of AD

Current treatment is focused on restoring epidermal barrier function, often with topical agents, such as moisturizers containing different amounts of emollients, occlusives, and humectants; corticosteroids; calcineurin inhibitors; and antimicrobials. Emollients such as glycol stearate, glyceryl stearate, and soy sterols function as lubricants, softening the skin. Occlusive agents include petrolatum, dimethicone, and mineral oil; they act by forming a layer to slow evaporation of water. Humectants including glycerol, lactic acid, and urea function by promoting water retention.¹¹ For acute flares, mid- to high-potency topical corticosteroids are recommended. Also, topical calcineurin inhibitors such as tacrolimus and pimecrolimus may be used alone or in combination with topical steroids. Finally, bleach baths and topical mupirocin applied to the nares also have proved helpful in moderate to severe AD with secondary bacterial infections.¹¹ Phototherapy can be used in adult and pediatric patients with acute and chronic AD if traditional treatments have failed.²

Systemic agents are indicated and recommended for the subset of adult and pediatric patients in whom optimized topical regimens and/or phototherapy do not adequately provide disease control or when QOL is substantially impacted. The systemic agents effective in the pediatric population include cyclosporine, azathioprine, mycophenolate mofetil, and possibly methotrexate.¹¹ Dupilumab recently was approved by the US Food and Drug Administration for patients 12 years and older with moderate to severe AD whose disease is not well controlled with topical medications.

Patients with AD are predisposed to secondary bacterial and viral infections because of their dysfunctional skin barrier; these infections most commonly are caused by S aureus and herpes simplex virus, respectively.² Systemic antibiotics are only recommended for patients with AD when there is clinical evidence of bacterial infection. In patients with evidence of eczema herpeticum, systemic antiviral agents should be used to treat the underlying herpes simplex virus infection.² Atopic dermatitis typically has been studied in white patients; however, patients with skin of color have higher frequencies of treatment-resistant AD. Further research on treatment efficacy for AD in this patient population is needed, as data are limited.⁴

Treatment of AV in Patients With AD

Two of the most prevalent skin diseases affecting the pediatric population are AD and AV, and both can remarkably impact QOL.¹² Acne is one of the most common reasons for adolescent patients to seek dermatologic care, including patients with skin of color (Fitzpatrick skin types IV to VI).¹³ Thus, it is to be expected that many black adolescents with AD also will have AV. For mild to moderate acne in patients with skin of color, topical retinoids and benzoyl peroxide typically are first line.¹³ These medications can be problematic for patients with AD, as retinoids and many other acne treatments can cause dryness, which may exacerbate AD.

Moisturizers containing ceramide can be a helpful adjunctive therapy in treating acne,¹⁴ especially in patients with AD. Modifications to application of acne medications, such as using topical retinoids every other night or mixing them with moisturizers to minimize dryness, may be beneficial to these patients. Dapsone gel 7.5% used daily also may be an option for adolescents with AD and AV. A double-blind, vehicle-controlled study demonstrated that dapsone is safe and effective for patients 12 years and older with moderate acne, and patients with Fitzpatrick skin types IV to VI rated local scaling, erythema, dryness, and stinging/burning as “none” in the study.¹⁵ Another potentially helpful topical agent in patients with AD and AV is sulfacetamide, as it is not likely to cause dryness of the skin. In a small study, sodium sulfacetamide 10% and sulfur 5% in an emollient foam vehicle showed no residual film or sulfur smell and resulted in acne reduction of 50%.¹⁶

Patients with skin of color often experience PIH in AD and acne or hypopigmentation from inflammatory dermatoses including AD.^17,18 In addition to the dryness from AD and topical retinoid use, patients with skin of color may develop irritant contact dermatitis, thus leading to PIH.¹³ Dryness and irritant contact dermatitis also can be seen with the use of benzoyl peroxide in black patients. Because of these effects, gentle moisturizers are recommended, and both benzoyl peroxide and retinoids should be initiated at lower doses in patients with skin of color.¹³

For patients with severe nodulocystic acne, isotretinoin is the treatment of choice in patients with skin of color,¹³ but there is a dearth of clinical studies addressing complications seen in black adolescents on this treatment, especially with respect to those with AD. Of note, systemic antibiotics typically are initiated before isotretinoin; however, this strategy is falling out of favor due to concern for antibiotic resistance with long-term use.¹⁹

Impact of Athletics on AD in Black Adolescents

Because of the exacerbating effects of perspiration and heat causing itch and irritation in patients with AD, it is frequently advised that pediatric patients limit their participation in athletics because of the exacerbating effects of strenuous physical exercise on their disease.¹² In one study, 429 pediatric patients or their parents/guardians completed QOL questionnaires; 89% of patients 15 years and younger with severe AD reported that their disease was impacted by athletics and outdoor activities, and 86% of these pediatric patients with severe AD responded that their social lives and leisure activities were impacted.²⁰ Because adolescents often are involved in athletics or have mandatory physical education classes, AD may be isolating and may have a severe impact on self-esteem.

Aggressive treatment of AD with topical and systemic medications may be helpful in adolescents who may be reluctant to participate in sports because of teasing, bullying, or worsening of symptoms with heat or sweating.²¹ Now that dupilumab is available for adolescents, there is a chance that patients with severe and/or recalcitrant disease managed on this medication can achieve better control of their symptoms without the laboratory requirement of methotrexate and the difficulties of topical medication application, allowing them to engage in mandatory athletic classes as well as desired organized sports.

Use of Cosmetics for AD

Many adolescents experiment with cosmetics, and those with AD may use cosmetic products to cover hyperpigmented or hypopigmented lesions.¹⁸ In patients with active AD or increased sensitivity to allergens in cosmetic products, use of makeup can be a contributing factor for AD flares. Acne associated with cosmetics is especially important to consider in darker-skinned patients who may use makeup that is opaque and contains oil to conceal acne or PIH.

Allergens can be present in both cosmetics and pharmaceutical topical agents, and a Brazilian study found that approximately 89% of 813 prescription and nonprescription products (eg, topical drugs, sunscreens, moisturizers, soaps, cleansing lotions, shampoos, cosmeceuticals) contained allergens.²² Patients with AD have a higher prevalence of contact sensitization to fragrances, including balsam of Peru.²³ Some AD treatments that contain fragrances have caused further skin issues in a few patients. In one case series, 3 pediatric patients developed allergic contact dermatitis to Myroxylon pereirae (balsam of Peru) when using topical treatments for their AD, and their symptoms of scalp inflammation and alopecia resolved with discontinuation.²³

In a Dutch study, sensitization to Fragrance Mix I and M pereirae as well as other ingredients (eg, lanolin alcohol, Amerchol™ L 101 [a lanolin product]) was notably more common in pediatric patients with AD than in patients without AD; however, no data on patients with skin of color were included in this study.²⁴

Because of the increased risk of sensitization to fragrances and other ingredients in patients with AD as well as the high percentage of allergens in prescription and nonprescription products, it is important to discuss all personal care products that patients may be using, not just their cosmetic products. Also, patch testing may be helpful in determining true allergens in some patients. Patch testing is recommended for patients with treatment-resistant AD, and a recent study suggested it should be done prior to long-term use of immunosuppressive agents.²⁵ Increased steroid phobia and a push toward alternative medicines are leading both patients with AD and guardians of children with AD to look for other forms of moisturization, such as olive oil, coconut oil, sunflower seed oil, and shea butter, to decrease transepidermal water loss.^26,27 An important factor in AD treatment efficacy is patient acceptability in using what is recommended.²⁷ One study showed there was no difference in efficacy or acceptability in using a cream containing shea butter extract vs the ceramide-precursor product.²⁷ Current data show olive oil may exacerbate dry skin and AD,²⁶ and recommendation of any over-the-counter oils and butters in patients with AD should be made with great caution, as many of these products contain fragrances and other potential allergens.

Alternative Therapies for AD

Patients with AD often seek alternative or integrative treatment options, including dietary modifications and holistic remedies. Studies investigating the role of vitamins and supplements in treating AD are limited by sample size.²⁸ However, there is some evidence that may support supplementation with vitamins D and E in addressing AD symptoms. The use of probiotics in treating AD is controversial, but there are studies suggesting that the use of probiotics may prove beneficial in preventing infantile AD.²⁸ Additionally, findings from an ex vivo and in vitro study show that some conditions, including AD and acne, may benefit from the same probiotics, despite the differences in these two diseases. Both AD and acne have inflammatory and skin dysbiosis characteristics, which may be the common thread leading to both conditions potentially responding to treatment with probiotics.²⁹

Preliminary evidence indicates that supplements containing fatty acids such as docosahexaenoic acid, sea buckthorn oil, and hemp seed oil may decrease the severity of AD.²⁸ In a 20-week, randomized, single-blind, crossover study published in 2005, dietary hemp seed oil showed an improvement of clinical symptoms, including dry skin and itchiness, in patients with AD.³⁰

In light of recent legalization in several states, patients may turn to use of cannabinoid products to manage AD. In a systematic review, cannabinoid use was reportedly a therapeutic option in the treatment of AD and AV; however, the data are based on preclinical work, and there are no randomized, placebo-controlled studies to support the use of cannabinoids.³¹ Furthermore, there is great concern that use of these products in adolescents is an even larger unknown.

Final Thoughts

Eighty percent of children diagnosed with AD experience symptom improvement before their early teens³²; for those with AD during their preteen and teenage years, there can be psychological ramifications, as teenagers with AD report having fewer friends, are less socially involved, participate in fewer sports, and are absent from classes more often than their peers.⁵ In black patients with AD, school absences are even more common.⁶ Given the social and emotional impact of AD on patients with skin of color, it is imperative to treat the condition appropriately.³³ There are areas of opportunity for further research on alternate dosing of existing treatments for AV in patients with AD, further recommendations for adolescent athletes with AD, and which cosmetic and alternative medicine products may be beneficial for this population to improve their QOL.

Providers should discuss medical management in a broader context considering patients’ extracurricular activities, treatment vehicle preferences, expectations, and personal care habits. It also is important to address the many possible factors that may influence treatment adherence early on, particularly in adolescents, as these could be barriers to treatment. This article highlights considerations for treating AD and comorbid conditions that may further complicate treatment in adolescent patients with skin of color. The information provided should serve as a guide in initial counseling and management of AD in adolescents with skin of color.

Data are limited on the management of atopic dermatitis (AD) in adolescents, particularly in patients with skin of color, making it important to identify factors that may improve AD management in this population. Comorbid conditions (eg, acne, postinflammatory hyperpigmentation [PIH]), extracurricular activities (eg, athletics), and experimentation with cosmetics in adolescents, all of which can undermine treatment efficacy and medication adherence, make it particularly challenging to devise a therapeutic regimen in this patient population. We review the management of AD in black adolescents, with special consideration of concomitant treatment of acne vulgaris (AV) as well as lifestyle and social choices (Table).

Prevalence and Epidemiology

Atopic dermatitis affects 13% to 25% of children and 2% to 10% of adults.^1,2 Population‐based studies in the United States show a higher prevalence of AD in black children (19.3%) compared to European American (EA) children (16.1%).^3,4

AD in Black Adolescents

Atopic dermatitis is a common skin condition that is defined as a chronic, pruritic, inflammatory dermatosis with recurrent scaling, papules, and plaques (Figure) that usually develop during infancy and early childhood.³ Although AD severity improves for some patients in adolescence, it can be a lifelong issue affecting performance in academic and occupational settings.⁵ One US study of 8015 children found that there are racial and ethnic disparities in school absences among children (age range, 2–17 years) with AD, with children with skin of color being absent more often than white children.⁶ The same study noted that black children had a 1.5-fold higher chance of being absent 6 days over a 6-month school period compared to white children. It is postulated that AD has a greater impact on quality of life (QOL) in children with skin of color, resulting in the increased number of school absences in this population.⁶

The origin of AD currently is thought to be complex and can involve skin barrier dysfunction, environmental factors, microbiome effects, genetic predisposition, and immune dysregulation.^1,4 Atopic dermatitis is a heterogeneous disease with variations in the prevalence, genetic background, and immune activation patterns across racial groups.⁴ It is now understood to be an immune-mediated disease with multiple inflammatory pathways, with type 2–associated inflammation being a primary pathway. Patients with AD have strong helper T cell (T_H2) activation, and black patients with AD have higher IgE serum levels as well as absent T_H17/T_H1 activation.⁴

Atopic dermatitis currently is seen as a defect of the epidermal barrier, with variable clinical manifestations and expressivity.⁷ Filaggrin is an epidermal barrier protein, encoded by the FLG gene, and plays a major role in barrier function by regulating pH and promoting hydration of the skin.⁴ Loss of function of the FLG gene is the most well-studied genetic risk factor for developing AD, and this mutation is seen in patients with more severe and persistent AD in addition to patients with more skin infections and allergic sensitizations.^3,4 However, in the skin of color population, FLG mutations are 6 times less common than in the EA population, despite the fact that AD is more prevalent in patients of African descent.⁴ Therefore, the role of the FLG loss-of-function mutation and AD is not as well defined in black patients, and some researchers have found no association.³ The FLG loss-of-function mutation seems to play a smaller role in black patients than in EA patients, and other genes may be involved in skin barrier dysfunction.^3,4 In a small study of patients with mild AD compared to nonaffected patients, those with AD had lower total ceramide levels in the stratum corneum of affected sites than normal skin sites in healthy individuals.⁸

Particular disturbances in the gut microbiome have the possibility of impacting the development of AD.⁹ Additionally, the development of AD may be influenced by the skin microbiome, which can change depending on body site, with fungal organisms thought to make up a large proportion of the microbiome of patients with AD. In patients with AD, there is a lack of microbial diversity and an overgrowth of Staphylococcus aureus.⁹

Diagnosis

Clinicians diagnose AD based on clinical characteristics, and the lack of objective criteria can hinder diagnosis.¹ Thus, diagnosing AD in children with dark skin can pose a particular challenge given the varied clinical presentation of AD across skin types. Severe cases of AD may not be diagnosed or treated adequately in deeply pigmented children because erythema, a defining characteristic of AD, may be hard to identify in darker skin types.¹⁰ Furthermore, clinical erythema scores among black children may be “strongly” underestimated using scoring systems such as Eczema Area and Severity Index and SCORing Atopic Dermatitis.⁴ It is estimated that the risk for severe AD may be 6 times higher in black children compared to white children.¹⁰ Additionally, patients with skin of color can present with more treatment-resistant AD.⁴

Treatment of AD

Current treatment is focused on restoring epidermal barrier function, often with topical agents, such as moisturizers containing different amounts of emollients, occlusives, and humectants; corticosteroids; calcineurin inhibitors; and antimicrobials. Emollients such as glycol stearate, glyceryl stearate, and soy sterols function as lubricants, softening the skin. Occlusive agents include petrolatum, dimethicone, and mineral oil; they act by forming a layer to slow evaporation of water. Humectants including glycerol, lactic acid, and urea function by promoting water retention.¹¹ For acute flares, mid- to high-potency topical corticosteroids are recommended. Also, topical calcineurin inhibitors such as tacrolimus and pimecrolimus may be used alone or in combination with topical steroids. Finally, bleach baths and topical mupirocin applied to the nares also have proved helpful in moderate to severe AD with secondary bacterial infections.¹¹ Phototherapy can be used in adult and pediatric patients with acute and chronic AD if traditional treatments have failed.²

Systemic agents are indicated and recommended for the subset of adult and pediatric patients in whom optimized topical regimens and/or phototherapy do not adequately provide disease control or when QOL is substantially impacted. The systemic agents effective in the pediatric population include cyclosporine, azathioprine, mycophenolate mofetil, and possibly methotrexate.¹¹ Dupilumab recently was approved by the US Food and Drug Administration for patients 12 years and older with moderate to severe AD whose disease is not well controlled with topical medications.

Patients with AD are predisposed to secondary bacterial and viral infections because of their dysfunctional skin barrier; these infections most commonly are caused by S aureus and herpes simplex virus, respectively.² Systemic antibiotics are only recommended for patients with AD when there is clinical evidence of bacterial infection. In patients with evidence of eczema herpeticum, systemic antiviral agents should be used to treat the underlying herpes simplex virus infection.² Atopic dermatitis typically has been studied in white patients; however, patients with skin of color have higher frequencies of treatment-resistant AD. Further research on treatment efficacy for AD in this patient population is needed, as data are limited.⁴

Treatment of AV in Patients With AD

Two of the most prevalent skin diseases affecting the pediatric population are AD and AV, and both can remarkably impact QOL.¹² Acne is one of the most common reasons for adolescent patients to seek dermatologic care, including patients with skin of color (Fitzpatrick skin types IV to VI).¹³ Thus, it is to be expected that many black adolescents with AD also will have AV. For mild to moderate acne in patients with skin of color, topical retinoids and benzoyl peroxide typically are first line.¹³ These medications can be problematic for patients with AD, as retinoids and many other acne treatments can cause dryness, which may exacerbate AD.

Moisturizers containing ceramide can be a helpful adjunctive therapy in treating acne,¹⁴ especially in patients with AD. Modifications to application of acne medications, such as using topical retinoids every other night or mixing them with moisturizers to minimize dryness, may be beneficial to these patients. Dapsone gel 7.5% used daily also may be an option for adolescents with AD and AV. A double-blind, vehicle-controlled study demonstrated that dapsone is safe and effective for patients 12 years and older with moderate acne, and patients with Fitzpatrick skin types IV to VI rated local scaling, erythema, dryness, and stinging/burning as “none” in the study.¹⁵ Another potentially helpful topical agent in patients with AD and AV is sulfacetamide, as it is not likely to cause dryness of the skin. In a small study, sodium sulfacetamide 10% and sulfur 5% in an emollient foam vehicle showed no residual film or sulfur smell and resulted in acne reduction of 50%.¹⁶

Patients with skin of color often experience PIH in AD and acne or hypopigmentation from inflammatory dermatoses including AD.^17,18 In addition to the dryness from AD and topical retinoid use, patients with skin of color may develop irritant contact dermatitis, thus leading to PIH.¹³ Dryness and irritant contact dermatitis also can be seen with the use of benzoyl peroxide in black patients. Because of these effects, gentle moisturizers are recommended, and both benzoyl peroxide and retinoids should be initiated at lower doses in patients with skin of color.¹³

For patients with severe nodulocystic acne, isotretinoin is the treatment of choice in patients with skin of color,¹³ but there is a dearth of clinical studies addressing complications seen in black adolescents on this treatment, especially with respect to those with AD. Of note, systemic antibiotics typically are initiated before isotretinoin; however, this strategy is falling out of favor due to concern for antibiotic resistance with long-term use.¹⁹

Impact of Athletics on AD in Black Adolescents

Because of the exacerbating effects of perspiration and heat causing itch and irritation in patients with AD, it is frequently advised that pediatric patients limit their participation in athletics because of the exacerbating effects of strenuous physical exercise on their disease.¹² In one study, 429 pediatric patients or their parents/guardians completed QOL questionnaires; 89% of patients 15 years and younger with severe AD reported that their disease was impacted by athletics and outdoor activities, and 86% of these pediatric patients with severe AD responded that their social lives and leisure activities were impacted.²⁰ Because adolescents often are involved in athletics or have mandatory physical education classes, AD may be isolating and may have a severe impact on self-esteem.

Aggressive treatment of AD with topical and systemic medications may be helpful in adolescents who may be reluctant to participate in sports because of teasing, bullying, or worsening of symptoms with heat or sweating.²¹ Now that dupilumab is available for adolescents, there is a chance that patients with severe and/or recalcitrant disease managed on this medication can achieve better control of their symptoms without the laboratory requirement of methotrexate and the difficulties of topical medication application, allowing them to engage in mandatory athletic classes as well as desired organized sports.

Use of Cosmetics for AD

Many adolescents experiment with cosmetics, and those with AD may use cosmetic products to cover hyperpigmented or hypopigmented lesions.¹⁸ In patients with active AD or increased sensitivity to allergens in cosmetic products, use of makeup can be a contributing factor for AD flares. Acne associated with cosmetics is especially important to consider in darker-skinned patients who may use makeup that is opaque and contains oil to conceal acne or PIH.

Allergens can be present in both cosmetics and pharmaceutical topical agents, and a Brazilian study found that approximately 89% of 813 prescription and nonprescription products (eg, topical drugs, sunscreens, moisturizers, soaps, cleansing lotions, shampoos, cosmeceuticals) contained allergens.²² Patients with AD have a higher prevalence of contact sensitization to fragrances, including balsam of Peru.²³ Some AD treatments that contain fragrances have caused further skin issues in a few patients. In one case series, 3 pediatric patients developed allergic contact dermatitis to Myroxylon pereirae (balsam of Peru) when using topical treatments for their AD, and their symptoms of scalp inflammation and alopecia resolved with discontinuation.²³

In a Dutch study, sensitization to Fragrance Mix I and M pereirae as well as other ingredients (eg, lanolin alcohol, Amerchol™ L 101 [a lanolin product]) was notably more common in pediatric patients with AD than in patients without AD; however, no data on patients with skin of color were included in this study.²⁴

Because of the increased risk of sensitization to fragrances and other ingredients in patients with AD as well as the high percentage of allergens in prescription and nonprescription products, it is important to discuss all personal care products that patients may be using, not just their cosmetic products. Also, patch testing may be helpful in determining true allergens in some patients. Patch testing is recommended for patients with treatment-resistant AD, and a recent study suggested it should be done prior to long-term use of immunosuppressive agents.²⁵ Increased steroid phobia and a push toward alternative medicines are leading both patients with AD and guardians of children with AD to look for other forms of moisturization, such as olive oil, coconut oil, sunflower seed oil, and shea butter, to decrease transepidermal water loss.^26,27 An important factor in AD treatment efficacy is patient acceptability in using what is recommended.²⁷ One study showed there was no difference in efficacy or acceptability in using a cream containing shea butter extract vs the ceramide-precursor product.²⁷ Current data show olive oil may exacerbate dry skin and AD,²⁶ and recommendation of any over-the-counter oils and butters in patients with AD should be made with great caution, as many of these products contain fragrances and other potential allergens.

Alternative Therapies for AD

Patients with AD often seek alternative or integrative treatment options, including dietary modifications and holistic remedies. Studies investigating the role of vitamins and supplements in treating AD are limited by sample size.²⁸ However, there is some evidence that may support supplementation with vitamins D and E in addressing AD symptoms. The use of probiotics in treating AD is controversial, but there are studies suggesting that the use of probiotics may prove beneficial in preventing infantile AD.²⁸ Additionally, findings from an ex vivo and in vitro study show that some conditions, including AD and acne, may benefit from the same probiotics, despite the differences in these two diseases. Both AD and acne have inflammatory and skin dysbiosis characteristics, which may be the common thread leading to both conditions potentially responding to treatment with probiotics.²⁹

Preliminary evidence indicates that supplements containing fatty acids such as docosahexaenoic acid, sea buckthorn oil, and hemp seed oil may decrease the severity of AD.²⁸ In a 20-week, randomized, single-blind, crossover study published in 2005, dietary hemp seed oil showed an improvement of clinical symptoms, including dry skin and itchiness, in patients with AD.³⁰

In light of recent legalization in several states, patients may turn to use of cannabinoid products to manage AD. In a systematic review, cannabinoid use was reportedly a therapeutic option in the treatment of AD and AV; however, the data are based on preclinical work, and there are no randomized, placebo-controlled studies to support the use of cannabinoids.³¹ Furthermore, there is great concern that use of these products in adolescents is an even larger unknown.

Final Thoughts

Eighty percent of children diagnosed with AD experience symptom improvement before their early teens³²; for those with AD during their preteen and teenage years, there can be psychological ramifications, as teenagers with AD report having fewer friends, are less socially involved, participate in fewer sports, and are absent from classes more often than their peers.⁵ In black patients with AD, school absences are even more common.⁶ Given the social and emotional impact of AD on patients with skin of color, it is imperative to treat the condition appropriately.³³ There are areas of opportunity for further research on alternate dosing of existing treatments for AV in patients with AD, further recommendations for adolescent athletes with AD, and which cosmetic and alternative medicine products may be beneficial for this population to improve their QOL.

Providers should discuss medical management in a broader context considering patients’ extracurricular activities, treatment vehicle preferences, expectations, and personal care habits. It also is important to address the many possible factors that may influence treatment adherence early on, particularly in adolescents, as these could be barriers to treatment. This article highlights considerations for treating AD and comorbid conditions that may further complicate treatment in adolescent patients with skin of color. The information provided should serve as a guide in initial counseling and management of AD in adolescents with skin of color.

Data are limited on the management of atopic dermatitis (AD) in adolescents, particularly in patients with skin of color, making it important to identify factors that may improve AD management in this population. Comorbid conditions (eg, acne, postinflammatory hyperpigmentation [PIH]), extracurricular activities (eg, athletics), and experimentation with cosmetics in adolescents, all of which can undermine treatment efficacy and medication adherence, make it particularly challenging to devise a therapeutic regimen in this patient population. We review the management of AD in black adolescents, with special consideration of concomitant treatment of acne vulgaris (AV) as well as lifestyle and social choices (Table).

Prevalence and Epidemiology

Atopic dermatitis affects 13% to 25% of children and 2% to 10% of adults.^1,2 Population‐based studies in the United States show a higher prevalence of AD in black children (19.3%) compared to European American (EA) children (16.1%).^3,4

AD in Black Adolescents

Atopic dermatitis is a common skin condition that is defined as a chronic, pruritic, inflammatory dermatosis with recurrent scaling, papules, and plaques (Figure) that usually develop during infancy and early childhood.³ Although AD severity improves for some patients in adolescence, it can be a lifelong issue affecting performance in academic and occupational settings.⁵ One US study of 8015 children found that there are racial and ethnic disparities in school absences among children (age range, 2–17 years) with AD, with children with skin of color being absent more often than white children.⁶ The same study noted that black children had a 1.5-fold higher chance of being absent 6 days over a 6-month school period compared to white children. It is postulated that AD has a greater impact on quality of life (QOL) in children with skin of color, resulting in the increased number of school absences in this population.⁶

The origin of AD currently is thought to be complex and can involve skin barrier dysfunction, environmental factors, microbiome effects, genetic predisposition, and immune dysregulation.^1,4 Atopic dermatitis is a heterogeneous disease with variations in the prevalence, genetic background, and immune activation patterns across racial groups.⁴ It is now understood to be an immune-mediated disease with multiple inflammatory pathways, with type 2–associated inflammation being a primary pathway. Patients with AD have strong helper T cell (T_H2) activation, and black patients with AD have higher IgE serum levels as well as absent T_H17/T_H1 activation.⁴

Atopic dermatitis currently is seen as a defect of the epidermal barrier, with variable clinical manifestations and expressivity.⁷ Filaggrin is an epidermal barrier protein, encoded by the FLG gene, and plays a major role in barrier function by regulating pH and promoting hydration of the skin.⁴ Loss of function of the FLG gene is the most well-studied genetic risk factor for developing AD, and this mutation is seen in patients with more severe and persistent AD in addition to patients with more skin infections and allergic sensitizations.^3,4 However, in the skin of color population, FLG mutations are 6 times less common than in the EA population, despite the fact that AD is more prevalent in patients of African descent.⁴ Therefore, the role of the FLG loss-of-function mutation and AD is not as well defined in black patients, and some researchers have found no association.³ The FLG loss-of-function mutation seems to play a smaller role in black patients than in EA patients, and other genes may be involved in skin barrier dysfunction.^3,4 In a small study of patients with mild AD compared to nonaffected patients, those with AD had lower total ceramide levels in the stratum corneum of affected sites than normal skin sites in healthy individuals.⁸

Particular disturbances in the gut microbiome have the possibility of impacting the development of AD.⁹ Additionally, the development of AD may be influenced by the skin microbiome, which can change depending on body site, with fungal organisms thought to make up a large proportion of the microbiome of patients with AD. In patients with AD, there is a lack of microbial diversity and an overgrowth of Staphylococcus aureus.⁹

Diagnosis

Clinicians diagnose AD based on clinical characteristics, and the lack of objective criteria can hinder diagnosis.¹ Thus, diagnosing AD in children with dark skin can pose a particular challenge given the varied clinical presentation of AD across skin types. Severe cases of AD may not be diagnosed or treated adequately in deeply pigmented children because erythema, a defining characteristic of AD, may be hard to identify in darker skin types.¹⁰ Furthermore, clinical erythema scores among black children may be “strongly” underestimated using scoring systems such as Eczema Area and Severity Index and SCORing Atopic Dermatitis.⁴ It is estimated that the risk for severe AD may be 6 times higher in black children compared to white children.¹⁰ Additionally, patients with skin of color can present with more treatment-resistant AD.⁴

Treatment of AD

Current treatment is focused on restoring epidermal barrier function, often with topical agents, such as moisturizers containing different amounts of emollients, occlusives, and humectants; corticosteroids; calcineurin inhibitors; and antimicrobials. Emollients such as glycol stearate, glyceryl stearate, and soy sterols function as lubricants, softening the skin. Occlusive agents include petrolatum, dimethicone, and mineral oil; they act by forming a layer to slow evaporation of water. Humectants including glycerol, lactic acid, and urea function by promoting water retention.¹¹ For acute flares, mid- to high-potency topical corticosteroids are recommended. Also, topical calcineurin inhibitors such as tacrolimus and pimecrolimus may be used alone or in combination with topical steroids. Finally, bleach baths and topical mupirocin applied to the nares also have proved helpful in moderate to severe AD with secondary bacterial infections.¹¹ Phototherapy can be used in adult and pediatric patients with acute and chronic AD if traditional treatments have failed.²

Systemic agents are indicated and recommended for the subset of adult and pediatric patients in whom optimized topical regimens and/or phototherapy do not adequately provide disease control or when QOL is substantially impacted. The systemic agents effective in the pediatric population include cyclosporine, azathioprine, mycophenolate mofetil, and possibly methotrexate.¹¹ Dupilumab recently was approved by the US Food and Drug Administration for patients 12 years and older with moderate to severe AD whose disease is not well controlled with topical medications.

Patients with AD are predisposed to secondary bacterial and viral infections because of their dysfunctional skin barrier; these infections most commonly are caused by S aureus and herpes simplex virus, respectively.² Systemic antibiotics are only recommended for patients with AD when there is clinical evidence of bacterial infection. In patients with evidence of eczema herpeticum, systemic antiviral agents should be used to treat the underlying herpes simplex virus infection.² Atopic dermatitis typically has been studied in white patients; however, patients with skin of color have higher frequencies of treatment-resistant AD. Further research on treatment efficacy for AD in this patient population is needed, as data are limited.⁴

Treatment of AV in Patients With AD

Two of the most prevalent skin diseases affecting the pediatric population are AD and AV, and both can remarkably impact QOL.¹² Acne is one of the most common reasons for adolescent patients to seek dermatologic care, including patients with skin of color (Fitzpatrick skin types IV to VI).¹³ Thus, it is to be expected that many black adolescents with AD also will have AV. For mild to moderate acne in patients with skin of color, topical retinoids and benzoyl peroxide typically are first line.¹³ These medications can be problematic for patients with AD, as retinoids and many other acne treatments can cause dryness, which may exacerbate AD.

Moisturizers containing ceramide can be a helpful adjunctive therapy in treating acne,¹⁴ especially in patients with AD. Modifications to application of acne medications, such as using topical retinoids every other night or mixing them with moisturizers to minimize dryness, may be beneficial to these patients. Dapsone gel 7.5% used daily also may be an option for adolescents with AD and AV. A double-blind, vehicle-controlled study demonstrated that dapsone is safe and effective for patients 12 years and older with moderate acne, and patients with Fitzpatrick skin types IV to VI rated local scaling, erythema, dryness, and stinging/burning as “none” in the study.¹⁵ Another potentially helpful topical agent in patients with AD and AV is sulfacetamide, as it is not likely to cause dryness of the skin. In a small study, sodium sulfacetamide 10% and sulfur 5% in an emollient foam vehicle showed no residual film or sulfur smell and resulted in acne reduction of 50%.¹⁶

Patients with skin of color often experience PIH in AD and acne or hypopigmentation from inflammatory dermatoses including AD.^17,18 In addition to the dryness from AD and topical retinoid use, patients with skin of color may develop irritant contact dermatitis, thus leading to PIH.¹³ Dryness and irritant contact dermatitis also can be seen with the use of benzoyl peroxide in black patients. Because of these effects, gentle moisturizers are recommended, and both benzoyl peroxide and retinoids should be initiated at lower doses in patients with skin of color.¹³

For patients with severe nodulocystic acne, isotretinoin is the treatment of choice in patients with skin of color,¹³ but there is a dearth of clinical studies addressing complications seen in black adolescents on this treatment, especially with respect to those with AD. Of note, systemic antibiotics typically are initiated before isotretinoin; however, this strategy is falling out of favor due to concern for antibiotic resistance with long-term use.¹⁹

Impact of Athletics on AD in Black Adolescents

Because of the exacerbating effects of perspiration and heat causing itch and irritation in patients with AD, it is frequently advised that pediatric patients limit their participation in athletics because of the exacerbating effects of strenuous physical exercise on their disease.¹² In one study, 429 pediatric patients or their parents/guardians completed QOL questionnaires; 89% of patients 15 years and younger with severe AD reported that their disease was impacted by athletics and outdoor activities, and 86% of these pediatric patients with severe AD responded that their social lives and leisure activities were impacted.²⁰ Because adolescents often are involved in athletics or have mandatory physical education classes, AD may be isolating and may have a severe impact on self-esteem.

Aggressive treatment of AD with topical and systemic medications may be helpful in adolescents who may be reluctant to participate in sports because of teasing, bullying, or worsening of symptoms with heat or sweating.²¹ Now that dupilumab is available for adolescents, there is a chance that patients with severe and/or recalcitrant disease managed on this medication can achieve better control of their symptoms without the laboratory requirement of methotrexate and the difficulties of topical medication application, allowing them to engage in mandatory athletic classes as well as desired organized sports.

Use of Cosmetics for AD

Many adolescents experiment with cosmetics, and those with AD may use cosmetic products to cover hyperpigmented or hypopigmented lesions.¹⁸ In patients with active AD or increased sensitivity to allergens in cosmetic products, use of makeup can be a contributing factor for AD flares. Acne associated with cosmetics is especially important to consider in darker-skinned patients who may use makeup that is opaque and contains oil to conceal acne or PIH.

Allergens can be present in both cosmetics and pharmaceutical topical agents, and a Brazilian study found that approximately 89% of 813 prescription and nonprescription products (eg, topical drugs, sunscreens, moisturizers, soaps, cleansing lotions, shampoos, cosmeceuticals) contained allergens.²² Patients with AD have a higher prevalence of contact sensitization to fragrances, including balsam of Peru.²³ Some AD treatments that contain fragrances have caused further skin issues in a few patients. In one case series, 3 pediatric patients developed allergic contact dermatitis to Myroxylon pereirae (balsam of Peru) when using topical treatments for their AD, and their symptoms of scalp inflammation and alopecia resolved with discontinuation.²³

In a Dutch study, sensitization to Fragrance Mix I and M pereirae as well as other ingredients (eg, lanolin alcohol, Amerchol™ L 101 [a lanolin product]) was notably more common in pediatric patients with AD than in patients without AD; however, no data on patients with skin of color were included in this study.²⁴

Because of the increased risk of sensitization to fragrances and other ingredients in patients with AD as well as the high percentage of allergens in prescription and nonprescription products, it is important to discuss all personal care products that patients may be using, not just their cosmetic products. Also, patch testing may be helpful in determining true allergens in some patients. Patch testing is recommended for patients with treatment-resistant AD, and a recent study suggested it should be done prior to long-term use of immunosuppressive agents.²⁵ Increased steroid phobia and a push toward alternative medicines are leading both patients with AD and guardians of children with AD to look for other forms of moisturization, such as olive oil, coconut oil, sunflower seed oil, and shea butter, to decrease transepidermal water loss.^26,27 An important factor in AD treatment efficacy is patient acceptability in using what is recommended.²⁷ One study showed there was no difference in efficacy or acceptability in using a cream containing shea butter extract vs the ceramide-precursor product.²⁷ Current data show olive oil may exacerbate dry skin and AD,²⁶ and recommendation of any over-the-counter oils and butters in patients with AD should be made with great caution, as many of these products contain fragrances and other potential allergens.

Alternative Therapies for AD

Patients with AD often seek alternative or integrative treatment options, including dietary modifications and holistic remedies. Studies investigating the role of vitamins and supplements in treating AD are limited by sample size.²⁸ However, there is some evidence that may support supplementation with vitamins D and E in addressing AD symptoms. The use of probiotics in treating AD is controversial, but there are studies suggesting that the use of probiotics may prove beneficial in preventing infantile AD.²⁸ Additionally, findings from an ex vivo and in vitro study show that some conditions, including AD and acne, may benefit from the same probiotics, despite the differences in these two diseases. Both AD and acne have inflammatory and skin dysbiosis characteristics, which may be the common thread leading to both conditions potentially responding to treatment with probiotics.²⁹

Preliminary evidence indicates that supplements containing fatty acids such as docosahexaenoic acid, sea buckthorn oil, and hemp seed oil may decrease the severity of AD.²⁸ In a 20-week, randomized, single-blind, crossover study published in 2005, dietary hemp seed oil showed an improvement of clinical symptoms, including dry skin and itchiness, in patients with AD.³⁰

In light of recent legalization in several states, patients may turn to use of cannabinoid products to manage AD. In a systematic review, cannabinoid use was reportedly a therapeutic option in the treatment of AD and AV; however, the data are based on preclinical work, and there are no randomized, placebo-controlled studies to support the use of cannabinoids.³¹ Furthermore, there is great concern that use of these products in adolescents is an even larger unknown.

Final Thoughts

Eighty percent of children diagnosed with AD experience symptom improvement before their early teens³²; for those with AD during their preteen and teenage years, there can be psychological ramifications, as teenagers with AD report having fewer friends, are less socially involved, participate in fewer sports, and are absent from classes more often than their peers.⁵ In black patients with AD, school absences are even more common.⁶ Given the social and emotional impact of AD on patients with skin of color, it is imperative to treat the condition appropriately.³³ There are areas of opportunity for further research on alternate dosing of existing treatments for AV in patients with AD, further recommendations for adolescent athletes with AD, and which cosmetic and alternative medicine products may be beneficial for this population to improve their QOL.

Providers should discuss medical management in a broader context considering patients’ extracurricular activities, treatment vehicle preferences, expectations, and personal care habits. It also is important to address the many possible factors that may influence treatment adherence early on, particularly in adolescents, as these could be barriers to treatment. This article highlights considerations for treating AD and comorbid conditions that may further complicate treatment in adolescent patients with skin of color. The information provided should serve as a guide in initial counseling and management of AD in adolescents with skin of color.

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.¹ Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.^1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.^2,3

It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,⁴ which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.⁴

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.⁵ Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.^4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.⁶ The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al⁷ showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.⁸ A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.⁹ However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.⁹ Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.¹⁰ Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.¹¹ Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.^6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,¹³ but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.⁵ Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.^5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P₀), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.⁶ Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).⁶ Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.⁵ Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.¹⁴ Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.^5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.^4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.¹⁵ A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.⁴ A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.^4,5

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.¹⁶ Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.^16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.¹⁸ They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.¹⁸ 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.¹⁹ Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer¹⁶; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”²⁰ They extended this statement to include isopropylparaben and isobutylparaben in a later review.²¹ In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.²² This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.^16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”²³ However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,¹⁶ and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.²⁴

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.²⁵ Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.¹⁷

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.¹⁶ Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.¹⁶

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.⁵ Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).¹⁶ However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.¹⁶

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.^2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.²⁸ It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.^2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.^26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.³¹ Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.³⁰ Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.^32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.²⁸ The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.³⁰ The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.³³ Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents^2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.²⁸ However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.^2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.³³ Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.³⁴ Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.³⁴

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.^5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.^36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.^36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.³⁸ Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.³⁸

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.¹ Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.^1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.^2,3

It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,⁴ which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.⁴

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.⁵ Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.^4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.⁶ The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al⁷ showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.⁸ A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.⁹ However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.⁹ Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.¹⁰ Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.¹¹ Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.^6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,¹³ but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.⁵ Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.^5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P₀), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.⁶ Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).⁶ Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.⁵ Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.¹⁴ Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.^5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.^4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.¹⁵ A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.⁴ A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.^4,5

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.¹⁶ Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.^16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.¹⁸ They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.¹⁸ 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.¹⁹ Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer¹⁶; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”²⁰ They extended this statement to include isopropylparaben and isobutylparaben in a later review.²¹ In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.²² This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.^16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”²³ However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,¹⁶ and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.²⁴

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.²⁵ Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.¹⁷

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.¹⁶ Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.¹⁶

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.⁵ Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).¹⁶ However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.¹⁶

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.^2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.²⁸ It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.^2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.^26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.³¹ Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.³⁰ Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.^32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.²⁸ The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.³⁰ The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.³³ Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents^2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.²⁸ However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.^2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.³³ Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.³⁴ Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.³⁴

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.^5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.^36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.^36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.³⁸ Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.³⁸

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.¹ Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.^1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.^2,3

It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,⁴ which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.⁴

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.⁵ Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.^4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.⁶ The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al⁷ showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.⁸ A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.⁹ However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.⁹ Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.¹⁰ Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.¹¹ Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.^6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,¹³ but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.⁵ Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.^5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P₀), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.⁶ Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).⁶ Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.⁵ Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.¹⁴ Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.^5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.^4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.¹⁵ A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.⁴ A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.^4,5

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.¹⁶ Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.^16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.¹⁸ They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.¹⁸ 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.¹⁹ Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer¹⁶; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”²⁰ They extended this statement to include isopropylparaben and isobutylparaben in a later review.²¹ In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.²² This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.^16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”²³ However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,¹⁶ and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.²⁴

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.²⁵ Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.¹⁷

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.¹⁶ Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.¹⁶

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.⁵ Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).¹⁶ However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.¹⁶

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.^2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.²⁸ It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.^2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.^26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.³¹ Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.³⁰ Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.^32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.²⁸ The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.³⁰ The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.³³ Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents^2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.²⁸ However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.^2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.³³ Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.³⁴ Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.³⁴

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.^5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.^36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.^36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.³⁸ Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.³⁸

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

The approach to the treatment of common skin disorders and cosmetic concerns in patients with skin of color (SOC) requires the clinician to understand the biological differences, nuances, and special considerations that are unique to patients with darker skin types.^1-3 This article addresses 4 common facial concerns in SOC patients—acne, rosacea, facial hyperpigmentation, and cosmetic enhancement—and provides treatment recommendations and management pearls to assist the clinician with optimal outcomes for SOC patients.

Acne in SOC Patients

Acne vulgaris is one of the most common conditions that dermatologists treat and is estimated to affect 40 to 50 million individuals in the United States.¹ Many of these acne patients are individuals with SOC.^2-4 A study of 2835 females (aged 10–70 years) conducted in 4 different cities—Los Angeles, California; London, United Kingdom; Akita, Japan; and Rome, Italy—demonstrated acne prevalence of 37% in blacks, 32% in Hispanics, 30% in Asians, 24% in whites, and 23% in Continental Indians.⁵ Blacks, Hispanics, and Continental Indians demonstrated equal prevalence with comedonal and inflammatory acne. Asians displayed more inflammatory acne lesions than comedones. In contrast, whites demonstrated more comedones than inflammatory acne. Dyspigmentation, postinflammatory hyperpigmentation (PIH), and atrophic scars were more common in black and Hispanic females than other ethnicities.⁵ This study illustrated that acne-induced PIH is a common sequela in SOC patients and is the main reason they seek treatment.^6,7

The pathogenesis of acne is the same in all racial and ethnic groups: (1) follicular hyperkeratinization and the formation of a microcomedone caused by abnormal desquamation of the keratinocytes within the sebaceous follicle, (2) production of sebum by circulating androgens, (3) proliferation of Propionibacterium acnes, and (4) inflammation. Subclinical inflammation is present throughout all stages of acne, including normal-appearing skin, inflammatory lesions, comedones, and scarring, and may contribute to PIH in acne patients with SOC (Figure 1).⁸ A thorough history should be obtained from acne patients, including answers to the following questions⁷:

• What skin and hair care products do you use?
• Do you use sunscreen daily?
• What cosmetic products or makeup do you use?
• Do you use any ethnic skin care products, including skin lightening creams?
• Do you have a history of keloids?

It is important to ask these questions to assess if the SOC patient has developed pomade acne,⁹ acne cosmetica,¹⁰ or a potential risk of skin irritation from the use of skin care practices. It is best to take total control of the patient’s skin care regimen and discontinue use of toners, astringents, witch hazel, exfoliants, and rubbing alcohol, which may lead to skin dryness and irritation, particularly when combined with topical acne medications.

Treatment
Treatment of acne in SOC patients is similar to generally recommended treatments, with special considerations. Consider the following key points when treating acne in SOC patients:

• Treat acne early and aggressively to prevent or minimize subsequent PIH and acne scarring.
• Balance aggressive treatment with nonirritating topical skin care.
• Most importantly, target PIH in addition to acne and choose a regimen that limits skin irritation that might exacerbate existing PIH.⁷

Develop a maintenance program to control future breakouts. Topical agents can be used as monotherapy or in fixed combinations and may include benzoyl peroxide, antibiotics, dapsone, azelaic acid (AZA), and retinoids. Similar to white patients, topical retinoids remain a first-line treatment for acne in patients with SOC.^11,12

Tolerability must be managed in SOC acne patients. Therapeutic maneuvers that can be instituted should include a discussion on using gentle skin care, initiating therapy with a retinoid applied every other night starting with a low concentration and gradually titrating up, and applying a moisturizer before or after applying acne medication. Oral therapies consist of antibiotics (doxycycline, minocycline), retinoids (isotretinoin), and hormonal modulators (oral contraceptives, spironolactone). Isotretinoin, recommended for patients with nodulocystic acne, may play a possible role in treating acne-induced PIH.¹³

Two common procedural therapies for acne include comedone extraction and intralesional corticosteroid injection. A 6- to 8-week course of a topical retinoid prior to comedonal extraction may facilitate the procedure and is recommended in SOC patients to help reduce cutaneous trauma and PIH.¹¹ Inflammatory acne lesions can be treated with intralesional injection of triamcinolone acetonide 2.5 or 5.0 mg/mL, which usually reduces inflammation within 2 to 5 days.¹¹

Treatment of acne-induced PIH includes sun protection, topical and oral medications, chemical peels, lasers, and energy devices. Treatment of hypertrophic scarring and keloids involves intralesional injection of triamcinolone acetonide 20, 30, or 40 mg/mL every 4 weeks until the lesion is flat.¹¹

Superficial chemical peels can be used to treat acne and PIH in SOC patients,¹⁴ such as salicylic acid (20%–30%), glycolic acid (20%–70%), trichloroacetic acid (15%–30%), and Jessner peels.

Acne Scarring
Surgical approaches to acne scarring in patients with SOC include elliptical excision, punch excision, punch elevation, punch autografting, dermal grafting, dermal planning, subcutaneous incision (subcision), dermabrasion, microneedling, fillers, and laser skin resurfacing. The treatment of choice depends on the size, type, and depth of the scar and the clinician’s preference.

Lasers
Fractional photothermolysis has emerged as a treatment option for acne scars in SOC patients. This procedure produces microscopic columns of thermal injury in the epidermis and dermis, sparing the surrounding tissue and minimizing downtime and adverse events. Because fractional photothermolysis does not target melanin and produces limited epidermal injury, darker Fitzpatrick skin types (IV–VI) can be safely and effectively treated with this procedure.¹⁵

Rosacea in SOC Patients

Rosacea is a chronic inflammatory disorder that affects the vasculature and pilosebaceous units of the face. It commonly is seen in Fitzpatrick skin types I and II; however, rosacea can occur in all skin types (Figure 2). Triggers include emotional stress, extreme environmental temperatures, hot and spicy foods, red wine or alcohol, and topical irritants or allergens found in common cosmetic products.¹⁶

Data suggest that 4% of rosacea patients in the United States are of African, Latino, or Asian descent.¹¹ National Ambulatory Medical Care Survey data revealed that of 31.5 million rosacea visits, 2% of patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino. In a 5-year longitudinal study of 2587 rosacea patients enrolled in Medicaid in North Carolina who were prescribed at least 1 topical treatment for rosacea, 16.27% were black and 10% were of a race other than white.¹⁷

Although the pathogenesis of rosacea is unclear, hypotheses include immune system abnormalities, neurogenic dysregulation, presence of microorganisms (eg, Demodex folliculorum), UV damage, and skin barrier dysfunction.¹⁸

The 4 major subtypes of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea.¹⁶ Interestingly, rosacea in SOC patients may present with hypopigmentation surrounding the borders of the facial erythema. For phymatous rosacea, isotretinoin may reduce incipient rhinophyma but must be carefully monitored and pregnancy must be excluded. Surgical or laser therapy may be indicated to recontour the nose if severe.

There are several skin conditions that can present with facial erythema in patients with SOC, including seborrheic dermatitis, systemic lupus erythematosus, and contact dermatitis. It is important to note that the detection of facial erythema in darker skin types may be difficult; therefore, laboratory evaluation (antinuclear antibodies), patch testing, and skin biopsy should be considered if the clinical diagnosis is unclear.

Treatment
Treatment of rosacea in SOC patients does not differ from other racial groups. Common strategies include gentle skin care, sun protection (sun protection factor 30+), and barrier repair creams. Topical agents include metronidazole, AZA, sodium sulfacetamide/sulfur, ivermectin, and retinoids.¹⁶ Oral treatments include antibiotics in the tetracycline family (eg, subantimicrobial dose doxycycline) and isotretinoin.¹⁶ Persistent erythema associated with rosacea can be treated with brimonidine¹⁹ and oxymetazoline.²⁰ Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea²¹; however, the latter is not recommended in Fitzpatrick skin types IV through VI.

Facial Hyperpigmentation in SOC Patients

Hyperpigmentation disorders can be divided into conditions that affect Fitzpatrick skin types I through III and IV though VI. Mottled hyperpigmentation (photodamage) and solar lentigines occur in patients with lighter skin types as compared to melasma, PIH, and age-related (UV-induced) hyperpigmentation, which occur more commonly in patients with darker skin types. Facial hyperpigmentation is a common concern in SOC patients. In a survey of cosmetic concerns of 100 women with SOC, hyperpigmentation or dark spots (86%) and blotchy uneven skin (80%) were the top concerns.²² In addition, facial hyperpigmentation has been shown to negatively impact quality of life.²³

Postinflammatory hyperpigmentation occurs from a pathophysiological response to inflammation, cutaneous irritation or injury, and subsequent melanocyte lability. Postinflammatory hyperpigmentation is a common presenting concern in patients with SOC and is seen as a result of many inflammatory skin disorders (eg, acne, eczema) and dermatologic procedures (eg, adverse reaction to electrodesiccation, microdermabrasion, chemical peels, laser surgery).²⁴

Melasma is an acquired idiopathic disorder of hyperpigmentation and often referred to as the mask of pregnancy (Figure 3). It occurs on sun-exposed areas of skin, mainly in women with Fitzpatrick skin types III through V. Associated factors or triggers include pregnancy, hormonal treatments, exposure to UV radiation, and medications.²⁵ Hereditary factors play a role in more than 40% of cases.²⁶

Other not-so-common facial dyschromias include contact dermatitis, acanthosis nigricans, exogenous ochronosis, lichen planus pigmentosus (associated with frontal fibrosing alopecia),²⁷ drug-induced hyperpigmentation (associated with minocycline or diltiazem),^28,29 and UV-induced (age-related) hyperpigmentation.

Treatment
The treatment of hyperpigmentation should provide the following: (1) protection from sun exposure; (2) inhibition of tyrosinase, the enzyme responsible for the conversion of tyrosine to melanin; (3) inhibition of melanosome transfer from the melanocyte to the keratinocyte; (4) removal of melanin from the epidermis through exfoliation; and (5) destruction or disruption of melanin in the dermis.³⁰ Therapies for facial hyperpigmentation are listed in Table 1.

Topical therapies include prescription medications and nonprescription cosmeceuticals. Prescription medications include hydroquinone (HQ), topical retinoids, and AZA. Hydroquinone, a tyrosinase inhibitor, is the gold standard for skin lightening and often is used as a first-line therapy. It is used as a monotherapy (HQ 4%) or as a fixed combination with tretinoin 0.05% and fluocinolone 0.01%.³¹ Use caution with HQ in high concentrations (6% and higher) and low concentrations (2% [over-the-counter strength]) used long-term due to the potential risk of exogenous ochronosis.

Topical retinoids have been shown to be effective therapeutic agents for melasma and PIH. Tretinoin,³² tazarotene,³³ and adapalene³⁴ all have demonstrated efficacy for acne and acne-induced PIH in SOC patients. Patients must be monitored for the development of retinoid dermatitis and worsening of hyperpigmentation.

Azelaic acid is a naturally occurring dicarboxylic acid obtained from cultures of Malassezia furfur. Azelaic acid inhibits tyrosinase activity, DNA synthesis, and mitochondrial enzymes, thus blocking direct cytotoxic effects toward melanocytes. Azelaic acid is approved by the US Food and Drug Administration for acne in a 20% cream formulation and rosacea in 15% gel and foam formulations, and it is used off label for melasma and PIH.³⁵

Oral tranexamic acid is currently used as a hemostatic agent due to its ability to inhibit the plasminogen-plasmin pathway. In melasma, it blocks the interaction between melanocytes and keratinocytes in the epidermis and modulates the vascular component of melasma in the dermis. In an open-label study, 561 Asian melasma patients were treated with oral tranexamic acid 250 mg twice daily for 4 months. Results demonstrated improvement in 90% of patients, and 7.1% reported adverse effects (eg, abdominal bloating and pain, nausea, vomiting, headache, tinnitus, numbness, menstrual irregularities).³⁶ Coagulation screening should be monitored monthly, and any patient with a history of clotting abnormalities should be excluded from off-label treatment with oral tranexamic acid.

Nonprescription cosmeceuticals are available over-the-counter or are office dispensed.³⁷ For optimal results, cosmeceutical agents for skin lightening are used in combination. Most of these combinations are HQ free and have additive benefits such as a multimodal skin lightening agent containing key ingredients that correct and prevent skin pigmentation via several pathways affecting melanogenesis.³⁸ It is an excellent alternative to HQ for mottled and diffuse UV-induced hyperpigmentation and can be used for maintenance therapy in patients with melasma.

Photoprotection is an essential component of therapy for melasma and PIH, but there is a paucity of data on the benefits for SOC patients. Halder et al³⁹ performed a randomized prospective study of 89 black and Hispanic patients who applied sunscreen with a sun protection factor of 30 or 60 daily for 8 weeks. Clinical grading, triplicate L*A*B chromameter, and clinical photography were taken at baseline and weeks 4 and 8. The results demonstrated skin lightening in both black and Hispanic patients and support the use of sunscreen in the prevention and management of dyschromia in SOC patients.³⁹ Visible light also may play a role in melasma development, and thus use of sunscreens or makeup containing iron oxides are recommended.⁴⁰

Procedural treatments for facial hyperpigmentation include microdermabrasion, chemical peels, lasers, energy-based devices, and microneedling. There are many types and formulations of chemical peeling agents available; however, superficial and medium-depth chemical peels are recommended for SOC patients (Table 2). Deep chemical peels are not recommended for SOC patients due to the potential increased risk for PIH and scarring.

Cosmetic Enhancement in SOC Patients

Cosmetic procedures are gaining popularity in the SOC population and account for more than 20% of cosmetic procedures in the United States.⁴¹ Facial cosmetic concerns in SOC include dyschromia, benign growths (dermatosis papulosa nigra), hyperkinetic facial lines, volume loss, and skin laxity.⁴² Key principles to consider when treating SOC patients are the impact of ethnicity on aging and facial structure, the patient’s desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient’s expectations for recommended therapies.

Aging in SOC Patients
Skin aging can be classified as intrinsic aging or extrinsic aging. Intrinsic aging is genetic and involves subsurface changes such as volume loss, muscle atrophy, and resorption of bony structure. Extrinsic aging (or photoaging) involves surface changes of the epidermis/dermis and manifests as mottled pigmentation, textural changes, and fine wrinkling. Due to the photoprotection of melanin (black skin=SPF 13.4), skin aging in SOC patients is delayed by 10 to 20 years.⁴³ In addition, SOC patients have more reactive collagen and can benefit from noninvasive cosmetic procedures such as fillers and skin-tightening procedures.⁴²

Cosmetic Treatments and Procedures
Dermatosis papulosa nigra (benign growths of skin that have a genetic predisposition)⁴⁴ occur mainly on the face but can involve the entire body. Treatment modalities include electrodesiccation, cryotherapy, scissor excision, and laser surgery.⁴⁵

Treatment of hyperkinetic facial lines with botulinum toxin type A is a safe and effective procedure in patients with SOC. Grimes and Shabazz⁴⁶ performed a 4-month, randomized, double-blind study that evaluated the treatment of glabellar lines in women with Fitzpatrick skin types V and VI. The results demonstrated that the duration of effects was the same in the patients who received either 20 or 30 U of botulinum toxin type A.⁴⁶ Dynamic rhytides (furrows and frown/scowl lines arising from laughing, frowning, or smiling) can be treated safely in patients with SOC using botulinum toxin type A off label for relaxation of the upper and lower hyperkinetic muscles that result in these unwanted signs of aging. Botulinum toxin type A often is used for etched-in crow’s-feet, which rarely are evident in SOC patients.⁴⁷ Facial shaping also can be accomplished by injecting botulinum toxin type A in combination with soft-tissue dermal fillers.⁴⁷

Although black individuals do not experience perioral rhytides at the frequency of white individuals, they experience a variety of other cosmetic issues related to skin sagging and sinking. Currently available hyaluronic acid (HA) fillers have been shown to be safe in patients with Fitzpatrick skin types IV through VI.⁴⁸ Two studies evaluated fillers in patients with SOC, specifically HA⁴⁹ and calcium hydroxylapatite,⁵⁰ focused on treatment of the nasolabial folds and the potential risk for dyspigmentation and keloidal scarring. Taylor et al⁴⁹ noted that the risk of hyperpigmentation was 6% to 9% for large- and small-particle HA, respectively, and was associated with the serial or multiple puncture injection technique. No hypertrophic or keloidal scarring occurred in both studies.^49,50

Facial contouring applications with fillers include glabellar lines, temples, nasal bridge, tear troughs, malar and submalar areas, nasolabial folds, radial lines, lips, marionette lines, mental crease, and chin. Hyaluronic acid fillers also can be used for lip enhancement.⁴⁷ Although white women are looking to increase the size of their lips, black women are seeking augmentation to restore their lip size to that of their youth. Black individuals do not experience the same frequency of perioral rhytides as white patients, but they experience a variety of other issues related to skin sagging and sinking. Unlike white women, enhancement of the vermilion border rarely is performed in black women due to development of rhytides, predominantly in the body of the lip below the vermilion border in response to volume loss in the upper lip while the lower lip usually maintains its same appearance.⁴⁷

Facial enhancement utilizing poly-L-lactic acid can be used safely in SOC patients.⁵¹ Poly-L-lactic acid microparticles induce collagen formation, leading to dermal thickening over 3 to 6 months; however, multiple sessions are required to achieve optimal aesthetic results.

Patients with more reactive collagen can benefit from noninvasive cosmetic procedures such as skin-tightening procedures.⁵² Radiofrequency and microfocused ultrasound are cosmetic procedures used to provide skin tightening and facial lifting. They are safe and effective treatments for patients with Fitzpatrick skin types IV to VI.⁵³ Histologically, there is less thinning of collagen bundles and elastic tissue in ethnic skin. Due to stimulation of collagen by these procedures, most SOC patients will experience a more enhanced response, requiring fewer treatment sessions than white individuals.

Conclusion

Medical and aesthetic facial concerns in SOC patients vary and can be a source of emotional and psychological distress that can negatively impact quality of life. The approach to the treatment of SOC patients should be a balance between tolerability and efficacy, considering the potential risk for PIH.

The approach to the treatment of common skin disorders and cosmetic concerns in patients with skin of color (SOC) requires the clinician to understand the biological differences, nuances, and special considerations that are unique to patients with darker skin types.^1-3 This article addresses 4 common facial concerns in SOC patients—acne, rosacea, facial hyperpigmentation, and cosmetic enhancement—and provides treatment recommendations and management pearls to assist the clinician with optimal outcomes for SOC patients.

Acne in SOC Patients

Acne vulgaris is one of the most common conditions that dermatologists treat and is estimated to affect 40 to 50 million individuals in the United States.¹ Many of these acne patients are individuals with SOC.^2-4 A study of 2835 females (aged 10–70 years) conducted in 4 different cities—Los Angeles, California; London, United Kingdom; Akita, Japan; and Rome, Italy—demonstrated acne prevalence of 37% in blacks, 32% in Hispanics, 30% in Asians, 24% in whites, and 23% in Continental Indians.⁵ Blacks, Hispanics, and Continental Indians demonstrated equal prevalence with comedonal and inflammatory acne. Asians displayed more inflammatory acne lesions than comedones. In contrast, whites demonstrated more comedones than inflammatory acne. Dyspigmentation, postinflammatory hyperpigmentation (PIH), and atrophic scars were more common in black and Hispanic females than other ethnicities.⁵ This study illustrated that acne-induced PIH is a common sequela in SOC patients and is the main reason they seek treatment.^6,7

The pathogenesis of acne is the same in all racial and ethnic groups: (1) follicular hyperkeratinization and the formation of a microcomedone caused by abnormal desquamation of the keratinocytes within the sebaceous follicle, (2) production of sebum by circulating androgens, (3) proliferation of Propionibacterium acnes, and (4) inflammation. Subclinical inflammation is present throughout all stages of acne, including normal-appearing skin, inflammatory lesions, comedones, and scarring, and may contribute to PIH in acne patients with SOC (Figure 1).⁸ A thorough history should be obtained from acne patients, including answers to the following questions⁷:

• What skin and hair care products do you use?
• Do you use sunscreen daily?
• What cosmetic products or makeup do you use?
• Do you use any ethnic skin care products, including skin lightening creams?
• Do you have a history of keloids?

It is important to ask these questions to assess if the SOC patient has developed pomade acne,⁹ acne cosmetica,¹⁰ or a potential risk of skin irritation from the use of skin care practices. It is best to take total control of the patient’s skin care regimen and discontinue use of toners, astringents, witch hazel, exfoliants, and rubbing alcohol, which may lead to skin dryness and irritation, particularly when combined with topical acne medications.

Treatment
Treatment of acne in SOC patients is similar to generally recommended treatments, with special considerations. Consider the following key points when treating acne in SOC patients:

• Treat acne early and aggressively to prevent or minimize subsequent PIH and acne scarring.
• Balance aggressive treatment with nonirritating topical skin care.
• Most importantly, target PIH in addition to acne and choose a regimen that limits skin irritation that might exacerbate existing PIH.⁷

Develop a maintenance program to control future breakouts. Topical agents can be used as monotherapy or in fixed combinations and may include benzoyl peroxide, antibiotics, dapsone, azelaic acid (AZA), and retinoids. Similar to white patients, topical retinoids remain a first-line treatment for acne in patients with SOC.^11,12

Tolerability must be managed in SOC acne patients. Therapeutic maneuvers that can be instituted should include a discussion on using gentle skin care, initiating therapy with a retinoid applied every other night starting with a low concentration and gradually titrating up, and applying a moisturizer before or after applying acne medication. Oral therapies consist of antibiotics (doxycycline, minocycline), retinoids (isotretinoin), and hormonal modulators (oral contraceptives, spironolactone). Isotretinoin, recommended for patients with nodulocystic acne, may play a possible role in treating acne-induced PIH.¹³

Two common procedural therapies for acne include comedone extraction and intralesional corticosteroid injection. A 6- to 8-week course of a topical retinoid prior to comedonal extraction may facilitate the procedure and is recommended in SOC patients to help reduce cutaneous trauma and PIH.¹¹ Inflammatory acne lesions can be treated with intralesional injection of triamcinolone acetonide 2.5 or 5.0 mg/mL, which usually reduces inflammation within 2 to 5 days.¹¹

Treatment of acne-induced PIH includes sun protection, topical and oral medications, chemical peels, lasers, and energy devices. Treatment of hypertrophic scarring and keloids involves intralesional injection of triamcinolone acetonide 20, 30, or 40 mg/mL every 4 weeks until the lesion is flat.¹¹

Superficial chemical peels can be used to treat acne and PIH in SOC patients,¹⁴ such as salicylic acid (20%–30%), glycolic acid (20%–70%), trichloroacetic acid (15%–30%), and Jessner peels.

Acne Scarring
Surgical approaches to acne scarring in patients with SOC include elliptical excision, punch excision, punch elevation, punch autografting, dermal grafting, dermal planning, subcutaneous incision (subcision), dermabrasion, microneedling, fillers, and laser skin resurfacing. The treatment of choice depends on the size, type, and depth of the scar and the clinician’s preference.

Lasers
Fractional photothermolysis has emerged as a treatment option for acne scars in SOC patients. This procedure produces microscopic columns of thermal injury in the epidermis and dermis, sparing the surrounding tissue and minimizing downtime and adverse events. Because fractional photothermolysis does not target melanin and produces limited epidermal injury, darker Fitzpatrick skin types (IV–VI) can be safely and effectively treated with this procedure.¹⁵

Rosacea in SOC Patients

Rosacea is a chronic inflammatory disorder that affects the vasculature and pilosebaceous units of the face. It commonly is seen in Fitzpatrick skin types I and II; however, rosacea can occur in all skin types (Figure 2). Triggers include emotional stress, extreme environmental temperatures, hot and spicy foods, red wine or alcohol, and topical irritants or allergens found in common cosmetic products.¹⁶

Data suggest that 4% of rosacea patients in the United States are of African, Latino, or Asian descent.¹¹ National Ambulatory Medical Care Survey data revealed that of 31.5 million rosacea visits, 2% of patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino. In a 5-year longitudinal study of 2587 rosacea patients enrolled in Medicaid in North Carolina who were prescribed at least 1 topical treatment for rosacea, 16.27% were black and 10% were of a race other than white.¹⁷

Although the pathogenesis of rosacea is unclear, hypotheses include immune system abnormalities, neurogenic dysregulation, presence of microorganisms (eg, Demodex folliculorum), UV damage, and skin barrier dysfunction.¹⁸

The 4 major subtypes of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea.¹⁶ Interestingly, rosacea in SOC patients may present with hypopigmentation surrounding the borders of the facial erythema. For phymatous rosacea, isotretinoin may reduce incipient rhinophyma but must be carefully monitored and pregnancy must be excluded. Surgical or laser therapy may be indicated to recontour the nose if severe.

There are several skin conditions that can present with facial erythema in patients with SOC, including seborrheic dermatitis, systemic lupus erythematosus, and contact dermatitis. It is important to note that the detection of facial erythema in darker skin types may be difficult; therefore, laboratory evaluation (antinuclear antibodies), patch testing, and skin biopsy should be considered if the clinical diagnosis is unclear.

Treatment
Treatment of rosacea in SOC patients does not differ from other racial groups. Common strategies include gentle skin care, sun protection (sun protection factor 30+), and barrier repair creams. Topical agents include metronidazole, AZA, sodium sulfacetamide/sulfur, ivermectin, and retinoids.¹⁶ Oral treatments include antibiotics in the tetracycline family (eg, subantimicrobial dose doxycycline) and isotretinoin.¹⁶ Persistent erythema associated with rosacea can be treated with brimonidine¹⁹ and oxymetazoline.²⁰ Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea²¹; however, the latter is not recommended in Fitzpatrick skin types IV through VI.

Facial Hyperpigmentation in SOC Patients

Hyperpigmentation disorders can be divided into conditions that affect Fitzpatrick skin types I through III and IV though VI. Mottled hyperpigmentation (photodamage) and solar lentigines occur in patients with lighter skin types as compared to melasma, PIH, and age-related (UV-induced) hyperpigmentation, which occur more commonly in patients with darker skin types. Facial hyperpigmentation is a common concern in SOC patients. In a survey of cosmetic concerns of 100 women with SOC, hyperpigmentation or dark spots (86%) and blotchy uneven skin (80%) were the top concerns.²² In addition, facial hyperpigmentation has been shown to negatively impact quality of life.²³

Postinflammatory hyperpigmentation occurs from a pathophysiological response to inflammation, cutaneous irritation or injury, and subsequent melanocyte lability. Postinflammatory hyperpigmentation is a common presenting concern in patients with SOC and is seen as a result of many inflammatory skin disorders (eg, acne, eczema) and dermatologic procedures (eg, adverse reaction to electrodesiccation, microdermabrasion, chemical peels, laser surgery).²⁴

Melasma is an acquired idiopathic disorder of hyperpigmentation and often referred to as the mask of pregnancy (Figure 3). It occurs on sun-exposed areas of skin, mainly in women with Fitzpatrick skin types III through V. Associated factors or triggers include pregnancy, hormonal treatments, exposure to UV radiation, and medications.²⁵ Hereditary factors play a role in more than 40% of cases.²⁶

Other not-so-common facial dyschromias include contact dermatitis, acanthosis nigricans, exogenous ochronosis, lichen planus pigmentosus (associated with frontal fibrosing alopecia),²⁷ drug-induced hyperpigmentation (associated with minocycline or diltiazem),^28,29 and UV-induced (age-related) hyperpigmentation.

Treatment
The treatment of hyperpigmentation should provide the following: (1) protection from sun exposure; (2) inhibition of tyrosinase, the enzyme responsible for the conversion of tyrosine to melanin; (3) inhibition of melanosome transfer from the melanocyte to the keratinocyte; (4) removal of melanin from the epidermis through exfoliation; and (5) destruction or disruption of melanin in the dermis.³⁰ Therapies for facial hyperpigmentation are listed in Table 1.

Topical therapies include prescription medications and nonprescription cosmeceuticals. Prescription medications include hydroquinone (HQ), topical retinoids, and AZA. Hydroquinone, a tyrosinase inhibitor, is the gold standard for skin lightening and often is used as a first-line therapy. It is used as a monotherapy (HQ 4%) or as a fixed combination with tretinoin 0.05% and fluocinolone 0.01%.³¹ Use caution with HQ in high concentrations (6% and higher) and low concentrations (2% [over-the-counter strength]) used long-term due to the potential risk of exogenous ochronosis.

Topical retinoids have been shown to be effective therapeutic agents for melasma and PIH. Tretinoin,³² tazarotene,³³ and adapalene³⁴ all have demonstrated efficacy for acne and acne-induced PIH in SOC patients. Patients must be monitored for the development of retinoid dermatitis and worsening of hyperpigmentation.

Azelaic acid is a naturally occurring dicarboxylic acid obtained from cultures of Malassezia furfur. Azelaic acid inhibits tyrosinase activity, DNA synthesis, and mitochondrial enzymes, thus blocking direct cytotoxic effects toward melanocytes. Azelaic acid is approved by the US Food and Drug Administration for acne in a 20% cream formulation and rosacea in 15% gel and foam formulations, and it is used off label for melasma and PIH.³⁵

Oral tranexamic acid is currently used as a hemostatic agent due to its ability to inhibit the plasminogen-plasmin pathway. In melasma, it blocks the interaction between melanocytes and keratinocytes in the epidermis and modulates the vascular component of melasma in the dermis. In an open-label study, 561 Asian melasma patients were treated with oral tranexamic acid 250 mg twice daily for 4 months. Results demonstrated improvement in 90% of patients, and 7.1% reported adverse effects (eg, abdominal bloating and pain, nausea, vomiting, headache, tinnitus, numbness, menstrual irregularities).³⁶ Coagulation screening should be monitored monthly, and any patient with a history of clotting abnormalities should be excluded from off-label treatment with oral tranexamic acid.

Nonprescription cosmeceuticals are available over-the-counter or are office dispensed.³⁷ For optimal results, cosmeceutical agents for skin lightening are used in combination. Most of these combinations are HQ free and have additive benefits such as a multimodal skin lightening agent containing key ingredients that correct and prevent skin pigmentation via several pathways affecting melanogenesis.³⁸ It is an excellent alternative to HQ for mottled and diffuse UV-induced hyperpigmentation and can be used for maintenance therapy in patients with melasma.

Photoprotection is an essential component of therapy for melasma and PIH, but there is a paucity of data on the benefits for SOC patients. Halder et al³⁹ performed a randomized prospective study of 89 black and Hispanic patients who applied sunscreen with a sun protection factor of 30 or 60 daily for 8 weeks. Clinical grading, triplicate L*A*B chromameter, and clinical photography were taken at baseline and weeks 4 and 8. The results demonstrated skin lightening in both black and Hispanic patients and support the use of sunscreen in the prevention and management of dyschromia in SOC patients.³⁹ Visible light also may play a role in melasma development, and thus use of sunscreens or makeup containing iron oxides are recommended.⁴⁰

Procedural treatments for facial hyperpigmentation include microdermabrasion, chemical peels, lasers, energy-based devices, and microneedling. There are many types and formulations of chemical peeling agents available; however, superficial and medium-depth chemical peels are recommended for SOC patients (Table 2). Deep chemical peels are not recommended for SOC patients due to the potential increased risk for PIH and scarring.

Cosmetic Enhancement in SOC Patients

Cosmetic procedures are gaining popularity in the SOC population and account for more than 20% of cosmetic procedures in the United States.⁴¹ Facial cosmetic concerns in SOC include dyschromia, benign growths (dermatosis papulosa nigra), hyperkinetic facial lines, volume loss, and skin laxity.⁴² Key principles to consider when treating SOC patients are the impact of ethnicity on aging and facial structure, the patient’s desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient’s expectations for recommended therapies.

Aging in SOC Patients
Skin aging can be classified as intrinsic aging or extrinsic aging. Intrinsic aging is genetic and involves subsurface changes such as volume loss, muscle atrophy, and resorption of bony structure. Extrinsic aging (or photoaging) involves surface changes of the epidermis/dermis and manifests as mottled pigmentation, textural changes, and fine wrinkling. Due to the photoprotection of melanin (black skin=SPF 13.4), skin aging in SOC patients is delayed by 10 to 20 years.⁴³ In addition, SOC patients have more reactive collagen and can benefit from noninvasive cosmetic procedures such as fillers and skin-tightening procedures.⁴²

Cosmetic Treatments and Procedures
Dermatosis papulosa nigra (benign growths of skin that have a genetic predisposition)⁴⁴ occur mainly on the face but can involve the entire body. Treatment modalities include electrodesiccation, cryotherapy, scissor excision, and laser surgery.⁴⁵

Treatment of hyperkinetic facial lines with botulinum toxin type A is a safe and effective procedure in patients with SOC. Grimes and Shabazz⁴⁶ performed a 4-month, randomized, double-blind study that evaluated the treatment of glabellar lines in women with Fitzpatrick skin types V and VI. The results demonstrated that the duration of effects was the same in the patients who received either 20 or 30 U of botulinum toxin type A.⁴⁶ Dynamic rhytides (furrows and frown/scowl lines arising from laughing, frowning, or smiling) can be treated safely in patients with SOC using botulinum toxin type A off label for relaxation of the upper and lower hyperkinetic muscles that result in these unwanted signs of aging. Botulinum toxin type A often is used for etched-in crow’s-feet, which rarely are evident in SOC patients.⁴⁷ Facial shaping also can be accomplished by injecting botulinum toxin type A in combination with soft-tissue dermal fillers.⁴⁷

Although black individuals do not experience perioral rhytides at the frequency of white individuals, they experience a variety of other cosmetic issues related to skin sagging and sinking. Currently available hyaluronic acid (HA) fillers have been shown to be safe in patients with Fitzpatrick skin types IV through VI.⁴⁸ Two studies evaluated fillers in patients with SOC, specifically HA⁴⁹ and calcium hydroxylapatite,⁵⁰ focused on treatment of the nasolabial folds and the potential risk for dyspigmentation and keloidal scarring. Taylor et al⁴⁹ noted that the risk of hyperpigmentation was 6% to 9% for large- and small-particle HA, respectively, and was associated with the serial or multiple puncture injection technique. No hypertrophic or keloidal scarring occurred in both studies.^49,50

Facial contouring applications with fillers include glabellar lines, temples, nasal bridge, tear troughs, malar and submalar areas, nasolabial folds, radial lines, lips, marionette lines, mental crease, and chin. Hyaluronic acid fillers also can be used for lip enhancement.⁴⁷ Although white women are looking to increase the size of their lips, black women are seeking augmentation to restore their lip size to that of their youth. Black individuals do not experience the same frequency of perioral rhytides as white patients, but they experience a variety of other issues related to skin sagging and sinking. Unlike white women, enhancement of the vermilion border rarely is performed in black women due to development of rhytides, predominantly in the body of the lip below the vermilion border in response to volume loss in the upper lip while the lower lip usually maintains its same appearance.⁴⁷

Facial enhancement utilizing poly-L-lactic acid can be used safely in SOC patients.⁵¹ Poly-L-lactic acid microparticles induce collagen formation, leading to dermal thickening over 3 to 6 months; however, multiple sessions are required to achieve optimal aesthetic results.

Patients with more reactive collagen can benefit from noninvasive cosmetic procedures such as skin-tightening procedures.⁵² Radiofrequency and microfocused ultrasound are cosmetic procedures used to provide skin tightening and facial lifting. They are safe and effective treatments for patients with Fitzpatrick skin types IV to VI.⁵³ Histologically, there is less thinning of collagen bundles and elastic tissue in ethnic skin. Due to stimulation of collagen by these procedures, most SOC patients will experience a more enhanced response, requiring fewer treatment sessions than white individuals.

Conclusion

Medical and aesthetic facial concerns in SOC patients vary and can be a source of emotional and psychological distress that can negatively impact quality of life. The approach to the treatment of SOC patients should be a balance between tolerability and efficacy, considering the potential risk for PIH.

The approach to the treatment of common skin disorders and cosmetic concerns in patients with skin of color (SOC) requires the clinician to understand the biological differences, nuances, and special considerations that are unique to patients with darker skin types.^1-3 This article addresses 4 common facial concerns in SOC patients—acne, rosacea, facial hyperpigmentation, and cosmetic enhancement—and provides treatment recommendations and management pearls to assist the clinician with optimal outcomes for SOC patients.

Acne in SOC Patients

Acne vulgaris is one of the most common conditions that dermatologists treat and is estimated to affect 40 to 50 million individuals in the United States.¹ Many of these acne patients are individuals with SOC.^2-4 A study of 2835 females (aged 10–70 years) conducted in 4 different cities—Los Angeles, California; London, United Kingdom; Akita, Japan; and Rome, Italy—demonstrated acne prevalence of 37% in blacks, 32% in Hispanics, 30% in Asians, 24% in whites, and 23% in Continental Indians.⁵ Blacks, Hispanics, and Continental Indians demonstrated equal prevalence with comedonal and inflammatory acne. Asians displayed more inflammatory acne lesions than comedones. In contrast, whites demonstrated more comedones than inflammatory acne. Dyspigmentation, postinflammatory hyperpigmentation (PIH), and atrophic scars were more common in black and Hispanic females than other ethnicities.⁵ This study illustrated that acne-induced PIH is a common sequela in SOC patients and is the main reason they seek treatment.^6,7

The pathogenesis of acne is the same in all racial and ethnic groups: (1) follicular hyperkeratinization and the formation of a microcomedone caused by abnormal desquamation of the keratinocytes within the sebaceous follicle, (2) production of sebum by circulating androgens, (3) proliferation of Propionibacterium acnes, and (4) inflammation. Subclinical inflammation is present throughout all stages of acne, including normal-appearing skin, inflammatory lesions, comedones, and scarring, and may contribute to PIH in acne patients with SOC (Figure 1).⁸ A thorough history should be obtained from acne patients, including answers to the following questions⁷:

• What skin and hair care products do you use?
• Do you use sunscreen daily?
• What cosmetic products or makeup do you use?
• Do you use any ethnic skin care products, including skin lightening creams?
• Do you have a history of keloids?

It is important to ask these questions to assess if the SOC patient has developed pomade acne,⁹ acne cosmetica,¹⁰ or a potential risk of skin irritation from the use of skin care practices. It is best to take total control of the patient’s skin care regimen and discontinue use of toners, astringents, witch hazel, exfoliants, and rubbing alcohol, which may lead to skin dryness and irritation, particularly when combined with topical acne medications.

Treatment
Treatment of acne in SOC patients is similar to generally recommended treatments, with special considerations. Consider the following key points when treating acne in SOC patients:

• Treat acne early and aggressively to prevent or minimize subsequent PIH and acne scarring.
• Balance aggressive treatment with nonirritating topical skin care.
• Most importantly, target PIH in addition to acne and choose a regimen that limits skin irritation that might exacerbate existing PIH.⁷

Develop a maintenance program to control future breakouts. Topical agents can be used as monotherapy or in fixed combinations and may include benzoyl peroxide, antibiotics, dapsone, azelaic acid (AZA), and retinoids. Similar to white patients, topical retinoids remain a first-line treatment for acne in patients with SOC.^11,12

Tolerability must be managed in SOC acne patients. Therapeutic maneuvers that can be instituted should include a discussion on using gentle skin care, initiating therapy with a retinoid applied every other night starting with a low concentration and gradually titrating up, and applying a moisturizer before or after applying acne medication. Oral therapies consist of antibiotics (doxycycline, minocycline), retinoids (isotretinoin), and hormonal modulators (oral contraceptives, spironolactone). Isotretinoin, recommended for patients with nodulocystic acne, may play a possible role in treating acne-induced PIH.¹³

Two common procedural therapies for acne include comedone extraction and intralesional corticosteroid injection. A 6- to 8-week course of a topical retinoid prior to comedonal extraction may facilitate the procedure and is recommended in SOC patients to help reduce cutaneous trauma and PIH.¹¹ Inflammatory acne lesions can be treated with intralesional injection of triamcinolone acetonide 2.5 or 5.0 mg/mL, which usually reduces inflammation within 2 to 5 days.¹¹

Treatment of acne-induced PIH includes sun protection, topical and oral medications, chemical peels, lasers, and energy devices. Treatment of hypertrophic scarring and keloids involves intralesional injection of triamcinolone acetonide 20, 30, or 40 mg/mL every 4 weeks until the lesion is flat.¹¹

Superficial chemical peels can be used to treat acne and PIH in SOC patients,¹⁴ such as salicylic acid (20%–30%), glycolic acid (20%–70%), trichloroacetic acid (15%–30%), and Jessner peels.

Acne Scarring
Surgical approaches to acne scarring in patients with SOC include elliptical excision, punch excision, punch elevation, punch autografting, dermal grafting, dermal planning, subcutaneous incision (subcision), dermabrasion, microneedling, fillers, and laser skin resurfacing. The treatment of choice depends on the size, type, and depth of the scar and the clinician’s preference.

Lasers
Fractional photothermolysis has emerged as a treatment option for acne scars in SOC patients. This procedure produces microscopic columns of thermal injury in the epidermis and dermis, sparing the surrounding tissue and minimizing downtime and adverse events. Because fractional photothermolysis does not target melanin and produces limited epidermal injury, darker Fitzpatrick skin types (IV–VI) can be safely and effectively treated with this procedure.¹⁵

Rosacea in SOC Patients

Rosacea is a chronic inflammatory disorder that affects the vasculature and pilosebaceous units of the face. It commonly is seen in Fitzpatrick skin types I and II; however, rosacea can occur in all skin types (Figure 2). Triggers include emotional stress, extreme environmental temperatures, hot and spicy foods, red wine or alcohol, and topical irritants or allergens found in common cosmetic products.¹⁶

Data suggest that 4% of rosacea patients in the United States are of African, Latino, or Asian descent.¹¹ National Ambulatory Medical Care Survey data revealed that of 31.5 million rosacea visits, 2% of patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino. In a 5-year longitudinal study of 2587 rosacea patients enrolled in Medicaid in North Carolina who were prescribed at least 1 topical treatment for rosacea, 16.27% were black and 10% were of a race other than white.¹⁷

Although the pathogenesis of rosacea is unclear, hypotheses include immune system abnormalities, neurogenic dysregulation, presence of microorganisms (eg, Demodex folliculorum), UV damage, and skin barrier dysfunction.¹⁸

The 4 major subtypes of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea.¹⁶ Interestingly, rosacea in SOC patients may present with hypopigmentation surrounding the borders of the facial erythema. For phymatous rosacea, isotretinoin may reduce incipient rhinophyma but must be carefully monitored and pregnancy must be excluded. Surgical or laser therapy may be indicated to recontour the nose if severe.

There are several skin conditions that can present with facial erythema in patients with SOC, including seborrheic dermatitis, systemic lupus erythematosus, and contact dermatitis. It is important to note that the detection of facial erythema in darker skin types may be difficult; therefore, laboratory evaluation (antinuclear antibodies), patch testing, and skin biopsy should be considered if the clinical diagnosis is unclear.

Treatment
Treatment of rosacea in SOC patients does not differ from other racial groups. Common strategies include gentle skin care, sun protection (sun protection factor 30+), and barrier repair creams. Topical agents include metronidazole, AZA, sodium sulfacetamide/sulfur, ivermectin, and retinoids.¹⁶ Oral treatments include antibiotics in the tetracycline family (eg, subantimicrobial dose doxycycline) and isotretinoin.¹⁶ Persistent erythema associated with rosacea can be treated with brimonidine¹⁹ and oxymetazoline.²⁰ Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea²¹; however, the latter is not recommended in Fitzpatrick skin types IV through VI.

Facial Hyperpigmentation in SOC Patients

Hyperpigmentation disorders can be divided into conditions that affect Fitzpatrick skin types I through III and IV though VI. Mottled hyperpigmentation (photodamage) and solar lentigines occur in patients with lighter skin types as compared to melasma, PIH, and age-related (UV-induced) hyperpigmentation, which occur more commonly in patients with darker skin types. Facial hyperpigmentation is a common concern in SOC patients. In a survey of cosmetic concerns of 100 women with SOC, hyperpigmentation or dark spots (86%) and blotchy uneven skin (80%) were the top concerns.²² In addition, facial hyperpigmentation has been shown to negatively impact quality of life.²³

Postinflammatory hyperpigmentation occurs from a pathophysiological response to inflammation, cutaneous irritation or injury, and subsequent melanocyte lability. Postinflammatory hyperpigmentation is a common presenting concern in patients with SOC and is seen as a result of many inflammatory skin disorders (eg, acne, eczema) and dermatologic procedures (eg, adverse reaction to electrodesiccation, microdermabrasion, chemical peels, laser surgery).²⁴

Melasma is an acquired idiopathic disorder of hyperpigmentation and often referred to as the mask of pregnancy (Figure 3). It occurs on sun-exposed areas of skin, mainly in women with Fitzpatrick skin types III through V. Associated factors or triggers include pregnancy, hormonal treatments, exposure to UV radiation, and medications.²⁵ Hereditary factors play a role in more than 40% of cases.²⁶

Other not-so-common facial dyschromias include contact dermatitis, acanthosis nigricans, exogenous ochronosis, lichen planus pigmentosus (associated with frontal fibrosing alopecia),²⁷ drug-induced hyperpigmentation (associated with minocycline or diltiazem),^28,29 and UV-induced (age-related) hyperpigmentation.

Treatment
The treatment of hyperpigmentation should provide the following: (1) protection from sun exposure; (2) inhibition of tyrosinase, the enzyme responsible for the conversion of tyrosine to melanin; (3) inhibition of melanosome transfer from the melanocyte to the keratinocyte; (4) removal of melanin from the epidermis through exfoliation; and (5) destruction or disruption of melanin in the dermis.³⁰ Therapies for facial hyperpigmentation are listed in Table 1.

Topical therapies include prescription medications and nonprescription cosmeceuticals. Prescription medications include hydroquinone (HQ), topical retinoids, and AZA. Hydroquinone, a tyrosinase inhibitor, is the gold standard for skin lightening and often is used as a first-line therapy. It is used as a monotherapy (HQ 4%) or as a fixed combination with tretinoin 0.05% and fluocinolone 0.01%.³¹ Use caution with HQ in high concentrations (6% and higher) and low concentrations (2% [over-the-counter strength]) used long-term due to the potential risk of exogenous ochronosis.

Topical retinoids have been shown to be effective therapeutic agents for melasma and PIH. Tretinoin,³² tazarotene,³³ and adapalene³⁴ all have demonstrated efficacy for acne and acne-induced PIH in SOC patients. Patients must be monitored for the development of retinoid dermatitis and worsening of hyperpigmentation.

Azelaic acid is a naturally occurring dicarboxylic acid obtained from cultures of Malassezia furfur. Azelaic acid inhibits tyrosinase activity, DNA synthesis, and mitochondrial enzymes, thus blocking direct cytotoxic effects toward melanocytes. Azelaic acid is approved by the US Food and Drug Administration for acne in a 20% cream formulation and rosacea in 15% gel and foam formulations, and it is used off label for melasma and PIH.³⁵

Oral tranexamic acid is currently used as a hemostatic agent due to its ability to inhibit the plasminogen-plasmin pathway. In melasma, it blocks the interaction between melanocytes and keratinocytes in the epidermis and modulates the vascular component of melasma in the dermis. In an open-label study, 561 Asian melasma patients were treated with oral tranexamic acid 250 mg twice daily for 4 months. Results demonstrated improvement in 90% of patients, and 7.1% reported adverse effects (eg, abdominal bloating and pain, nausea, vomiting, headache, tinnitus, numbness, menstrual irregularities).³⁶ Coagulation screening should be monitored monthly, and any patient with a history of clotting abnormalities should be excluded from off-label treatment with oral tranexamic acid.

Nonprescription cosmeceuticals are available over-the-counter or are office dispensed.³⁷ For optimal results, cosmeceutical agents for skin lightening are used in combination. Most of these combinations are HQ free and have additive benefits such as a multimodal skin lightening agent containing key ingredients that correct and prevent skin pigmentation via several pathways affecting melanogenesis.³⁸ It is an excellent alternative to HQ for mottled and diffuse UV-induced hyperpigmentation and can be used for maintenance therapy in patients with melasma.

Photoprotection is an essential component of therapy for melasma and PIH, but there is a paucity of data on the benefits for SOC patients. Halder et al³⁹ performed a randomized prospective study of 89 black and Hispanic patients who applied sunscreen with a sun protection factor of 30 or 60 daily for 8 weeks. Clinical grading, triplicate L*A*B chromameter, and clinical photography were taken at baseline and weeks 4 and 8. The results demonstrated skin lightening in both black and Hispanic patients and support the use of sunscreen in the prevention and management of dyschromia in SOC patients.³⁹ Visible light also may play a role in melasma development, and thus use of sunscreens or makeup containing iron oxides are recommended.⁴⁰

Procedural treatments for facial hyperpigmentation include microdermabrasion, chemical peels, lasers, energy-based devices, and microneedling. There are many types and formulations of chemical peeling agents available; however, superficial and medium-depth chemical peels are recommended for SOC patients (Table 2). Deep chemical peels are not recommended for SOC patients due to the potential increased risk for PIH and scarring.

Cosmetic Enhancement in SOC Patients

Cosmetic procedures are gaining popularity in the SOC population and account for more than 20% of cosmetic procedures in the United States.⁴¹ Facial cosmetic concerns in SOC include dyschromia, benign growths (dermatosis papulosa nigra), hyperkinetic facial lines, volume loss, and skin laxity.⁴² Key principles to consider when treating SOC patients are the impact of ethnicity on aging and facial structure, the patient’s desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient’s expectations for recommended therapies.

Aging in SOC Patients
Skin aging can be classified as intrinsic aging or extrinsic aging. Intrinsic aging is genetic and involves subsurface changes such as volume loss, muscle atrophy, and resorption of bony structure. Extrinsic aging (or photoaging) involves surface changes of the epidermis/dermis and manifests as mottled pigmentation, textural changes, and fine wrinkling. Due to the photoprotection of melanin (black skin=SPF 13.4), skin aging in SOC patients is delayed by 10 to 20 years.⁴³ In addition, SOC patients have more reactive collagen and can benefit from noninvasive cosmetic procedures such as fillers and skin-tightening procedures.⁴²

Cosmetic Treatments and Procedures
Dermatosis papulosa nigra (benign growths of skin that have a genetic predisposition)⁴⁴ occur mainly on the face but can involve the entire body. Treatment modalities include electrodesiccation, cryotherapy, scissor excision, and laser surgery.⁴⁵

Treatment of hyperkinetic facial lines with botulinum toxin type A is a safe and effective procedure in patients with SOC. Grimes and Shabazz⁴⁶ performed a 4-month, randomized, double-blind study that evaluated the treatment of glabellar lines in women with Fitzpatrick skin types V and VI. The results demonstrated that the duration of effects was the same in the patients who received either 20 or 30 U of botulinum toxin type A.⁴⁶ Dynamic rhytides (furrows and frown/scowl lines arising from laughing, frowning, or smiling) can be treated safely in patients with SOC using botulinum toxin type A off label for relaxation of the upper and lower hyperkinetic muscles that result in these unwanted signs of aging. Botulinum toxin type A often is used for etched-in crow’s-feet, which rarely are evident in SOC patients.⁴⁷ Facial shaping also can be accomplished by injecting botulinum toxin type A in combination with soft-tissue dermal fillers.⁴⁷

Although black individuals do not experience perioral rhytides at the frequency of white individuals, they experience a variety of other cosmetic issues related to skin sagging and sinking. Currently available hyaluronic acid (HA) fillers have been shown to be safe in patients with Fitzpatrick skin types IV through VI.⁴⁸ Two studies evaluated fillers in patients with SOC, specifically HA⁴⁹ and calcium hydroxylapatite,⁵⁰ focused on treatment of the nasolabial folds and the potential risk for dyspigmentation and keloidal scarring. Taylor et al⁴⁹ noted that the risk of hyperpigmentation was 6% to 9% for large- and small-particle HA, respectively, and was associated with the serial or multiple puncture injection technique. No hypertrophic or keloidal scarring occurred in both studies.^49,50

Facial contouring applications with fillers include glabellar lines, temples, nasal bridge, tear troughs, malar and submalar areas, nasolabial folds, radial lines, lips, marionette lines, mental crease, and chin. Hyaluronic acid fillers also can be used for lip enhancement.⁴⁷ Although white women are looking to increase the size of their lips, black women are seeking augmentation to restore their lip size to that of their youth. Black individuals do not experience the same frequency of perioral rhytides as white patients, but they experience a variety of other issues related to skin sagging and sinking. Unlike white women, enhancement of the vermilion border rarely is performed in black women due to development of rhytides, predominantly in the body of the lip below the vermilion border in response to volume loss in the upper lip while the lower lip usually maintains its same appearance.⁴⁷

Facial enhancement utilizing poly-L-lactic acid can be used safely in SOC patients.⁵¹ Poly-L-lactic acid microparticles induce collagen formation, leading to dermal thickening over 3 to 6 months; however, multiple sessions are required to achieve optimal aesthetic results.

Patients with more reactive collagen can benefit from noninvasive cosmetic procedures such as skin-tightening procedures.⁵² Radiofrequency and microfocused ultrasound are cosmetic procedures used to provide skin tightening and facial lifting. They are safe and effective treatments for patients with Fitzpatrick skin types IV to VI.⁵³ Histologically, there is less thinning of collagen bundles and elastic tissue in ethnic skin. Due to stimulation of collagen by these procedures, most SOC patients will experience a more enhanced response, requiring fewer treatment sessions than white individuals.

Conclusion

Medical and aesthetic facial concerns in SOC patients vary and can be a source of emotional and psychological distress that can negatively impact quality of life. The approach to the treatment of SOC patients should be a balance between tolerability and efficacy, considering the potential risk for PIH.

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.¹ Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.² Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.³ Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.^4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.^6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.⁶

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).⁸ Another study by Hall et al⁹ of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al⁶ investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al¹⁰ examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.¹¹ Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.¹² Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.¹³ Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.¹⁴ The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan¹⁵ revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.¹⁶

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling¹⁷ demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.^18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.^20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard²² shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.²² Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.^23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.²⁵ Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.^26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.²⁸ Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).⁸ Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.¹ Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.² Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.³ Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.^4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.^6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.⁶

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).⁸ Another study by Hall et al⁹ of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al⁶ investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al¹⁰ examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.¹¹ Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.¹² Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.¹³ Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.¹⁴ The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan¹⁵ revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.¹⁶

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling¹⁷ demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.^18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.^20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard²² shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.²² Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.^23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.²⁵ Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.^26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.²⁸ Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).⁸ Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.¹ Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.² Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.³ Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.^4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.^6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.⁶

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).⁸ Another study by Hall et al⁹ of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al⁶ investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al¹⁰ examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.¹¹ Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.¹² Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.¹³ Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.¹⁴ The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan¹⁵ revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.¹⁶

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling¹⁷ demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.^18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.^20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard²² shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.²² Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.^23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.²⁵ Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.^26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.²⁸ Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).⁸ Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.