Cutis

THE DIAGNOSIS: White Fibrous Papulosis

Given the histopathology findings, location on a sun-exposed site, lack of any additional systemic signs or symptoms, and no family history of similar lesions to suggest an underlying genetic condition, a diagnosis of white fibrous papulosis (WFP) was made. White fibrous papulosis is a relatively rare cutaneous disorder that was first reported by Shimizu et al¹ in 1985. It is characterized by numerous grouped, 2- to 3-mm, white to flesh-colored papules that in most cases are confined to the neck in middle-aged to elderly individuals; however, cases involving the upper trunk and axillae also have been reported.^1-3 The etiology of this condition is unclear but is thought to be related to aging and chronic exposure to UV light. Although treatment is not required, various modalities including tretinoin, excision, and laser therapy have been trialed with varying success.^2,4 Our patient elected not to proceed with treatment.

Histologically, WFP may manifest similarly to connective tissue nevi; the overall architecture is nonspecific with focally thickened collagen and often elastic fibers that may be normal to reduced and/or fragmented, as well as an overall decrease in superficial dermal elastic tissue.^3,5 Therefore, the differential diagnosis may include connective tissue nevi and require clinical correlation to make a correct diagnosis.

Pseudoxanthoma elasticum (PXE) is an autosomalrecessive disorder most commonly related to mutations in the ATP binding cassette subfamily C member 6 (ABCC6) gene that tends to manifest clinically on the neck and flexural extremities.⁶ This disease affects elastic fibers, which may become calcified over time. Pseudoxanthoma elasticum is associated with ocular complications relating to the Bruch membrane of the retina and angioid streaks; choroidal neovascularization involving the damaged Bruch membrane and episodes of acute retinopathy may result in vision loss in later stages of the disease.⁷ Involvement of the elastic laminae of arteries can be associated with cardiovascular and cerebrovascular complications such as stroke, coronary artery disease, claudication, and aneurysms. Involvement of the gastrointestinal or genitourinary tracts also may occur and most commonly manifests with bleeding. Pathologic alterations in the elastic fibers of the lungs also have been reported in patients with PXE.⁸ Histologically, PXE exhibits increased abnormally clumped and fragmented elastic fibers in the superficial dermis, often with calcification (Figure 1). Pseudo-PXE related to D-penicillamine use often lacks calcification and has a bramble bush appearance.⁹

Fibrofolliculomas may manifest alone or in association with an underlying condition such as Birt-Hogg-Dubé syndrome, in which lesions are most frequently seen scattered on the scalp, face, ears, neck, or upper trunk.¹⁰ This condition is related to a folliculin (FLCN) gene germline mutation. Birt-Hogg-Dubé syndrome also may be associated with acrochordons, trichodiscomas, renal cancer, and lung cysts with or without spontaneous pneumothorax. Less frequently noted findings include oral papules, epidermal cysts, angiofibromas, lipomas/angiolipomas, parotid gland tumors, and thyroid neoplasms. Connective tissue nevi/collagenomas can appear clinically similar to fibrofolliculomas; true connective tissue nevi are reported less commonly in Birt-Hogg-Dubé syndrome.¹¹ Histologically, a fibrofolliculoma manifests with epidermal strands originating from a hair follicle associated with prominent surrounding connective tissue (Figure 2).

Elastofibroma dorsi is a benign tumor of connective tissue that most commonly manifests clinically as a solitary subcutaneous mass on the back near the inferior angle of the scapula; it typically develops below the rhomboid major and latissimus dorsi muscles.¹² The pathogenesis is uncertain, but some patients have reported a family history of the condition or a history of repetitive shoulder movement/trauma prior to onset; the mass may be asymptomatic or associated with pain and/or swelling. Those affected tend to be older than 50 years.¹³ Histologically, thickened and rounded to beaded elastic fibers are seen admixed with collagen (Figure 3).

Actinic (solar) elastosis frequently is encountered in many skin biopsies and is caused by chronic photodamage. More hypertrophic variants, such as papular or nodular solar elastosis, may clinically manifest similarly to WFP.¹⁴ Histologically, actinic elastosis manifests as a considerable increase in elastic tissue in the papillary and superficial reticular dermis (Figure 4).

THE DIAGNOSIS: White Fibrous Papulosis

Given the histopathology findings, location on a sun-exposed site, lack of any additional systemic signs or symptoms, and no family history of similar lesions to suggest an underlying genetic condition, a diagnosis of white fibrous papulosis (WFP) was made. White fibrous papulosis is a relatively rare cutaneous disorder that was first reported by Shimizu et al¹ in 1985. It is characterized by numerous grouped, 2- to 3-mm, white to flesh-colored papules that in most cases are confined to the neck in middle-aged to elderly individuals; however, cases involving the upper trunk and axillae also have been reported.^1-3 The etiology of this condition is unclear but is thought to be related to aging and chronic exposure to UV light. Although treatment is not required, various modalities including tretinoin, excision, and laser therapy have been trialed with varying success.^2,4 Our patient elected not to proceed with treatment.

Histologically, WFP may manifest similarly to connective tissue nevi; the overall architecture is nonspecific with focally thickened collagen and often elastic fibers that may be normal to reduced and/or fragmented, as well as an overall decrease in superficial dermal elastic tissue.^3,5 Therefore, the differential diagnosis may include connective tissue nevi and require clinical correlation to make a correct diagnosis.

Pseudoxanthoma elasticum (PXE) is an autosomalrecessive disorder most commonly related to mutations in the ATP binding cassette subfamily C member 6 (ABCC6) gene that tends to manifest clinically on the neck and flexural extremities.⁶ This disease affects elastic fibers, which may become calcified over time. Pseudoxanthoma elasticum is associated with ocular complications relating to the Bruch membrane of the retina and angioid streaks; choroidal neovascularization involving the damaged Bruch membrane and episodes of acute retinopathy may result in vision loss in later stages of the disease.⁷ Involvement of the elastic laminae of arteries can be associated with cardiovascular and cerebrovascular complications such as stroke, coronary artery disease, claudication, and aneurysms. Involvement of the gastrointestinal or genitourinary tracts also may occur and most commonly manifests with bleeding. Pathologic alterations in the elastic fibers of the lungs also have been reported in patients with PXE.⁸ Histologically, PXE exhibits increased abnormally clumped and fragmented elastic fibers in the superficial dermis, often with calcification (Figure 1). Pseudo-PXE related to D-penicillamine use often lacks calcification and has a bramble bush appearance.⁹

Fibrofolliculomas may manifest alone or in association with an underlying condition such as Birt-Hogg-Dubé syndrome, in which lesions are most frequently seen scattered on the scalp, face, ears, neck, or upper trunk.¹⁰ This condition is related to a folliculin (FLCN) gene germline mutation. Birt-Hogg-Dubé syndrome also may be associated with acrochordons, trichodiscomas, renal cancer, and lung cysts with or without spontaneous pneumothorax. Less frequently noted findings include oral papules, epidermal cysts, angiofibromas, lipomas/angiolipomas, parotid gland tumors, and thyroid neoplasms. Connective tissue nevi/collagenomas can appear clinically similar to fibrofolliculomas; true connective tissue nevi are reported less commonly in Birt-Hogg-Dubé syndrome.¹¹ Histologically, a fibrofolliculoma manifests with epidermal strands originating from a hair follicle associated with prominent surrounding connective tissue (Figure 2).

Elastofibroma dorsi is a benign tumor of connective tissue that most commonly manifests clinically as a solitary subcutaneous mass on the back near the inferior angle of the scapula; it typically develops below the rhomboid major and latissimus dorsi muscles.¹² The pathogenesis is uncertain, but some patients have reported a family history of the condition or a history of repetitive shoulder movement/trauma prior to onset; the mass may be asymptomatic or associated with pain and/or swelling. Those affected tend to be older than 50 years.¹³ Histologically, thickened and rounded to beaded elastic fibers are seen admixed with collagen (Figure 3).

Actinic (solar) elastosis frequently is encountered in many skin biopsies and is caused by chronic photodamage. More hypertrophic variants, such as papular or nodular solar elastosis, may clinically manifest similarly to WFP.¹⁴ Histologically, actinic elastosis manifests as a considerable increase in elastic tissue in the papillary and superficial reticular dermis (Figure 4).

THE DIAGNOSIS: White Fibrous Papulosis

Given the histopathology findings, location on a sun-exposed site, lack of any additional systemic signs or symptoms, and no family history of similar lesions to suggest an underlying genetic condition, a diagnosis of white fibrous papulosis (WFP) was made. White fibrous papulosis is a relatively rare cutaneous disorder that was first reported by Shimizu et al¹ in 1985. It is characterized by numerous grouped, 2- to 3-mm, white to flesh-colored papules that in most cases are confined to the neck in middle-aged to elderly individuals; however, cases involving the upper trunk and axillae also have been reported.^1-3 The etiology of this condition is unclear but is thought to be related to aging and chronic exposure to UV light. Although treatment is not required, various modalities including tretinoin, excision, and laser therapy have been trialed with varying success.^2,4 Our patient elected not to proceed with treatment.

Histologically, WFP may manifest similarly to connective tissue nevi; the overall architecture is nonspecific with focally thickened collagen and often elastic fibers that may be normal to reduced and/or fragmented, as well as an overall decrease in superficial dermal elastic tissue.^3,5 Therefore, the differential diagnosis may include connective tissue nevi and require clinical correlation to make a correct diagnosis.

Pseudoxanthoma elasticum (PXE) is an autosomalrecessive disorder most commonly related to mutations in the ATP binding cassette subfamily C member 6 (ABCC6) gene that tends to manifest clinically on the neck and flexural extremities.⁶ This disease affects elastic fibers, which may become calcified over time. Pseudoxanthoma elasticum is associated with ocular complications relating to the Bruch membrane of the retina and angioid streaks; choroidal neovascularization involving the damaged Bruch membrane and episodes of acute retinopathy may result in vision loss in later stages of the disease.⁷ Involvement of the elastic laminae of arteries can be associated with cardiovascular and cerebrovascular complications such as stroke, coronary artery disease, claudication, and aneurysms. Involvement of the gastrointestinal or genitourinary tracts also may occur and most commonly manifests with bleeding. Pathologic alterations in the elastic fibers of the lungs also have been reported in patients with PXE.⁸ Histologically, PXE exhibits increased abnormally clumped and fragmented elastic fibers in the superficial dermis, often with calcification (Figure 1). Pseudo-PXE related to D-penicillamine use often lacks calcification and has a bramble bush appearance.⁹

Fibrofolliculomas may manifest alone or in association with an underlying condition such as Birt-Hogg-Dubé syndrome, in which lesions are most frequently seen scattered on the scalp, face, ears, neck, or upper trunk.¹⁰ This condition is related to a folliculin (FLCN) gene germline mutation. Birt-Hogg-Dubé syndrome also may be associated with acrochordons, trichodiscomas, renal cancer, and lung cysts with or without spontaneous pneumothorax. Less frequently noted findings include oral papules, epidermal cysts, angiofibromas, lipomas/angiolipomas, parotid gland tumors, and thyroid neoplasms. Connective tissue nevi/collagenomas can appear clinically similar to fibrofolliculomas; true connective tissue nevi are reported less commonly in Birt-Hogg-Dubé syndrome.¹¹ Histologically, a fibrofolliculoma manifests with epidermal strands originating from a hair follicle associated with prominent surrounding connective tissue (Figure 2).

Elastofibroma dorsi is a benign tumor of connective tissue that most commonly manifests clinically as a solitary subcutaneous mass on the back near the inferior angle of the scapula; it typically develops below the rhomboid major and latissimus dorsi muscles.¹² The pathogenesis is uncertain, but some patients have reported a family history of the condition or a history of repetitive shoulder movement/trauma prior to onset; the mass may be asymptomatic or associated with pain and/or swelling. Those affected tend to be older than 50 years.¹³ Histologically, thickened and rounded to beaded elastic fibers are seen admixed with collagen (Figure 3).

Actinic (solar) elastosis frequently is encountered in many skin biopsies and is caused by chronic photodamage. More hypertrophic variants, such as papular or nodular solar elastosis, may clinically manifest similarly to WFP.¹⁴ Histologically, actinic elastosis manifests as a considerable increase in elastic tissue in the papillary and superficial reticular dermis (Figure 4).

Current evidence indicates that obesity may initiate psoriasis or worsen existing disease. Various factors contribute to the development of obesity, including eating disorders (EDs). The aim of this study was to screen for and identify factors associated with EDs in patients with psoriasis and their impact on the development of obesity in this population. Demographic information including body mass index (BMI), Eating Attitude Test (EAT-26), Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale 21 (DASS-21) scores were statistically analyzed for 82 participants with psoriasis at a tertiary dermatology clinic. It is important to manage obesity and other comorbidities of psoriasis in addition to treating its cutaneous manifestations, which may require a biopsychosocial approach.

Psoriasis is a chronic multisystemic inflammatory skin disease with a worldwide prevalence of 2% to 3%.¹ Psoriasis can be accompanied by other conditions such as psoriatic arthritis, obesity, metabolic syndrome, diabetes mellitus, hypertension, dyslipidemia, atherosclerotic disease, inflammatory bowel disease, and anxiety/depression. It is important to manage comorbidities of psoriasis in addition to treating the cutaneous manifestations of the disease.¹

Obesity is a major public health concern worldwide. Numerous observational and epidemiologic studies have reported a high prevalence of obesity among patients with psoriasis.² Current evidence indicates that obesity may initiate or worsen psoriasis; furthermore, it is important to note that obesity may negatively impact the effectiveness of psoriasis-specific treatments or increase the incidence of adverse effects. Therefore, managing obesity is crucial in the treatment of psoriasis.³ Numerous studies have investigated the association between psoriasis and obesity, and they commonly conclude that both conditions share the same genetic metabolic pathways.^2-4 However, it is important to consider environmental factors such as dietary habits, smoking, alcohol consumption, and a sedentary lifestyle—all of which are associated with psoriasis and also can contribute to the development of obesity.⁵ Because of the effects of obesity in psoriasis patients, factors that impact the development of obesity have become a popular research topic.

Eating disorders (EDs) are a crucial risk factor for both developing and maintaining obesity. In particular, two EDs that are associated with obesity include binge eating disorder and bulimia nervosa.⁶ According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,⁷ binge eating disorder can be diagnosed when a patient has at least 1 episode of binge eating per week over a 3-month period. Bulimia nervosa can be diagnosed when a patient is excessively concerned with their body weight and shape and engages in behaviors to prevent weight gain (eg, forced vomiting, excessive use of laxatives).⁷ Psychiatrists who specialize in EDs make diagnoses based on these criteria. In daily practice, there are several quick and simple questionnaires available to screen for EDs that can be used by nonpsychiatrist physicians, including the commonly used 26-item Eating Attitudes Test (EAT-26).⁸ The EAT-26 has been used to screen for EDs in patients with inflammatory disorders.⁹

The aim of this study was to screen for EDs in patients with psoriasis to identify potential risk factors for development of obesity.

Materials and Methods

This study included patients with psoriasis who were screened for EDs at a tertiary dermatology clinic in Turkey between January 2021 and December 2023. This study was approved by the local ethics committee and was in accordance with the Declaration of Helsinki (decision number E-93471371-514.99-225000079).

Study Design and Patient Inclusion Criteria—This quantitative cross-sectional study utilized EAT-26, Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale-21 (DASS-21) scores. All the questionnaire scales used in the study were adapted and validated in Turkey.^8,10-12 The inclusion criteria consisted of being older than 18 years of age, being literate, having psoriasis for at least 1 year that was not treated topically or systemically, and having no psychiatric diseases outside an ED. The questionnaires were presented in written format following the clinical examination. Literacy was an inclusion criterion in this study due to the absence of auxiliary health personnel.

Study Variables—The study variables included age, sex, marital status (single/divorced or married), education status (primary/secondary school or high school/university), employment status (employed or unemployed/retired), body mass index (BMI), smoking status, alcohol-consumption status, Psoriasis Area Severity Index score, presence of nail psoriasis and psoriatic arthritis, duration of psoriasis, family history of psoriasis, EAT-26 score, ASHN score, DLQI score, and DASS-21 score. Body mass index was calculated by taking a participant’s weight in kilograms and dividing it by their height in meters squared. The BMI values were classified into 3 categories: normal (18.5–24.9 kg/m²), overweight (25.0–29.9 kg/m²), and obese (≥30 kg/m²).¹³

Questionnaires—The EAT-26 questionnaire includes 26 questions that are used to detect EDs. Responses to each question include Likert-type answer options (ie, “always,” “usually,” “often,” “sometimes,” “rarely,” and “never.”) Patients with scores of 20 points or higher (range, 0–78) are classified as high risk for EDs.⁸ In our study, EAT-26 scores were grouped into 2 categories: patients scoring less than 20 points and those scoring 20 points or higher.

The DLQI questionnaire includes 10 questions to measure dermatologic symptoms and qualiy of life. Responses to each question include Likert-type answer options (ie, “not at all,” “a little,” “a lot,” or “very much.”) On the DLQI scale, the higher the score, the lower the quality of life (score range, 0–30).¹⁰

The ASHN questionnaire includes 21 questions that measure attitudes toward healthy nutrition with 5 possible answer options (“strongly disagree,” “disagree,” “undecided,” “agree,” and “strongly agree”). On this scale, higher scores indicate the participant is more knowledgeable about healthy nutrition (score range, 0–78).¹¹

The DASS-21 questionnaire includes 21 questions that measure the severity of a range of symptoms common to depression, anxiety, and stress. Responses include Likert-type answer options (eg, “never,” “sometimes,” “often,” and “almost always.”) On this scale, a higher score (range of 0–21 for each) indicates higher levels of depression, anxiety, and stress.¹²

Statistical Analysis—Descriptive statistics were analyzed using SPSS software version 22.0 (IBM). The Shapiro-Wilk test was applied to determine whether the data were normally distributed. For categorical variables, frequency differences among groups were compared using the Pearson χ² test. A t test was used to compare the means of 2 independent groups with a normal distribution. One-way analysis of variance and Tukey Honest Significant Difference post hoc analysis were used to test whether there was a statistically significant difference among the normally distributed means of independent groups. Pearson correlation analysis was used to determine whether there was a linear relationship between 2 numeric measurements and, if so, to determine the direction and severity of this relationship. P<.05 indicated statistical significance in this study.

Results

Study Participant Demographics—This study included 82 participants with a mean age of 44.3 years; 52.4% (43/82) were female, and 85.4% (70/82) were married. The questionnaire took an average of 4.2 minutes for participants to complete. A total of 57.3% (47/82) of patients had completed primary/secondary education and 59.8% (49/82) were employed. The mean BMI was 28.1 kg/m². According to the BMI classification, 26.8% (22/82) participants had a normal weight, 36.6% (30/82) were overweight, and 43.9% (36/82) were obese. A total of 48.8% (40/82) of participants smoked, and 4.9% (4/82) consumed alcohol. The mean Psoriasis Area and Severity Index score was 5.4. A total of 54.9% (45/82) of participants had nail psoriasis, and 24.4% (20/82) had psoriatic arthritis. The mean duration of psoriasis was 153 months. A total of 29.3% (24/82) of participants had a positive family history of psoriasis. The mean EAT-26 score was 11.1. A total of 12.2% (10/82) of participants had an EAT-26 score of 20 points or higher and were considered at high risk for an ED. The mean ASHN score was 72.9; the mean DLQI score was 5.5; and on the DASS-21 scale, mean scores for depression, anxiety, and stress were 6.3, 8.7, and 10.0, respectively (Table).

Comparative Evaluation of the BMI Groups—The only statistically significant differences among the 3 BMI groups were related to marital status, EAT-26 score, and anxiety and stress scores (P=.02, <.01, <.01, and <.01, respectively)(eTable 1). The number of single/divorced participants in the overweight group was significantly (P=.02) greater than in the normal weight group. The mean EAT-26 score for the normal weight group was significantly (P<.01) lower than for the overweight and obese groups; there was no significant difference in mean EAT-26 scores between the overweight and obese groups. The mean anxiety score was significantly (P<.01) lower in the normal weight group compared with the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean depression score. The mean stress and anxiety scores were significantly (P<.01) lower in the normal weight group than in the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean anxiety score.

Comparative Evaluation of the EAT-26 Scores—There were statistically significant differences among the EAT-26 scores related to sex; BMI; and depression, anxiety, and stress scores (P=.04, .02, <.01, <.01, and <.01, respectively). The number of females in the group with a score of 20 points or higher was significantly (P=.04) less than that in the group scoring less than 20 points. The mean BMI in the group with a score of 20 points or higher was significantly (P=.02) greater than in group scoring less than 20 points. The mean depression, anxiety, and stress scores of the group scoring 20 points or higher were significantly (P<.01 for all) greater than in the group scoring less than 20 points (eTable 2).

Correlation Analysis of the Study Variables—The EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress (P<.01 for all)(eTable 3).

Comment

Eating disorders are psychiatric conditions that require a multidisciplinary approach. Nonpsychiatric medical departments may be involved due to the severe consequences (eg, various skin changes¹⁴) of these disorders. Psoriasis is not known to be directly affected by the presence of an ED; however, it is possible that EDs could indirectly affect patients with psoriasis by influencing obesity. Therefore, this study aimed to examine the relationship between ED risk factors and obesity in this population.

The relationship between psoriasis and obesity has been a popular research topic in dermatology since the 1990s.¹⁵ Epidemiologic and observational studies have reported that patients with psoriasis are more likely to be overweight or have obesity, which is an independent risk factor for psoriasis.^3,16 However, the causal relationship between psoriasis and obesity remains unclear. In a comprehensive review, Barros et al¹⁷ emphasized the causal relationship between obesity and psoriasis under several headings. Firstly, a higher BMI increases the risk for psoriasis by promoting cytokine release and immune system dysregulation. Secondly, a Western diet (eg, processed foods and fast food) triggers obesity and psoriasis by increasing adipose tissue. Thirdly, the alteration of the skin and gut microbiota triggers chronic inflammation as a result of bacterial translocation in patients with obesity. Fourthly, a high-fat diet and palmitic acid disrupt the intestinal integrity of the gut and increase the risk for psoriasis and obesity by triggering chronic inflammation of bacterial fragments that pass into the blood. Finally, the decrease in the amount of adiponectin and the increase in the amount of leptin in patients with obesity may cause psoriasis by increasing proinflammatory cytokines, which are similar to those involved in the pathogenesis of psoriasis.¹⁷ Additionally, psoriatic inflammation can cause insulin resistance and metabolic dysfunction, leading to obesity.¹⁸ The relationship between psoriasis and obesity cannot be solely explained by metabolic pathways. Smoking, alcohol consumption, and a sedentary lifestyle all are associated with psoriasis and also can contribute to obesity.⁵ Our study revealed no significant difference in smoking or alcohol consumption between the normal weight and overweight/obesity groups. Based on our data, we determined that smoking and alcohol consumption did not affect obesity in our patients with psoriasis.

Observational and epidemiologic studies have shown that patients with psoriasis experience increased rates of depression, anxiety, and stress.¹⁹ In studies of pathogenesis, a connection between depression and psoriatic inflammation has been established.²⁰ It is known that inflammatory cytokines similar to those in psoriasis are involved in the development of obesity.¹⁸ In addition, depression and anxiety can lead to binge eating, unhealthy food choices, and a more sedentary lifestyle.⁵ All of these variables may contribute to the associations between depression and anxiety with psoriasis and obesity. Zafiriou et al²¹ conducted a study to investigate the relationship between psoriasis, obesity, and depression through inflammatory pathways with a focus on the importance of IL-17. Data showing that IL-17–producing Th17-cell subgroups play a considerable role in the development of obesity and depression prompted the authors to suggest that psoriasis, obesity, and ­anxiety/depression may be interconnected manifestations of immune dysregulation, potentially linked to IL-17 and its associated cells.²¹ Mrowietz et al²² also suggested that metabolic inflammation may contribute to obesity and depression in patients with psoriasis and highlighted the importance of several cytokines, including tumor necrosis factor α, IL-6, IL-8, IL-17, and IL-23. Our study revealed no significant differences in depression scores between BMI groups. Another meta-analysis reported conflicting findings on the incidence of depression in obese patients with psoriasis.²³ Some of the studies had a small number of participants. Compared to depression, anxiety has received less attention in studies of patients with obesity with psoriasis. However, these studies have shown a positive correlation between anxiety scores and BMI in patients with psoriasis.^24,25 In our study, similar to the findings of previous studies, overweight patients and those with obesitywho have psoriasis had significantly (P<.01) greater anxiety and stress scores than did normal weight patients with psoriasis.

Obesity should be assessed in patients with psoriasis via a biopsychosocial approach that takes into account genetic, behavioral, and environmental factors.²⁶ Eating disorders are considered to be one of the factors contributing to obesity. Numerous studies in the literature have demonstrated a greater incidence of EDs in patients with obesity vs those without obesity.^5,6,27 Obesity and EDs have a bidirectional relationship: individuals with obesity are at risk for EDs due to body dissatisfaction, dieting habits, and depressive states. Conversely, poor eating behaviors in individuals with a normal weight can lead to obesity.²⁸

There are few studies in the literature exploring the relationship between psoriasis and EDs. Crosta et al²⁹ demonstrated that patients with psoriasis had impaired results on ED screening tests and that these scores deteriorated further as BMI increased. Moreover, Altunay et al³⁰ demonstrated that patients with psoriasis and metabolic syndrome had higher scores on the ED screening test. In this study, patients with higher scores also exhibited high levels of anxiety.³⁰ In our study, similar to the findings of previous studies, patients with psoriasis who were overweight or had obesity had significantly (P<.01) greater EAT-26 scores than those in the normal weight group. Patients with high EAT-26 scores also exhibited elevated levels of depression, anxiety, and stress. Additionally, EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress scores. Our study as well as other studies in the literature indicate that additional research is needed to determine the associations between EDs and obesity in psoriasis.

Conclusion

Managing obesity is crucial for patients with psoriasis. This study showed that EAT-26 scores were higher in patients with psoriasis who were overweight or had obesity than in those who were normal weight. Participants with high EAT-26 scores (≥20 points) were more likely to be female and have higher anxiety and stress scores. In addition, EAT-26 scores were positively correlated with BMI as well as depression, anxiety, and stress scores. Eating disorders may contribute to the development of obesity in patients with psoriasis. Although our study was limited by a small sample size, the results suggest that there is a need for large-scale multicenter studies to investigate the relationship between psoriasis and EDs.

References

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21. Zafiriou E, Daponte AI, Siokas V, et al. Depression and obesity in patients with psoriasis and psoriatic arthritis: is IL-17–mediated immune dysregulation the connecting link? Front Immunol. 2021;12:699848.

22. Mrowietz U, Sümbül M, Gerdes S. Depression, a major comorbidity of psoriatic disease, is caused by metabolic inflammation. J Eur Acad Dermatol Venereol. 2023;37:1731-1738.

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25. Tabolli S, Naldi L, Pagliarello C, et al. Evaluation of the impact of writing exercises interventions on quality of life in patients with psoriasis undergoing systemic treatments. Br J Dermatol. 2012;167:1254‐1264.

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28. Jebeile H, Lister NB, Baur LA, et al. Eating disorder risk in adolescents with obesity. Obes Rev. 2021;22:E13173.

29. Crosta ML, Caldarola G, Fraietta S, et al. Psychopathology and eating disorders in patients with psoriasis. G Ital Dermatol Venereol. 2014;149:355-361.

30. Altunay I, Demirci GT, Ates B, et al. Do eating disorders accompany metabolic syndrome in psoriasis patients? results of a preliminary study. Clin Cosmet Investig Dermatol. 2011;4:139-143.

Current evidence indicates that obesity may initiate psoriasis or worsen existing disease. Various factors contribute to the development of obesity, including eating disorders (EDs). The aim of this study was to screen for and identify factors associated with EDs in patients with psoriasis and their impact on the development of obesity in this population. Demographic information including body mass index (BMI), Eating Attitude Test (EAT-26), Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale 21 (DASS-21) scores were statistically analyzed for 82 participants with psoriasis at a tertiary dermatology clinic. It is important to manage obesity and other comorbidities of psoriasis in addition to treating its cutaneous manifestations, which may require a biopsychosocial approach.

Psoriasis is a chronic multisystemic inflammatory skin disease with a worldwide prevalence of 2% to 3%.¹ Psoriasis can be accompanied by other conditions such as psoriatic arthritis, obesity, metabolic syndrome, diabetes mellitus, hypertension, dyslipidemia, atherosclerotic disease, inflammatory bowel disease, and anxiety/depression. It is important to manage comorbidities of psoriasis in addition to treating the cutaneous manifestations of the disease.¹

Obesity is a major public health concern worldwide. Numerous observational and epidemiologic studies have reported a high prevalence of obesity among patients with psoriasis.² Current evidence indicates that obesity may initiate or worsen psoriasis; furthermore, it is important to note that obesity may negatively impact the effectiveness of psoriasis-specific treatments or increase the incidence of adverse effects. Therefore, managing obesity is crucial in the treatment of psoriasis.³ Numerous studies have investigated the association between psoriasis and obesity, and they commonly conclude that both conditions share the same genetic metabolic pathways.^2-4 However, it is important to consider environmental factors such as dietary habits, smoking, alcohol consumption, and a sedentary lifestyle—all of which are associated with psoriasis and also can contribute to the development of obesity.⁵ Because of the effects of obesity in psoriasis patients, factors that impact the development of obesity have become a popular research topic.

Eating disorders (EDs) are a crucial risk factor for both developing and maintaining obesity. In particular, two EDs that are associated with obesity include binge eating disorder and bulimia nervosa.⁶ According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,⁷ binge eating disorder can be diagnosed when a patient has at least 1 episode of binge eating per week over a 3-month period. Bulimia nervosa can be diagnosed when a patient is excessively concerned with their body weight and shape and engages in behaviors to prevent weight gain (eg, forced vomiting, excessive use of laxatives).⁷ Psychiatrists who specialize in EDs make diagnoses based on these criteria. In daily practice, there are several quick and simple questionnaires available to screen for EDs that can be used by nonpsychiatrist physicians, including the commonly used 26-item Eating Attitudes Test (EAT-26).⁸ The EAT-26 has been used to screen for EDs in patients with inflammatory disorders.⁹

The aim of this study was to screen for EDs in patients with psoriasis to identify potential risk factors for development of obesity.

Materials and Methods

This study included patients with psoriasis who were screened for EDs at a tertiary dermatology clinic in Turkey between January 2021 and December 2023. This study was approved by the local ethics committee and was in accordance with the Declaration of Helsinki (decision number E-93471371-514.99-225000079).

Study Design and Patient Inclusion Criteria—This quantitative cross-sectional study utilized EAT-26, Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale-21 (DASS-21) scores. All the questionnaire scales used in the study were adapted and validated in Turkey.^8,10-12 The inclusion criteria consisted of being older than 18 years of age, being literate, having psoriasis for at least 1 year that was not treated topically or systemically, and having no psychiatric diseases outside an ED. The questionnaires were presented in written format following the clinical examination. Literacy was an inclusion criterion in this study due to the absence of auxiliary health personnel.

Study Variables—The study variables included age, sex, marital status (single/divorced or married), education status (primary/secondary school or high school/university), employment status (employed or unemployed/retired), body mass index (BMI), smoking status, alcohol-consumption status, Psoriasis Area Severity Index score, presence of nail psoriasis and psoriatic arthritis, duration of psoriasis, family history of psoriasis, EAT-26 score, ASHN score, DLQI score, and DASS-21 score. Body mass index was calculated by taking a participant’s weight in kilograms and dividing it by their height in meters squared. The BMI values were classified into 3 categories: normal (18.5–24.9 kg/m²), overweight (25.0–29.9 kg/m²), and obese (≥30 kg/m²).¹³

Questionnaires—The EAT-26 questionnaire includes 26 questions that are used to detect EDs. Responses to each question include Likert-type answer options (ie, “always,” “usually,” “often,” “sometimes,” “rarely,” and “never.”) Patients with scores of 20 points or higher (range, 0–78) are classified as high risk for EDs.⁸ In our study, EAT-26 scores were grouped into 2 categories: patients scoring less than 20 points and those scoring 20 points or higher.

The DLQI questionnaire includes 10 questions to measure dermatologic symptoms and qualiy of life. Responses to each question include Likert-type answer options (ie, “not at all,” “a little,” “a lot,” or “very much.”) On the DLQI scale, the higher the score, the lower the quality of life (score range, 0–30).¹⁰

The ASHN questionnaire includes 21 questions that measure attitudes toward healthy nutrition with 5 possible answer options (“strongly disagree,” “disagree,” “undecided,” “agree,” and “strongly agree”). On this scale, higher scores indicate the participant is more knowledgeable about healthy nutrition (score range, 0–78).¹¹

The DASS-21 questionnaire includes 21 questions that measure the severity of a range of symptoms common to depression, anxiety, and stress. Responses include Likert-type answer options (eg, “never,” “sometimes,” “often,” and “almost always.”) On this scale, a higher score (range of 0–21 for each) indicates higher levels of depression, anxiety, and stress.¹²

Statistical Analysis—Descriptive statistics were analyzed using SPSS software version 22.0 (IBM). The Shapiro-Wilk test was applied to determine whether the data were normally distributed. For categorical variables, frequency differences among groups were compared using the Pearson χ² test. A t test was used to compare the means of 2 independent groups with a normal distribution. One-way analysis of variance and Tukey Honest Significant Difference post hoc analysis were used to test whether there was a statistically significant difference among the normally distributed means of independent groups. Pearson correlation analysis was used to determine whether there was a linear relationship between 2 numeric measurements and, if so, to determine the direction and severity of this relationship. P<.05 indicated statistical significance in this study.

Results

Study Participant Demographics—This study included 82 participants with a mean age of 44.3 years; 52.4% (43/82) were female, and 85.4% (70/82) were married. The questionnaire took an average of 4.2 minutes for participants to complete. A total of 57.3% (47/82) of patients had completed primary/secondary education and 59.8% (49/82) were employed. The mean BMI was 28.1 kg/m². According to the BMI classification, 26.8% (22/82) participants had a normal weight, 36.6% (30/82) were overweight, and 43.9% (36/82) were obese. A total of 48.8% (40/82) of participants smoked, and 4.9% (4/82) consumed alcohol. The mean Psoriasis Area and Severity Index score was 5.4. A total of 54.9% (45/82) of participants had nail psoriasis, and 24.4% (20/82) had psoriatic arthritis. The mean duration of psoriasis was 153 months. A total of 29.3% (24/82) of participants had a positive family history of psoriasis. The mean EAT-26 score was 11.1. A total of 12.2% (10/82) of participants had an EAT-26 score of 20 points or higher and were considered at high risk for an ED. The mean ASHN score was 72.9; the mean DLQI score was 5.5; and on the DASS-21 scale, mean scores for depression, anxiety, and stress were 6.3, 8.7, and 10.0, respectively (Table).

Comparative Evaluation of the BMI Groups—The only statistically significant differences among the 3 BMI groups were related to marital status, EAT-26 score, and anxiety and stress scores (P=.02, <.01, <.01, and <.01, respectively)(eTable 1). The number of single/divorced participants in the overweight group was significantly (P=.02) greater than in the normal weight group. The mean EAT-26 score for the normal weight group was significantly (P<.01) lower than for the overweight and obese groups; there was no significant difference in mean EAT-26 scores between the overweight and obese groups. The mean anxiety score was significantly (P<.01) lower in the normal weight group compared with the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean depression score. The mean stress and anxiety scores were significantly (P<.01) lower in the normal weight group than in the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean anxiety score.

Comparative Evaluation of the EAT-26 Scores—There were statistically significant differences among the EAT-26 scores related to sex; BMI; and depression, anxiety, and stress scores (P=.04, .02, <.01, <.01, and <.01, respectively). The number of females in the group with a score of 20 points or higher was significantly (P=.04) less than that in the group scoring less than 20 points. The mean BMI in the group with a score of 20 points or higher was significantly (P=.02) greater than in group scoring less than 20 points. The mean depression, anxiety, and stress scores of the group scoring 20 points or higher were significantly (P<.01 for all) greater than in the group scoring less than 20 points (eTable 2).

Correlation Analysis of the Study Variables—The EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress (P<.01 for all)(eTable 3).

Comment

Eating disorders are psychiatric conditions that require a multidisciplinary approach. Nonpsychiatric medical departments may be involved due to the severe consequences (eg, various skin changes¹⁴) of these disorders. Psoriasis is not known to be directly affected by the presence of an ED; however, it is possible that EDs could indirectly affect patients with psoriasis by influencing obesity. Therefore, this study aimed to examine the relationship between ED risk factors and obesity in this population.

The relationship between psoriasis and obesity has been a popular research topic in dermatology since the 1990s.¹⁵ Epidemiologic and observational studies have reported that patients with psoriasis are more likely to be overweight or have obesity, which is an independent risk factor for psoriasis.^3,16 However, the causal relationship between psoriasis and obesity remains unclear. In a comprehensive review, Barros et al¹⁷ emphasized the causal relationship between obesity and psoriasis under several headings. Firstly, a higher BMI increases the risk for psoriasis by promoting cytokine release and immune system dysregulation. Secondly, a Western diet (eg, processed foods and fast food) triggers obesity and psoriasis by increasing adipose tissue. Thirdly, the alteration of the skin and gut microbiota triggers chronic inflammation as a result of bacterial translocation in patients with obesity. Fourthly, a high-fat diet and palmitic acid disrupt the intestinal integrity of the gut and increase the risk for psoriasis and obesity by triggering chronic inflammation of bacterial fragments that pass into the blood. Finally, the decrease in the amount of adiponectin and the increase in the amount of leptin in patients with obesity may cause psoriasis by increasing proinflammatory cytokines, which are similar to those involved in the pathogenesis of psoriasis.¹⁷ Additionally, psoriatic inflammation can cause insulin resistance and metabolic dysfunction, leading to obesity.¹⁸ The relationship between psoriasis and obesity cannot be solely explained by metabolic pathways. Smoking, alcohol consumption, and a sedentary lifestyle all are associated with psoriasis and also can contribute to obesity.⁵ Our study revealed no significant difference in smoking or alcohol consumption between the normal weight and overweight/obesity groups. Based on our data, we determined that smoking and alcohol consumption did not affect obesity in our patients with psoriasis.

Observational and epidemiologic studies have shown that patients with psoriasis experience increased rates of depression, anxiety, and stress.¹⁹ In studies of pathogenesis, a connection between depression and psoriatic inflammation has been established.²⁰ It is known that inflammatory cytokines similar to those in psoriasis are involved in the development of obesity.¹⁸ In addition, depression and anxiety can lead to binge eating, unhealthy food choices, and a more sedentary lifestyle.⁵ All of these variables may contribute to the associations between depression and anxiety with psoriasis and obesity. Zafiriou et al²¹ conducted a study to investigate the relationship between psoriasis, obesity, and depression through inflammatory pathways with a focus on the importance of IL-17. Data showing that IL-17–producing Th17-cell subgroups play a considerable role in the development of obesity and depression prompted the authors to suggest that psoriasis, obesity, and ­anxiety/depression may be interconnected manifestations of immune dysregulation, potentially linked to IL-17 and its associated cells.²¹ Mrowietz et al²² also suggested that metabolic inflammation may contribute to obesity and depression in patients with psoriasis and highlighted the importance of several cytokines, including tumor necrosis factor α, IL-6, IL-8, IL-17, and IL-23. Our study revealed no significant differences in depression scores between BMI groups. Another meta-analysis reported conflicting findings on the incidence of depression in obese patients with psoriasis.²³ Some of the studies had a small number of participants. Compared to depression, anxiety has received less attention in studies of patients with obesity with psoriasis. However, these studies have shown a positive correlation between anxiety scores and BMI in patients with psoriasis.^24,25 In our study, similar to the findings of previous studies, overweight patients and those with obesitywho have psoriasis had significantly (P<.01) greater anxiety and stress scores than did normal weight patients with psoriasis.

Obesity should be assessed in patients with psoriasis via a biopsychosocial approach that takes into account genetic, behavioral, and environmental factors.²⁶ Eating disorders are considered to be one of the factors contributing to obesity. Numerous studies in the literature have demonstrated a greater incidence of EDs in patients with obesity vs those without obesity.^5,6,27 Obesity and EDs have a bidirectional relationship: individuals with obesity are at risk for EDs due to body dissatisfaction, dieting habits, and depressive states. Conversely, poor eating behaviors in individuals with a normal weight can lead to obesity.²⁸

There are few studies in the literature exploring the relationship between psoriasis and EDs. Crosta et al²⁹ demonstrated that patients with psoriasis had impaired results on ED screening tests and that these scores deteriorated further as BMI increased. Moreover, Altunay et al³⁰ demonstrated that patients with psoriasis and metabolic syndrome had higher scores on the ED screening test. In this study, patients with higher scores also exhibited high levels of anxiety.³⁰ In our study, similar to the findings of previous studies, patients with psoriasis who were overweight or had obesity had significantly (P<.01) greater EAT-26 scores than those in the normal weight group. Patients with high EAT-26 scores also exhibited elevated levels of depression, anxiety, and stress. Additionally, EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress scores. Our study as well as other studies in the literature indicate that additional research is needed to determine the associations between EDs and obesity in psoriasis.

Conclusion

Managing obesity is crucial for patients with psoriasis. This study showed that EAT-26 scores were higher in patients with psoriasis who were overweight or had obesity than in those who were normal weight. Participants with high EAT-26 scores (≥20 points) were more likely to be female and have higher anxiety and stress scores. In addition, EAT-26 scores were positively correlated with BMI as well as depression, anxiety, and stress scores. Eating disorders may contribute to the development of obesity in patients with psoriasis. Although our study was limited by a small sample size, the results suggest that there is a need for large-scale multicenter studies to investigate the relationship between psoriasis and EDs.

References

1. Kalkan G. Comorbidities in psoriasis: the recognition of psoriasis as a systemic disease and current management. Turkderm-Turk Arch Dermatol Venereol. 2017;51:71-77.

2. Armstrong AW, Harskamp CT, Armstrong EJ. The association between psoriasis and obesity: a systematic review and meta-analysis of observational studies. Nutr Diabetes. 2012;2:E54.

3. Jensen P, Skov L. Psoriasis and obesity. Dermatology. 2016;232:633-639.

4. Mirghani H, Altemani AT, Altemani ST, et al. The cross talk between psoriasis, obesity, and dyslipidemia: a meta-analysis. Cureus. 2023;15:e49253.

5. Roehring M, Mashep MR, White MA, et al. The metabolic syndrome and behavioral correlates in obese patients with binge disorders. Obesity. 2009;17:481-486.

6. da Luz FQ, Hay P, Touyz S, et al. Obesity with comorbid eating disorders: associated health risks and treatment approaches. Nutrients. 2018;10:829.

7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Association; 2013.

8. Ergüney Okumus¸ FE, Sertel Berk HÖ. The psychometric properties of the Eating Attitudes Test short form (EAT-26) in a college sample. Stud Psychol. 2020;40:57-78.

9. Stoleru G, Leopold A, Auerbach A, et al. Female gender, dissatisfaction with weight, and number of IBD related surgeries as independent risk factors for eating disorders among patients with inflammatory bowel diseases. BMC Gastroenterol. 2022;22:438.

10. Öztürkcan S, Ermertcan AT, Eser E, et al. Cross validation of the Turkish version of dermatology life quality index. Int J Dermatol. 2006;45:1300-1307.

11. Demir GT, Ciciog˘lu HI˙. Attitude scale for healthy nutrition (ASHN): validity and reliability study. Gaziantep Univ J Sport Sci. 2019;4:256-274.

12. Yılmaz O, Boz H, Arslan A. The validity and reliability of depression stress and anxiety scale (DASS 21) Turkish short form. Res Financial Econ Soc Stud. 2017;2:78-91.

13. Nuttall FQ. Body mass index: obesity, BMI, and health: a critical review. Nutr Today. 2015;50:117-128.

14. Strumia R, Manzata E, Gualandi M. Is there a role for dermatologists in eating disorders? Expert Rev Dermatol. 2017; 2:109-112.

15. Henseler T, Christophers E. Disease concomitance in psoriasis. J Am Acad Dermatol. 1995;32:982-986.

16. Naldi L, Addis A, Chimenti S, et al. Impact of body mass index and obesity on clinical response to systemic treatment for psoriasis. evidence from the Psocare project. Dermatology. 2008;217:365-373.

17. Barros G, Duran P, Vera I, et al. Exploring the links between obesity and psoriasis: a comprehensive review. Int J Mol Sci. 2022;23:7499.

18. Hao Y, Zhu YJ, Zou S, et al. Metabolic syndrome and psoriasis: mechanisms and future directions. Front Immunol. 2021;12:711060.

19. Jing D, Xiao H, Shen M, et al. Association of psoriasis with anxiety and depression: a case–control study in Chinese patients. Front Med (Lausanne). 2021;8:771645.

20. Sahi FM, Masood A, Danawar NA, et al. Association between psoriasis and depression: a traditional review. Cureus. 2020;12:E9708.

21. Zafiriou E, Daponte AI, Siokas V, et al. Depression and obesity in patients with psoriasis and psoriatic arthritis: is IL-17–mediated immune dysregulation the connecting link? Front Immunol. 2021;12:699848.

22. Mrowietz U, Sümbül M, Gerdes S. Depression, a major comorbidity of psoriatic disease, is caused by metabolic inflammation. J Eur Acad Dermatol Venereol. 2023;37:1731-1738.

23. Pavlova NT, Kioskli K, Smith C, et al. Psychosocial aspects of obesity in adults with psoriasis: a systematic review. Skin Health Dis. 2021;1:E33.

24. Innamorati M, Quinto RM, Imperatori C, et al. Health-related quality of life and its association with alexithymia and difficulties in emotion regulation in patients with psoriasis. Compr Psychiatry. 2016;70:200-208.

25. Tabolli S, Naldi L, Pagliarello C, et al. Evaluation of the impact of writing exercises interventions on quality of life in patients with psoriasis undergoing systemic treatments. Br J Dermatol. 2012;167:1254‐1264.

26. Albuquerque D, Nóbrega C, Manco L, et al. The contribution of genetics and environment to obesity. Br Med Bull. 2017;123:159‐173.

27. Balantekin KN, Grammer AC, Fitzsimmons-Craft EE, et al. Overweight and obesity are associated with increased eating disorder correlates and general psychopathology in university women with eating disorders. Eat Behav. 2021;41:101482.

28. Jebeile H, Lister NB, Baur LA, et al. Eating disorder risk in adolescents with obesity. Obes Rev. 2021;22:E13173.

29. Crosta ML, Caldarola G, Fraietta S, et al. Psychopathology and eating disorders in patients with psoriasis. G Ital Dermatol Venereol. 2014;149:355-361.

30. Altunay I, Demirci GT, Ates B, et al. Do eating disorders accompany metabolic syndrome in psoriasis patients? results of a preliminary study. Clin Cosmet Investig Dermatol. 2011;4:139-143.

Current evidence indicates that obesity may initiate psoriasis or worsen existing disease. Various factors contribute to the development of obesity, including eating disorders (EDs). The aim of this study was to screen for and identify factors associated with EDs in patients with psoriasis and their impact on the development of obesity in this population. Demographic information including body mass index (BMI), Eating Attitude Test (EAT-26), Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale 21 (DASS-21) scores were statistically analyzed for 82 participants with psoriasis at a tertiary dermatology clinic. It is important to manage obesity and other comorbidities of psoriasis in addition to treating its cutaneous manifestations, which may require a biopsychosocial approach.

Psoriasis is a chronic multisystemic inflammatory skin disease with a worldwide prevalence of 2% to 3%.¹ Psoriasis can be accompanied by other conditions such as psoriatic arthritis, obesity, metabolic syndrome, diabetes mellitus, hypertension, dyslipidemia, atherosclerotic disease, inflammatory bowel disease, and anxiety/depression. It is important to manage comorbidities of psoriasis in addition to treating the cutaneous manifestations of the disease.¹

Obesity is a major public health concern worldwide. Numerous observational and epidemiologic studies have reported a high prevalence of obesity among patients with psoriasis.² Current evidence indicates that obesity may initiate or worsen psoriasis; furthermore, it is important to note that obesity may negatively impact the effectiveness of psoriasis-specific treatments or increase the incidence of adverse effects. Therefore, managing obesity is crucial in the treatment of psoriasis.³ Numerous studies have investigated the association between psoriasis and obesity, and they commonly conclude that both conditions share the same genetic metabolic pathways.^2-4 However, it is important to consider environmental factors such as dietary habits, smoking, alcohol consumption, and a sedentary lifestyle—all of which are associated with psoriasis and also can contribute to the development of obesity.⁵ Because of the effects of obesity in psoriasis patients, factors that impact the development of obesity have become a popular research topic.

Eating disorders (EDs) are a crucial risk factor for both developing and maintaining obesity. In particular, two EDs that are associated with obesity include binge eating disorder and bulimia nervosa.⁶ According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,⁷ binge eating disorder can be diagnosed when a patient has at least 1 episode of binge eating per week over a 3-month period. Bulimia nervosa can be diagnosed when a patient is excessively concerned with their body weight and shape and engages in behaviors to prevent weight gain (eg, forced vomiting, excessive use of laxatives).⁷ Psychiatrists who specialize in EDs make diagnoses based on these criteria. In daily practice, there are several quick and simple questionnaires available to screen for EDs that can be used by nonpsychiatrist physicians, including the commonly used 26-item Eating Attitudes Test (EAT-26).⁸ The EAT-26 has been used to screen for EDs in patients with inflammatory disorders.⁹

The aim of this study was to screen for EDs in patients with psoriasis to identify potential risk factors for development of obesity.

Materials and Methods

This study included patients with psoriasis who were screened for EDs at a tertiary dermatology clinic in Turkey between January 2021 and December 2023. This study was approved by the local ethics committee and was in accordance with the Declaration of Helsinki (decision number E-93471371-514.99-225000079).

Study Design and Patient Inclusion Criteria—This quantitative cross-sectional study utilized EAT-26, Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale-21 (DASS-21) scores. All the questionnaire scales used in the study were adapted and validated in Turkey.^8,10-12 The inclusion criteria consisted of being older than 18 years of age, being literate, having psoriasis for at least 1 year that was not treated topically or systemically, and having no psychiatric diseases outside an ED. The questionnaires were presented in written format following the clinical examination. Literacy was an inclusion criterion in this study due to the absence of auxiliary health personnel.

Study Variables—The study variables included age, sex, marital status (single/divorced or married), education status (primary/secondary school or high school/university), employment status (employed or unemployed/retired), body mass index (BMI), smoking status, alcohol-consumption status, Psoriasis Area Severity Index score, presence of nail psoriasis and psoriatic arthritis, duration of psoriasis, family history of psoriasis, EAT-26 score, ASHN score, DLQI score, and DASS-21 score. Body mass index was calculated by taking a participant’s weight in kilograms and dividing it by their height in meters squared. The BMI values were classified into 3 categories: normal (18.5–24.9 kg/m²), overweight (25.0–29.9 kg/m²), and obese (≥30 kg/m²).¹³

Questionnaires—The EAT-26 questionnaire includes 26 questions that are used to detect EDs. Responses to each question include Likert-type answer options (ie, “always,” “usually,” “often,” “sometimes,” “rarely,” and “never.”) Patients with scores of 20 points or higher (range, 0–78) are classified as high risk for EDs.⁸ In our study, EAT-26 scores were grouped into 2 categories: patients scoring less than 20 points and those scoring 20 points or higher.

The DLQI questionnaire includes 10 questions to measure dermatologic symptoms and qualiy of life. Responses to each question include Likert-type answer options (ie, “not at all,” “a little,” “a lot,” or “very much.”) On the DLQI scale, the higher the score, the lower the quality of life (score range, 0–30).¹⁰

The ASHN questionnaire includes 21 questions that measure attitudes toward healthy nutrition with 5 possible answer options (“strongly disagree,” “disagree,” “undecided,” “agree,” and “strongly agree”). On this scale, higher scores indicate the participant is more knowledgeable about healthy nutrition (score range, 0–78).¹¹

The DASS-21 questionnaire includes 21 questions that measure the severity of a range of symptoms common to depression, anxiety, and stress. Responses include Likert-type answer options (eg, “never,” “sometimes,” “often,” and “almost always.”) On this scale, a higher score (range of 0–21 for each) indicates higher levels of depression, anxiety, and stress.¹²

Statistical Analysis—Descriptive statistics were analyzed using SPSS software version 22.0 (IBM). The Shapiro-Wilk test was applied to determine whether the data were normally distributed. For categorical variables, frequency differences among groups were compared using the Pearson χ² test. A t test was used to compare the means of 2 independent groups with a normal distribution. One-way analysis of variance and Tukey Honest Significant Difference post hoc analysis were used to test whether there was a statistically significant difference among the normally distributed means of independent groups. Pearson correlation analysis was used to determine whether there was a linear relationship between 2 numeric measurements and, if so, to determine the direction and severity of this relationship. P<.05 indicated statistical significance in this study.

Results

Study Participant Demographics—This study included 82 participants with a mean age of 44.3 years; 52.4% (43/82) were female, and 85.4% (70/82) were married. The questionnaire took an average of 4.2 minutes for participants to complete. A total of 57.3% (47/82) of patients had completed primary/secondary education and 59.8% (49/82) were employed. The mean BMI was 28.1 kg/m². According to the BMI classification, 26.8% (22/82) participants had a normal weight, 36.6% (30/82) were overweight, and 43.9% (36/82) were obese. A total of 48.8% (40/82) of participants smoked, and 4.9% (4/82) consumed alcohol. The mean Psoriasis Area and Severity Index score was 5.4. A total of 54.9% (45/82) of participants had nail psoriasis, and 24.4% (20/82) had psoriatic arthritis. The mean duration of psoriasis was 153 months. A total of 29.3% (24/82) of participants had a positive family history of psoriasis. The mean EAT-26 score was 11.1. A total of 12.2% (10/82) of participants had an EAT-26 score of 20 points or higher and were considered at high risk for an ED. The mean ASHN score was 72.9; the mean DLQI score was 5.5; and on the DASS-21 scale, mean scores for depression, anxiety, and stress were 6.3, 8.7, and 10.0, respectively (Table).

Comparative Evaluation of the BMI Groups—The only statistically significant differences among the 3 BMI groups were related to marital status, EAT-26 score, and anxiety and stress scores (P=.02, <.01, <.01, and <.01, respectively)(eTable 1). The number of single/divorced participants in the overweight group was significantly (P=.02) greater than in the normal weight group. The mean EAT-26 score for the normal weight group was significantly (P<.01) lower than for the overweight and obese groups; there was no significant difference in mean EAT-26 scores between the overweight and obese groups. The mean anxiety score was significantly (P<.01) lower in the normal weight group compared with the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean depression score. The mean stress and anxiety scores were significantly (P<.01) lower in the normal weight group than in the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean anxiety score.

Comparative Evaluation of the EAT-26 Scores—There were statistically significant differences among the EAT-26 scores related to sex; BMI; and depression, anxiety, and stress scores (P=.04, .02, <.01, <.01, and <.01, respectively). The number of females in the group with a score of 20 points or higher was significantly (P=.04) less than that in the group scoring less than 20 points. The mean BMI in the group with a score of 20 points or higher was significantly (P=.02) greater than in group scoring less than 20 points. The mean depression, anxiety, and stress scores of the group scoring 20 points or higher were significantly (P<.01 for all) greater than in the group scoring less than 20 points (eTable 2).

Correlation Analysis of the Study Variables—The EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress (P<.01 for all)(eTable 3).

Comment

Eating disorders are psychiatric conditions that require a multidisciplinary approach. Nonpsychiatric medical departments may be involved due to the severe consequences (eg, various skin changes¹⁴) of these disorders. Psoriasis is not known to be directly affected by the presence of an ED; however, it is possible that EDs could indirectly affect patients with psoriasis by influencing obesity. Therefore, this study aimed to examine the relationship between ED risk factors and obesity in this population.

The relationship between psoriasis and obesity has been a popular research topic in dermatology since the 1990s.¹⁵ Epidemiologic and observational studies have reported that patients with psoriasis are more likely to be overweight or have obesity, which is an independent risk factor for psoriasis.^3,16 However, the causal relationship between psoriasis and obesity remains unclear. In a comprehensive review, Barros et al¹⁷ emphasized the causal relationship between obesity and psoriasis under several headings. Firstly, a higher BMI increases the risk for psoriasis by promoting cytokine release and immune system dysregulation. Secondly, a Western diet (eg, processed foods and fast food) triggers obesity and psoriasis by increasing adipose tissue. Thirdly, the alteration of the skin and gut microbiota triggers chronic inflammation as a result of bacterial translocation in patients with obesity. Fourthly, a high-fat diet and palmitic acid disrupt the intestinal integrity of the gut and increase the risk for psoriasis and obesity by triggering chronic inflammation of bacterial fragments that pass into the blood. Finally, the decrease in the amount of adiponectin and the increase in the amount of leptin in patients with obesity may cause psoriasis by increasing proinflammatory cytokines, which are similar to those involved in the pathogenesis of psoriasis.¹⁷ Additionally, psoriatic inflammation can cause insulin resistance and metabolic dysfunction, leading to obesity.¹⁸ The relationship between psoriasis and obesity cannot be solely explained by metabolic pathways. Smoking, alcohol consumption, and a sedentary lifestyle all are associated with psoriasis and also can contribute to obesity.⁵ Our study revealed no significant difference in smoking or alcohol consumption between the normal weight and overweight/obesity groups. Based on our data, we determined that smoking and alcohol consumption did not affect obesity in our patients with psoriasis.

Observational and epidemiologic studies have shown that patients with psoriasis experience increased rates of depression, anxiety, and stress.¹⁹ In studies of pathogenesis, a connection between depression and psoriatic inflammation has been established.²⁰ It is known that inflammatory cytokines similar to those in psoriasis are involved in the development of obesity.¹⁸ In addition, depression and anxiety can lead to binge eating, unhealthy food choices, and a more sedentary lifestyle.⁵ All of these variables may contribute to the associations between depression and anxiety with psoriasis and obesity. Zafiriou et al²¹ conducted a study to investigate the relationship between psoriasis, obesity, and depression through inflammatory pathways with a focus on the importance of IL-17. Data showing that IL-17–producing Th17-cell subgroups play a considerable role in the development of obesity and depression prompted the authors to suggest that psoriasis, obesity, and ­anxiety/depression may be interconnected manifestations of immune dysregulation, potentially linked to IL-17 and its associated cells.²¹ Mrowietz et al²² also suggested that metabolic inflammation may contribute to obesity and depression in patients with psoriasis and highlighted the importance of several cytokines, including tumor necrosis factor α, IL-6, IL-8, IL-17, and IL-23. Our study revealed no significant differences in depression scores between BMI groups. Another meta-analysis reported conflicting findings on the incidence of depression in obese patients with psoriasis.²³ Some of the studies had a small number of participants. Compared to depression, anxiety has received less attention in studies of patients with obesity with psoriasis. However, these studies have shown a positive correlation between anxiety scores and BMI in patients with psoriasis.^24,25 In our study, similar to the findings of previous studies, overweight patients and those with obesitywho have psoriasis had significantly (P<.01) greater anxiety and stress scores than did normal weight patients with psoriasis.

Obesity should be assessed in patients with psoriasis via a biopsychosocial approach that takes into account genetic, behavioral, and environmental factors.²⁶ Eating disorders are considered to be one of the factors contributing to obesity. Numerous studies in the literature have demonstrated a greater incidence of EDs in patients with obesity vs those without obesity.^5,6,27 Obesity and EDs have a bidirectional relationship: individuals with obesity are at risk for EDs due to body dissatisfaction, dieting habits, and depressive states. Conversely, poor eating behaviors in individuals with a normal weight can lead to obesity.²⁸

There are few studies in the literature exploring the relationship between psoriasis and EDs. Crosta et al²⁹ demonstrated that patients with psoriasis had impaired results on ED screening tests and that these scores deteriorated further as BMI increased. Moreover, Altunay et al³⁰ demonstrated that patients with psoriasis and metabolic syndrome had higher scores on the ED screening test. In this study, patients with higher scores also exhibited high levels of anxiety.³⁰ In our study, similar to the findings of previous studies, patients with psoriasis who were overweight or had obesity had significantly (P<.01) greater EAT-26 scores than those in the normal weight group. Patients with high EAT-26 scores also exhibited elevated levels of depression, anxiety, and stress. Additionally, EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress scores. Our study as well as other studies in the literature indicate that additional research is needed to determine the associations between EDs and obesity in psoriasis.

Conclusion

Managing obesity is crucial for patients with psoriasis. This study showed that EAT-26 scores were higher in patients with psoriasis who were overweight or had obesity than in those who were normal weight. Participants with high EAT-26 scores (≥20 points) were more likely to be female and have higher anxiety and stress scores. In addition, EAT-26 scores were positively correlated with BMI as well as depression, anxiety, and stress scores. Eating disorders may contribute to the development of obesity in patients with psoriasis. Although our study was limited by a small sample size, the results suggest that there is a need for large-scale multicenter studies to investigate the relationship between psoriasis and EDs.

References

1. Kalkan G. Comorbidities in psoriasis: the recognition of psoriasis as a systemic disease and current management. Turkderm-Turk Arch Dermatol Venereol. 2017;51:71-77.

2. Armstrong AW, Harskamp CT, Armstrong EJ. The association between psoriasis and obesity: a systematic review and meta-analysis of observational studies. Nutr Diabetes. 2012;2:E54.

3. Jensen P, Skov L. Psoriasis and obesity. Dermatology. 2016;232:633-639.

4. Mirghani H, Altemani AT, Altemani ST, et al. The cross talk between psoriasis, obesity, and dyslipidemia: a meta-analysis. Cureus. 2023;15:e49253.

5. Roehring M, Mashep MR, White MA, et al. The metabolic syndrome and behavioral correlates in obese patients with binge disorders. Obesity. 2009;17:481-486.

6. da Luz FQ, Hay P, Touyz S, et al. Obesity with comorbid eating disorders: associated health risks and treatment approaches. Nutrients. 2018;10:829.

7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Association; 2013.

8. Ergüney Okumus¸ FE, Sertel Berk HÖ. The psychometric properties of the Eating Attitudes Test short form (EAT-26) in a college sample. Stud Psychol. 2020;40:57-78.

9. Stoleru G, Leopold A, Auerbach A, et al. Female gender, dissatisfaction with weight, and number of IBD related surgeries as independent risk factors for eating disorders among patients with inflammatory bowel diseases. BMC Gastroenterol. 2022;22:438.

10. Öztürkcan S, Ermertcan AT, Eser E, et al. Cross validation of the Turkish version of dermatology life quality index. Int J Dermatol. 2006;45:1300-1307.

11. Demir GT, Ciciog˘lu HI˙. Attitude scale for healthy nutrition (ASHN): validity and reliability study. Gaziantep Univ J Sport Sci. 2019;4:256-274.

12. Yılmaz O, Boz H, Arslan A. The validity and reliability of depression stress and anxiety scale (DASS 21) Turkish short form. Res Financial Econ Soc Stud. 2017;2:78-91.

13. Nuttall FQ. Body mass index: obesity, BMI, and health: a critical review. Nutr Today. 2015;50:117-128.

14. Strumia R, Manzata E, Gualandi M. Is there a role for dermatologists in eating disorders? Expert Rev Dermatol. 2017; 2:109-112.

15. Henseler T, Christophers E. Disease concomitance in psoriasis. J Am Acad Dermatol. 1995;32:982-986.

16. Naldi L, Addis A, Chimenti S, et al. Impact of body mass index and obesity on clinical response to systemic treatment for psoriasis. evidence from the Psocare project. Dermatology. 2008;217:365-373.

17. Barros G, Duran P, Vera I, et al. Exploring the links between obesity and psoriasis: a comprehensive review. Int J Mol Sci. 2022;23:7499.

18. Hao Y, Zhu YJ, Zou S, et al. Metabolic syndrome and psoriasis: mechanisms and future directions. Front Immunol. 2021;12:711060.

19. Jing D, Xiao H, Shen M, et al. Association of psoriasis with anxiety and depression: a case–control study in Chinese patients. Front Med (Lausanne). 2021;8:771645.

20. Sahi FM, Masood A, Danawar NA, et al. Association between psoriasis and depression: a traditional review. Cureus. 2020;12:E9708.

21. Zafiriou E, Daponte AI, Siokas V, et al. Depression and obesity in patients with psoriasis and psoriatic arthritis: is IL-17–mediated immune dysregulation the connecting link? Front Immunol. 2021;12:699848.

22. Mrowietz U, Sümbül M, Gerdes S. Depression, a major comorbidity of psoriatic disease, is caused by metabolic inflammation. J Eur Acad Dermatol Venereol. 2023;37:1731-1738.

23. Pavlova NT, Kioskli K, Smith C, et al. Psychosocial aspects of obesity in adults with psoriasis: a systematic review. Skin Health Dis. 2021;1:E33.

24. Innamorati M, Quinto RM, Imperatori C, et al. Health-related quality of life and its association with alexithymia and difficulties in emotion regulation in patients with psoriasis. Compr Psychiatry. 2016;70:200-208.

25. Tabolli S, Naldi L, Pagliarello C, et al. Evaluation of the impact of writing exercises interventions on quality of life in patients with psoriasis undergoing systemic treatments. Br J Dermatol. 2012;167:1254‐1264.

26. Albuquerque D, Nóbrega C, Manco L, et al. The contribution of genetics and environment to obesity. Br Med Bull. 2017;123:159‐173.

27. Balantekin KN, Grammer AC, Fitzsimmons-Craft EE, et al. Overweight and obesity are associated with increased eating disorder correlates and general psychopathology in university women with eating disorders. Eat Behav. 2021;41:101482.

28. Jebeile H, Lister NB, Baur LA, et al. Eating disorder risk in adolescents with obesity. Obes Rev. 2021;22:E13173.

29. Crosta ML, Caldarola G, Fraietta S, et al. Psychopathology and eating disorders in patients with psoriasis. G Ital Dermatol Venereol. 2014;149:355-361.

30. Altunay I, Demirci GT, Ates B, et al. Do eating disorders accompany metabolic syndrome in psoriasis patients? results of a preliminary study. Clin Cosmet Investig Dermatol. 2011;4:139-143.

The Latine/Hispanic population in the United States comprises one of the largest and youngest skin of color communities.^1,2 In 2020, this group accounted for 19% of all Americans—a percentage expected to increase to more than 25% by 2060.³

It must be emphasized that the Latine/Hispanic community in the United States is incredibly diverse.⁴ Approximately one-third of individuals in this group are foreign-born, and this community is made up of people from all racialized groups, religions, languages, and cultural identities.² The heterogeneity of the Latine/Hispanic population translates into a wide representation of skin tones, reflecting a rich range of ancestries, ethnicities, and cultures. The percentage of individuals from each origin group may differ according to where they live in the United States; for instance, individuals who identify as Mexican comprise more than 80% of the Latine/Hispanic population in both Texas and California but only 17% in Florida, where more than half of Latine/Hispanic people identify as Cuban or Puerto Rican.^4,5 As a result, when it comes to skin cancer epidemiology, variations in incidence and mortality may exist within each of these subgroups who identify as part of the Latine/Hispanic community, as reported for other cancers.^6,7 Further research is needed to investigate these potential differences.Unfortunately, considerable health disparities persist among this rapidly growing population, including increased morbidity and mortality from melanoma and keratinocyte carcinomas (KCs) despite overall low lifetime incidence.^8,9 In this review, the epidemiology, clinical manifestation, and ethnic disparities for skin cancer among the US Latine/Hispanic population are summarized; other factors impacting overall health and health care, including sociocultural factors, also are briefly discussed.

Terminology

Before a meaningful dialogue can be had about skin cancer in the Latine/Hispanic population, it is important to contextualize the terms used to identify this patient population, including Latino/Latine and Hispanic. In the early 1970s, the United States adopted the term Hispanic as a way of conglomerating Spanish-speaking individuals from Spain, the Caribbean, and Central and South America. The goal was to implement a common identifier that enabled the US government to study the economic and social development of these groups.¹⁰ Nevertheless, considerable differences (eg, variations in skin pigmentation, sun sensitivity) exist among Hispanic communities, with some having stronger European, African, or Amerindian influences due to colonization of their ­distinct countries.¹¹

In contrast, Latino is a geographic term and refers to people with roots in Latin America and the Caribbean (Table 1).^12,13 For example, a person from Brazil may be considered Latino but not Hispanic as Brazilians speak Portuguese; alternatively, Spaniards (who are considered Hispanic) are not Latino because Spain is not a Latin American country. A person from Mexico would be considered both Latino and Hispanic.¹³

Melanoma

Melanoma, the deadliest form of skin cancer, is more likely to metastasize compared to other forms of skin cancer, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). For Latine/Hispanic individuals living in the United States, the lifetime risk for melanoma is 1 in 200 compared to 1 in 33 for NHW individuals.¹⁴ While the lifetime risk for melanoma is low for the Latine/Hispanic population, Hispanic individuals are diagnosed with melanoma at an earlier age (mean, 56 years), and the rate of new cases is marginally higher for women (4.9 per 100,000) compared to men (4.8 per 100,000).^15,16

Typical sites of melanoma manifestation in Latine/Hispanic individuals include the torso (most common site in Hispanic men), lower extremities (most common site in Hispanic women), and acral sites (palms, soles, and nails).^9,16,17 Anatomic location also can vary according to age for both men and women. For men, the incidence of melanoma on the trunk appears to decrease with age, while the incidence on the head and neck may increase. For women, the incidence of melanoma on the lower extremities and hip increases with age. Cutaneous melanoma may manifest as a lesion with asymmetry, irregular borders, variation in pigmentation, large diameter (>6 mm), and evolution over time. In patients with skin of color, melanoma easily can be missed, as it also typically mimics more benign skin conditions and may develop from an existing black- or dark brown–­pigmented macule.¹⁸ The most common histologic subtype reported among Latine/Hispanic individuals in the United States is superficial spreading melanoma (20%–23%) followed by nodular melanoma and acral lentiginous melanoma.^16,19 Until additional risk factors associated with melanoma susceptibility in Hispanic/Latine people are better elucidated, it may be appropriate to use an alternative acronym, such as CUBED (Table 2), in addition to the standard ABCDE system to help recognize potential melanoma on acral sites.¹⁸

Keratinocyte Carcinomas

Keratinocyte carcinomas, also known as nonmelanoma skin cancers, include BCC and SCC. In comparison to the high-quality data available for melanoma from cancer registries, there are less reliable incidence data for KCs, especially among individuals with skin of color.²⁵ As a result, KC epidemiology in the United States is drawn largely from case series (especially for individuals with skin of color) or claims data from small data sets often from geographically restricted regions within the United States.^25,26

Basal Cell Carcinoma—Basal cell carcinoma is the most common malignant skin cancer in Latine/Hispanic individuals. Among those with lighter skin tones, the lifetime risk for BCC is about 30%.^27,28 Men typically are affected at a higher rate than women, and the median age for diagnosis is 68 years.²⁹ The development of BCC primarily is linked to lifetime accumulated UV radiation exposure. Even though BCC has a low mortality rate, it can lead to substantial morbidity due to factors such as tumor location, size, and rate of invasion, resulting in cosmetic and functional issues. Given its low metastatic potential, treatment of BCC typically is aimed at local control.³⁰ Options for treatment include Mohs micrographic surgery (MMS), curettage and electrodessication, cryosurgery, photodynamic therapy, radiation therapy, and topical therapies. Systemic therapies are reserved for patients with locally advanced or metastatic disease.³⁰

Latine/Hispanic patients characteristically present with BCCs on sun-exposed areas of the skin such as the head and neck region. In most patients, BCC manifests as a translucent pearly nodule with superficial telangiectasias and/or a nonhealing ulcer with a central depression and rolled nontender borders. However, in patients with skin of color, 66% of BCCs manifest with pigmentation; in fact, pigmented BCC (a subtype of BCC) has been shown to have a higher prevalence among Hispanic individuals, with an incidence twice as frequent as in NHW individuals.³¹ In addition, there are reports of increased tendency among Latine/Hispanic individuals to develop multiple BCCs.^32,33

The relationship between UV exposure and KCs could explain the relatively higher incidence in populations with skin of color living in warmer climates, including Hispanic individuals.³⁴ Even so, the development of BCCs appears to correlate directly with the degree of pigmentation in the skin, as it is most common in individuals with lighter skin tones within the Hispanic population.^25,34,35 Other risk factors associated with BCC development include albinism, arsenic ingestion, chronic infections, immunosuppression, history of radiation treatment, and history of scars or ulcers due to physical/thermal trauma.^35-37

Squamous Cell Carcinoma—Squamous cell carcinoma is the second most common skin cancer among Latine/Hispanic patients. In contrast with NHW patients, evidence supporting the role of UV exposure as a primary risk factor for SCC in patients with skin of color remains limited.^25,38 Reports linking UV exposure and KCs in Hispanic and Black individuals predominantly include case series or population-based studies that do not consider levels of UV exposure.²⁵

More recently, genetic ancestry analyses of a large multiethnic cohort found an increased risk for cutaneous SCC among Latine/Hispanic individuals with European ancestry compared to those with Native American or African ancestry; however, these genetic ancestry associations were attenuated (although not eliminated) after considering skin pigmentation (using loci associated with skin pigmentation), history of sun exposure (using actinic keratoses as a covariate for chronic sun exposure), and sun-protected vs sun-exposed anatomic sites, supporting the role of other environmental or sociocultural factors in the development of SCC.³⁹ Similar to BCCs, immunosuppression, chronic scarring, skin irritation, and inflammatory disease also are documented risk factors.^9,32

Among NHW individuals with lighter skin tones, SCC characteristically manifests on sun-exposed areas of the skin such as the head and neck region. Typically, a lesion may appear as a scaly erythematous papule or plaque that may be verrucous in nature or a nonhealing bleeding ulcer. In patients with more deeply pigmented skin, SCC tends to develop in the perianal region and on the penis and lower legs; pigmented lesions also may be present (as commonly reported in BCCs).^9,32,36

Unfortunately, the lower incidence of KCs and lack of surveillance in populations with skin of color result in a low index of clinical suspicion, leading to delayed diagnoses and increased morbidity.⁴⁰ Keratinocyte carcinomas are more costly to treat and require more health care resources for Latine/Hispanic and Black patients compared to their NHW counterparts; for example, KCs are associated with more ambulatory visits, more prescription medications, and greater cost on a per-person, per-year basis in Latine/Hispanic and Black patients compared with NHW patients.⁴¹ Moreover, a recent multicenter retrospective study found Hispanic patients had 17% larger MMS defects following treatment for KCs compared to NHW patients after adjustment for age, sex, and insurance type.⁴²

Hispanic patients tend to present initially with SCCs in areas associated with advanced disease, such as the anogenital region, penis, and the lower extremities. Latine and Black men have the highest incidence of penile SCC, which is rare with high morbidity and mortality.^32,43,44 The higher incidence of penile SCC among Hispanic individuals living in southern states could correspond to circumcision or HPV infection rates,⁴⁴ ultimately impacting incidence.⁴⁵

Dermatofibrosarcoma Protuberans

Dermatofibrosarcoma protuberans (DFSP) is a rare locally aggressive cutaneous sarcoma. According to population studies, overall incidence of DFSP is around 4.1 to 4.2 per million in the United States. Population-based studies on DFSP are limited, but available data suggest that Black patients as well as women have the highest incidence.⁴⁶

Dermatofibrosarcoma protuberans is characterized by its capacity to invade surrounding tissues in a tentaclelike pattern.⁴⁷ This characteristic often leads to inadequate initial resection of the lesion as well as a high recurrence rate despite its low metastatic potential.⁴⁸ In early stages, DFSP typically manifests as an asymptomatic plaque with a slow growth rate. The color of the lesion ranges from reddish brown to flesh colored. The pigmented form of DFSP, known as Bednar tumor, is the most common among Black patients.⁴⁷ As the tumor grows, it tends to become firm and nodular. The most common location for DFSP is on the trunk or the upper and lower extremities.⁴⁷

Although current guidelines designate MMS as the first-line treatment for DFSP, the procedure may be inaccessible for certain populations.⁴⁹ Patients with skin of color are more likely to undergo wide local excision (WLE) than MMS; however, WLE is less effective, with a recurrence rate of 30% compared with 3% in those treated with MMS.⁵⁰ A retrospective cohort study of more than 2000 patients revealed that Hispanic and Black patients were less likely to undergo MMS. In addition, the authors noted that WLE recipients more commonly were deceased at the end of the study.⁵¹

Despite undergoing treatment for a primary DFSP, Hispanic patients also appear to be at increased risk for a second surgery.⁵² Additional studies are needed to elucidate the reasons behind higher recurrence rates in Latine/Hispanic patients compared to NHW individuals.

Factors Influencing Skin Cancer Outcomes

In recent years, racial and ethnic disparities in health care use, medical treatment, and quality of care among minoritized populations (including Latine/Hispanic groups) have been documented in the medical literature.^53,54 These systemic inequities, which are rooted in structural racism,⁵⁵ have contributed to poorer health outcomes, worse health status, and lower-quality care for minoritized patients living in the United States, including those impacted by dermatologic conditions.^8,43,55-57 Becoming familiar with the sociocultural factors influencing skin cancer outcomes in the Latine/Hispanic community (including the lack of or inadequate health insurance, medical mistrust, language, and other cultural elements) and the paucity of research in this domain could help eliminate existing health inequities in this population.

Health Insurance Coverage—Although the uninsured rates in the Latine population have decreased since the passage of the Affordable Care Act (from 30% in 2013 to a low of 19% in 2017),⁵⁸ inadequate health insurance coverage remains one of the largest barriers to health care access and a contributor to health disparities among the Latine community. Nearly 1 in 5 Latine individuals in the United States are uninsured compared to 8% of NHW individuals.⁵⁸ Even though Latine individuals are more likely than non-Latine individuals to be part of the workforce, Latine employees are less likely to receive employer-sponsored coverage (27% vs 53% for NHW individuals).⁵⁹

Not surprisingly, noncitizens are far less likely to be insured; this includes lawfully present immigrants (ie, permanent residents or green card holders, refugees, asylees, and others who are authorized to live in the United States temporarily or permanently) and undocumented immigrants (including individuals who entered the country without authorization and individuals who entered the country lawfully and stayed after their visa or status expired). The higher uninsured rate among noncitizens reflects not only limited access to employer-sponsored coverage but includes immigrant eligibility restrictions for federal programs such as Medicaid, the Children’s Health Insurance Program, and the Affordable Care Act Marketplace coverage.⁶⁰

With approximately 9 million Americans living in mixed-status families (and nearly 10% of babies born each year with at least one undocumented parent), restrictive federal or state health care policies may extend beyond their stated target and impact both Latine citizens and noncitizens.^61-65 For instance, Vargas et al⁶⁴ found that both Latine citizens and noncitizens who lived in states with a high number of immigration-related laws had decreased odds of reporting optimal health as compared to Latine respondents in states with fewer immigration-related laws.Other barriers to enrollment include fears and confusion about program qualification, even if eligible.⁵⁸

Medical Mistrust and Unfamiliarity—Mistrust of medical professionals has been shown to reduce patient adherence to treatment as prescribed by their medical provider and can negatively influence health outcomes.⁵³ For racial/ethnic minoritized groups (including Latine/Hispanic patients), medical mistrust may be rooted in patients’ experience of discrimination in the health care setting. In a recent cross-sectional study, results from a survey of California adults (including 704 non-Hispanic Black, 711 Hispanic, and 913 NHW adults) found links between levels of medical mistrust and perceived discrimination based on race/ethnicity and language as well as perceived discrimination due to income level and type or lack of insurance.⁵³ Interestingly, discrimination attributed to income level and insurance status remained after controlling for race/ethnicity and language. As expected, patients reliant on public insurance programs such as Medicare have been reported to have greater medical mistrust and suspicion compared with private insurance holders.⁶⁵ Together, these findings support the notion that individuals who have low socioeconomic status and lack insurance coverage—disproportionately historically marginalized populations—are more likely to perceive discrimination in health care settings, have greater medical mistrust, and experience poorer health outcomes.⁵³

It also is important for health care providers to consider that the US health care system is unfamiliar to many Latine/Hispanic individuals. Costs of medical services tend to be substantially higher in the United States, which can contribute to mistrust in the system.⁶⁶ In addition, unethical medical experimentations have negatively affected both Latine and especially non-Hispanic Black populations, with long-lasting perceptions of deception and exploitation.⁶⁷ These beliefs have undermined the trust that these populations have in clinicians and the health care system.^54,67

Language and Other Cultural Elements—The inability to effectively communicate with health care providers could contribute to disparities in access to and use of health care services among Latine/Hispanic individuals. In a Medical Expenditure Panel Survey analysis, half of Hispanic patients with limited comfort speaking English did not have a usual source of care, and almost 90% of those with a usual source of care had a provider who spoke Spanish or used interpreters—indicating that few Hispanic individuals with limited comfort speaking English selected a usual source of care without language assistance.^68,69 In other examples, language barriers ­contributed to disparities in cancer screening, and individuals with limited English proficiency were more likely to have difficulty understanding their physician due to language barriers.^68,70

Improving cultural misconceptions regarding skin conditions, especially skin cancer, is another important consideration in the Latine/Hispanic community. Many Latine/Hispanic individuals wrongly believe they cannot develop skin cancer due to their darker skin tones and lack of family history.²⁶ Moreover, multiple studies assessing melanoma knowledge and perception among participants with skin of color (including one with an equal number of Latine/Hispanic, Black/African American, and Asian individuals for a total of 120 participants) revealed that many were unaware of the risk for melanoma on acral sites.⁷¹ Participants expressed a need for more culturally relevant content from both clinicians and public materials (eg, images of acral melanoma in a person with skin of color).^71-73

Paucity of Research—There is limited research regarding skin cancer risks and methods of prevention for patients with skin of color, including the Latine/Hispanic population. Efforts to engage and include patients from these communities, as well as clinicians or investigators from similar backgrounds, in clinical studies are desperately needed. It also is important that clinical studies collect data beyond population descriptors to account for both clinical and genetic variations observed in the Latine/Hispanic population. 

Latine/Hispanic individuals are quite diverse with many variable factors that may influence skin cancer outcomes. Often, cancer surveillance data are available in aggregate only, which could mask this heterogeneity.⁷⁴ Rigorous studies that collect more granular data, including objective measures of skin pigmentation beyond self-reported Fitzpatrick skin type, culture/beliefs, lifestyle/behavior, geographic location, socioeconomic status, genetics, or epigenetics could help fully elucidate skin cancer risks and mitigate health disparities among individuals who identify as part of this population.

Final Thoughts

The Latine/Hispanic community—the largest ethnic minoritized group in the United States—is disproportionately affected by dermatologic health disparities. We hope this review helps to increase recognition of the clinical manifestations of skin cancer in Latine/Hispanic patients. Other factors that may impact skin cancer outcomes in this population include (but are not limited to) lack of or inadequate health insurance, medical mistrust, linguistic barriers and/or individual/cultural perspectives, along with limited research. Recognizing and addressing these (albeit complex) barriers that contribute to the inequitable access to health care in this population remains a critical step toward improving skin cancer outcomes.

The Latine/Hispanic population in the United States comprises one of the largest and youngest skin of color communities.^1,2 In 2020, this group accounted for 19% of all Americans—a percentage expected to increase to more than 25% by 2060.³

It must be emphasized that the Latine/Hispanic community in the United States is incredibly diverse.⁴ Approximately one-third of individuals in this group are foreign-born, and this community is made up of people from all racialized groups, religions, languages, and cultural identities.² The heterogeneity of the Latine/Hispanic population translates into a wide representation of skin tones, reflecting a rich range of ancestries, ethnicities, and cultures. The percentage of individuals from each origin group may differ according to where they live in the United States; for instance, individuals who identify as Mexican comprise more than 80% of the Latine/Hispanic population in both Texas and California but only 17% in Florida, where more than half of Latine/Hispanic people identify as Cuban or Puerto Rican.^4,5 As a result, when it comes to skin cancer epidemiology, variations in incidence and mortality may exist within each of these subgroups who identify as part of the Latine/Hispanic community, as reported for other cancers.^6,7 Further research is needed to investigate these potential differences.Unfortunately, considerable health disparities persist among this rapidly growing population, including increased morbidity and mortality from melanoma and keratinocyte carcinomas (KCs) despite overall low lifetime incidence.^8,9 In this review, the epidemiology, clinical manifestation, and ethnic disparities for skin cancer among the US Latine/Hispanic population are summarized; other factors impacting overall health and health care, including sociocultural factors, also are briefly discussed.

Terminology

Before a meaningful dialogue can be had about skin cancer in the Latine/Hispanic population, it is important to contextualize the terms used to identify this patient population, including Latino/Latine and Hispanic. In the early 1970s, the United States adopted the term Hispanic as a way of conglomerating Spanish-speaking individuals from Spain, the Caribbean, and Central and South America. The goal was to implement a common identifier that enabled the US government to study the economic and social development of these groups.¹⁰ Nevertheless, considerable differences (eg, variations in skin pigmentation, sun sensitivity) exist among Hispanic communities, with some having stronger European, African, or Amerindian influences due to colonization of their ­distinct countries.¹¹

In contrast, Latino is a geographic term and refers to people with roots in Latin America and the Caribbean (Table 1).^12,13 For example, a person from Brazil may be considered Latino but not Hispanic as Brazilians speak Portuguese; alternatively, Spaniards (who are considered Hispanic) are not Latino because Spain is not a Latin American country. A person from Mexico would be considered both Latino and Hispanic.¹³

Melanoma

Melanoma, the deadliest form of skin cancer, is more likely to metastasize compared to other forms of skin cancer, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). For Latine/Hispanic individuals living in the United States, the lifetime risk for melanoma is 1 in 200 compared to 1 in 33 for NHW individuals.¹⁴ While the lifetime risk for melanoma is low for the Latine/Hispanic population, Hispanic individuals are diagnosed with melanoma at an earlier age (mean, 56 years), and the rate of new cases is marginally higher for women (4.9 per 100,000) compared to men (4.8 per 100,000).^15,16

Typical sites of melanoma manifestation in Latine/Hispanic individuals include the torso (most common site in Hispanic men), lower extremities (most common site in Hispanic women), and acral sites (palms, soles, and nails).^9,16,17 Anatomic location also can vary according to age for both men and women. For men, the incidence of melanoma on the trunk appears to decrease with age, while the incidence on the head and neck may increase. For women, the incidence of melanoma on the lower extremities and hip increases with age. Cutaneous melanoma may manifest as a lesion with asymmetry, irregular borders, variation in pigmentation, large diameter (>6 mm), and evolution over time. In patients with skin of color, melanoma easily can be missed, as it also typically mimics more benign skin conditions and may develop from an existing black- or dark brown–­pigmented macule.¹⁸ The most common histologic subtype reported among Latine/Hispanic individuals in the United States is superficial spreading melanoma (20%–23%) followed by nodular melanoma and acral lentiginous melanoma.^16,19 Until additional risk factors associated with melanoma susceptibility in Hispanic/Latine people are better elucidated, it may be appropriate to use an alternative acronym, such as CUBED (Table 2), in addition to the standard ABCDE system to help recognize potential melanoma on acral sites.¹⁸

Keratinocyte Carcinomas

Keratinocyte carcinomas, also known as nonmelanoma skin cancers, include BCC and SCC. In comparison to the high-quality data available for melanoma from cancer registries, there are less reliable incidence data for KCs, especially among individuals with skin of color.²⁵ As a result, KC epidemiology in the United States is drawn largely from case series (especially for individuals with skin of color) or claims data from small data sets often from geographically restricted regions within the United States.^25,26

Basal Cell Carcinoma—Basal cell carcinoma is the most common malignant skin cancer in Latine/Hispanic individuals. Among those with lighter skin tones, the lifetime risk for BCC is about 30%.^27,28 Men typically are affected at a higher rate than women, and the median age for diagnosis is 68 years.²⁹ The development of BCC primarily is linked to lifetime accumulated UV radiation exposure. Even though BCC has a low mortality rate, it can lead to substantial morbidity due to factors such as tumor location, size, and rate of invasion, resulting in cosmetic and functional issues. Given its low metastatic potential, treatment of BCC typically is aimed at local control.³⁰ Options for treatment include Mohs micrographic surgery (MMS), curettage and electrodessication, cryosurgery, photodynamic therapy, radiation therapy, and topical therapies. Systemic therapies are reserved for patients with locally advanced or metastatic disease.³⁰

Latine/Hispanic patients characteristically present with BCCs on sun-exposed areas of the skin such as the head and neck region. In most patients, BCC manifests as a translucent pearly nodule with superficial telangiectasias and/or a nonhealing ulcer with a central depression and rolled nontender borders. However, in patients with skin of color, 66% of BCCs manifest with pigmentation; in fact, pigmented BCC (a subtype of BCC) has been shown to have a higher prevalence among Hispanic individuals, with an incidence twice as frequent as in NHW individuals.³¹ In addition, there are reports of increased tendency among Latine/Hispanic individuals to develop multiple BCCs.^32,33

The relationship between UV exposure and KCs could explain the relatively higher incidence in populations with skin of color living in warmer climates, including Hispanic individuals.³⁴ Even so, the development of BCCs appears to correlate directly with the degree of pigmentation in the skin, as it is most common in individuals with lighter skin tones within the Hispanic population.^25,34,35 Other risk factors associated with BCC development include albinism, arsenic ingestion, chronic infections, immunosuppression, history of radiation treatment, and history of scars or ulcers due to physical/thermal trauma.^35-37

Squamous Cell Carcinoma—Squamous cell carcinoma is the second most common skin cancer among Latine/Hispanic patients. In contrast with NHW patients, evidence supporting the role of UV exposure as a primary risk factor for SCC in patients with skin of color remains limited.^25,38 Reports linking UV exposure and KCs in Hispanic and Black individuals predominantly include case series or population-based studies that do not consider levels of UV exposure.²⁵

More recently, genetic ancestry analyses of a large multiethnic cohort found an increased risk for cutaneous SCC among Latine/Hispanic individuals with European ancestry compared to those with Native American or African ancestry; however, these genetic ancestry associations were attenuated (although not eliminated) after considering skin pigmentation (using loci associated with skin pigmentation), history of sun exposure (using actinic keratoses as a covariate for chronic sun exposure), and sun-protected vs sun-exposed anatomic sites, supporting the role of other environmental or sociocultural factors in the development of SCC.³⁹ Similar to BCCs, immunosuppression, chronic scarring, skin irritation, and inflammatory disease also are documented risk factors.^9,32

Among NHW individuals with lighter skin tones, SCC characteristically manifests on sun-exposed areas of the skin such as the head and neck region. Typically, a lesion may appear as a scaly erythematous papule or plaque that may be verrucous in nature or a nonhealing bleeding ulcer. In patients with more deeply pigmented skin, SCC tends to develop in the perianal region and on the penis and lower legs; pigmented lesions also may be present (as commonly reported in BCCs).^9,32,36

Unfortunately, the lower incidence of KCs and lack of surveillance in populations with skin of color result in a low index of clinical suspicion, leading to delayed diagnoses and increased morbidity.⁴⁰ Keratinocyte carcinomas are more costly to treat and require more health care resources for Latine/Hispanic and Black patients compared to their NHW counterparts; for example, KCs are associated with more ambulatory visits, more prescription medications, and greater cost on a per-person, per-year basis in Latine/Hispanic and Black patients compared with NHW patients.⁴¹ Moreover, a recent multicenter retrospective study found Hispanic patients had 17% larger MMS defects following treatment for KCs compared to NHW patients after adjustment for age, sex, and insurance type.⁴²

Hispanic patients tend to present initially with SCCs in areas associated with advanced disease, such as the anogenital region, penis, and the lower extremities. Latine and Black men have the highest incidence of penile SCC, which is rare with high morbidity and mortality.^32,43,44 The higher incidence of penile SCC among Hispanic individuals living in southern states could correspond to circumcision or HPV infection rates,⁴⁴ ultimately impacting incidence.⁴⁵

Dermatofibrosarcoma Protuberans

Dermatofibrosarcoma protuberans (DFSP) is a rare locally aggressive cutaneous sarcoma. According to population studies, overall incidence of DFSP is around 4.1 to 4.2 per million in the United States. Population-based studies on DFSP are limited, but available data suggest that Black patients as well as women have the highest incidence.⁴⁶

Dermatofibrosarcoma protuberans is characterized by its capacity to invade surrounding tissues in a tentaclelike pattern.⁴⁷ This characteristic often leads to inadequate initial resection of the lesion as well as a high recurrence rate despite its low metastatic potential.⁴⁸ In early stages, DFSP typically manifests as an asymptomatic plaque with a slow growth rate. The color of the lesion ranges from reddish brown to flesh colored. The pigmented form of DFSP, known as Bednar tumor, is the most common among Black patients.⁴⁷ As the tumor grows, it tends to become firm and nodular. The most common location for DFSP is on the trunk or the upper and lower extremities.⁴⁷

Although current guidelines designate MMS as the first-line treatment for DFSP, the procedure may be inaccessible for certain populations.⁴⁹ Patients with skin of color are more likely to undergo wide local excision (WLE) than MMS; however, WLE is less effective, with a recurrence rate of 30% compared with 3% in those treated with MMS.⁵⁰ A retrospective cohort study of more than 2000 patients revealed that Hispanic and Black patients were less likely to undergo MMS. In addition, the authors noted that WLE recipients more commonly were deceased at the end of the study.⁵¹

Despite undergoing treatment for a primary DFSP, Hispanic patients also appear to be at increased risk for a second surgery.⁵² Additional studies are needed to elucidate the reasons behind higher recurrence rates in Latine/Hispanic patients compared to NHW individuals.

Factors Influencing Skin Cancer Outcomes

In recent years, racial and ethnic disparities in health care use, medical treatment, and quality of care among minoritized populations (including Latine/Hispanic groups) have been documented in the medical literature.^53,54 These systemic inequities, which are rooted in structural racism,⁵⁵ have contributed to poorer health outcomes, worse health status, and lower-quality care for minoritized patients living in the United States, including those impacted by dermatologic conditions.^8,43,55-57 Becoming familiar with the sociocultural factors influencing skin cancer outcomes in the Latine/Hispanic community (including the lack of or inadequate health insurance, medical mistrust, language, and other cultural elements) and the paucity of research in this domain could help eliminate existing health inequities in this population.

Health Insurance Coverage—Although the uninsured rates in the Latine population have decreased since the passage of the Affordable Care Act (from 30% in 2013 to a low of 19% in 2017),⁵⁸ inadequate health insurance coverage remains one of the largest barriers to health care access and a contributor to health disparities among the Latine community. Nearly 1 in 5 Latine individuals in the United States are uninsured compared to 8% of NHW individuals.⁵⁸ Even though Latine individuals are more likely than non-Latine individuals to be part of the workforce, Latine employees are less likely to receive employer-sponsored coverage (27% vs 53% for NHW individuals).⁵⁹

Not surprisingly, noncitizens are far less likely to be insured; this includes lawfully present immigrants (ie, permanent residents or green card holders, refugees, asylees, and others who are authorized to live in the United States temporarily or permanently) and undocumented immigrants (including individuals who entered the country without authorization and individuals who entered the country lawfully and stayed after their visa or status expired). The higher uninsured rate among noncitizens reflects not only limited access to employer-sponsored coverage but includes immigrant eligibility restrictions for federal programs such as Medicaid, the Children’s Health Insurance Program, and the Affordable Care Act Marketplace coverage.⁶⁰

With approximately 9 million Americans living in mixed-status families (and nearly 10% of babies born each year with at least one undocumented parent), restrictive federal or state health care policies may extend beyond their stated target and impact both Latine citizens and noncitizens.^61-65 For instance, Vargas et al⁶⁴ found that both Latine citizens and noncitizens who lived in states with a high number of immigration-related laws had decreased odds of reporting optimal health as compared to Latine respondents in states with fewer immigration-related laws.Other barriers to enrollment include fears and confusion about program qualification, even if eligible.⁵⁸

Medical Mistrust and Unfamiliarity—Mistrust of medical professionals has been shown to reduce patient adherence to treatment as prescribed by their medical provider and can negatively influence health outcomes.⁵³ For racial/ethnic minoritized groups (including Latine/Hispanic patients), medical mistrust may be rooted in patients’ experience of discrimination in the health care setting. In a recent cross-sectional study, results from a survey of California adults (including 704 non-Hispanic Black, 711 Hispanic, and 913 NHW adults) found links between levels of medical mistrust and perceived discrimination based on race/ethnicity and language as well as perceived discrimination due to income level and type or lack of insurance.⁵³ Interestingly, discrimination attributed to income level and insurance status remained after controlling for race/ethnicity and language. As expected, patients reliant on public insurance programs such as Medicare have been reported to have greater medical mistrust and suspicion compared with private insurance holders.⁶⁵ Together, these findings support the notion that individuals who have low socioeconomic status and lack insurance coverage—disproportionately historically marginalized populations—are more likely to perceive discrimination in health care settings, have greater medical mistrust, and experience poorer health outcomes.⁵³

It also is important for health care providers to consider that the US health care system is unfamiliar to many Latine/Hispanic individuals. Costs of medical services tend to be substantially higher in the United States, which can contribute to mistrust in the system.⁶⁶ In addition, unethical medical experimentations have negatively affected both Latine and especially non-Hispanic Black populations, with long-lasting perceptions of deception and exploitation.⁶⁷ These beliefs have undermined the trust that these populations have in clinicians and the health care system.^54,67

Language and Other Cultural Elements—The inability to effectively communicate with health care providers could contribute to disparities in access to and use of health care services among Latine/Hispanic individuals. In a Medical Expenditure Panel Survey analysis, half of Hispanic patients with limited comfort speaking English did not have a usual source of care, and almost 90% of those with a usual source of care had a provider who spoke Spanish or used interpreters—indicating that few Hispanic individuals with limited comfort speaking English selected a usual source of care without language assistance.^68,69 In other examples, language barriers ­contributed to disparities in cancer screening, and individuals with limited English proficiency were more likely to have difficulty understanding their physician due to language barriers.^68,70

Improving cultural misconceptions regarding skin conditions, especially skin cancer, is another important consideration in the Latine/Hispanic community. Many Latine/Hispanic individuals wrongly believe they cannot develop skin cancer due to their darker skin tones and lack of family history.²⁶ Moreover, multiple studies assessing melanoma knowledge and perception among participants with skin of color (including one with an equal number of Latine/Hispanic, Black/African American, and Asian individuals for a total of 120 participants) revealed that many were unaware of the risk for melanoma on acral sites.⁷¹ Participants expressed a need for more culturally relevant content from both clinicians and public materials (eg, images of acral melanoma in a person with skin of color).^71-73

Paucity of Research—There is limited research regarding skin cancer risks and methods of prevention for patients with skin of color, including the Latine/Hispanic population. Efforts to engage and include patients from these communities, as well as clinicians or investigators from similar backgrounds, in clinical studies are desperately needed. It also is important that clinical studies collect data beyond population descriptors to account for both clinical and genetic variations observed in the Latine/Hispanic population. 

Latine/Hispanic individuals are quite diverse with many variable factors that may influence skin cancer outcomes. Often, cancer surveillance data are available in aggregate only, which could mask this heterogeneity.⁷⁴ Rigorous studies that collect more granular data, including objective measures of skin pigmentation beyond self-reported Fitzpatrick skin type, culture/beliefs, lifestyle/behavior, geographic location, socioeconomic status, genetics, or epigenetics could help fully elucidate skin cancer risks and mitigate health disparities among individuals who identify as part of this population.

Final Thoughts

The Latine/Hispanic community—the largest ethnic minoritized group in the United States—is disproportionately affected by dermatologic health disparities. We hope this review helps to increase recognition of the clinical manifestations of skin cancer in Latine/Hispanic patients. Other factors that may impact skin cancer outcomes in this population include (but are not limited to) lack of or inadequate health insurance, medical mistrust, linguistic barriers and/or individual/cultural perspectives, along with limited research. Recognizing and addressing these (albeit complex) barriers that contribute to the inequitable access to health care in this population remains a critical step toward improving skin cancer outcomes.

The Latine/Hispanic population in the United States comprises one of the largest and youngest skin of color communities.^1,2 In 2020, this group accounted for 19% of all Americans—a percentage expected to increase to more than 25% by 2060.³

It must be emphasized that the Latine/Hispanic community in the United States is incredibly diverse.⁴ Approximately one-third of individuals in this group are foreign-born, and this community is made up of people from all racialized groups, religions, languages, and cultural identities.² The heterogeneity of the Latine/Hispanic population translates into a wide representation of skin tones, reflecting a rich range of ancestries, ethnicities, and cultures. The percentage of individuals from each origin group may differ according to where they live in the United States; for instance, individuals who identify as Mexican comprise more than 80% of the Latine/Hispanic population in both Texas and California but only 17% in Florida, where more than half of Latine/Hispanic people identify as Cuban or Puerto Rican.^4,5 As a result, when it comes to skin cancer epidemiology, variations in incidence and mortality may exist within each of these subgroups who identify as part of the Latine/Hispanic community, as reported for other cancers.^6,7 Further research is needed to investigate these potential differences.Unfortunately, considerable health disparities persist among this rapidly growing population, including increased morbidity and mortality from melanoma and keratinocyte carcinomas (KCs) despite overall low lifetime incidence.^8,9 In this review, the epidemiology, clinical manifestation, and ethnic disparities for skin cancer among the US Latine/Hispanic population are summarized; other factors impacting overall health and health care, including sociocultural factors, also are briefly discussed.

Terminology

Before a meaningful dialogue can be had about skin cancer in the Latine/Hispanic population, it is important to contextualize the terms used to identify this patient population, including Latino/Latine and Hispanic. In the early 1970s, the United States adopted the term Hispanic as a way of conglomerating Spanish-speaking individuals from Spain, the Caribbean, and Central and South America. The goal was to implement a common identifier that enabled the US government to study the economic and social development of these groups.¹⁰ Nevertheless, considerable differences (eg, variations in skin pigmentation, sun sensitivity) exist among Hispanic communities, with some having stronger European, African, or Amerindian influences due to colonization of their ­distinct countries.¹¹

In contrast, Latino is a geographic term and refers to people with roots in Latin America and the Caribbean (Table 1).^12,13 For example, a person from Brazil may be considered Latino but not Hispanic as Brazilians speak Portuguese; alternatively, Spaniards (who are considered Hispanic) are not Latino because Spain is not a Latin American country. A person from Mexico would be considered both Latino and Hispanic.¹³

Melanoma

Melanoma, the deadliest form of skin cancer, is more likely to metastasize compared to other forms of skin cancer, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). For Latine/Hispanic individuals living in the United States, the lifetime risk for melanoma is 1 in 200 compared to 1 in 33 for NHW individuals.¹⁴ While the lifetime risk for melanoma is low for the Latine/Hispanic population, Hispanic individuals are diagnosed with melanoma at an earlier age (mean, 56 years), and the rate of new cases is marginally higher for women (4.9 per 100,000) compared to men (4.8 per 100,000).^15,16

Typical sites of melanoma manifestation in Latine/Hispanic individuals include the torso (most common site in Hispanic men), lower extremities (most common site in Hispanic women), and acral sites (palms, soles, and nails).^9,16,17 Anatomic location also can vary according to age for both men and women. For men, the incidence of melanoma on the trunk appears to decrease with age, while the incidence on the head and neck may increase. For women, the incidence of melanoma on the lower extremities and hip increases with age. Cutaneous melanoma may manifest as a lesion with asymmetry, irregular borders, variation in pigmentation, large diameter (>6 mm), and evolution over time. In patients with skin of color, melanoma easily can be missed, as it also typically mimics more benign skin conditions and may develop from an existing black- or dark brown–­pigmented macule.¹⁸ The most common histologic subtype reported among Latine/Hispanic individuals in the United States is superficial spreading melanoma (20%–23%) followed by nodular melanoma and acral lentiginous melanoma.^16,19 Until additional risk factors associated with melanoma susceptibility in Hispanic/Latine people are better elucidated, it may be appropriate to use an alternative acronym, such as CUBED (Table 2), in addition to the standard ABCDE system to help recognize potential melanoma on acral sites.¹⁸

Keratinocyte Carcinomas

Keratinocyte carcinomas, also known as nonmelanoma skin cancers, include BCC and SCC. In comparison to the high-quality data available for melanoma from cancer registries, there are less reliable incidence data for KCs, especially among individuals with skin of color.²⁵ As a result, KC epidemiology in the United States is drawn largely from case series (especially for individuals with skin of color) or claims data from small data sets often from geographically restricted regions within the United States.^25,26

Basal Cell Carcinoma—Basal cell carcinoma is the most common malignant skin cancer in Latine/Hispanic individuals. Among those with lighter skin tones, the lifetime risk for BCC is about 30%.^27,28 Men typically are affected at a higher rate than women, and the median age for diagnosis is 68 years.²⁹ The development of BCC primarily is linked to lifetime accumulated UV radiation exposure. Even though BCC has a low mortality rate, it can lead to substantial morbidity due to factors such as tumor location, size, and rate of invasion, resulting in cosmetic and functional issues. Given its low metastatic potential, treatment of BCC typically is aimed at local control.³⁰ Options for treatment include Mohs micrographic surgery (MMS), curettage and electrodessication, cryosurgery, photodynamic therapy, radiation therapy, and topical therapies. Systemic therapies are reserved for patients with locally advanced or metastatic disease.³⁰

Latine/Hispanic patients characteristically present with BCCs on sun-exposed areas of the skin such as the head and neck region. In most patients, BCC manifests as a translucent pearly nodule with superficial telangiectasias and/or a nonhealing ulcer with a central depression and rolled nontender borders. However, in patients with skin of color, 66% of BCCs manifest with pigmentation; in fact, pigmented BCC (a subtype of BCC) has been shown to have a higher prevalence among Hispanic individuals, with an incidence twice as frequent as in NHW individuals.³¹ In addition, there are reports of increased tendency among Latine/Hispanic individuals to develop multiple BCCs.^32,33

The relationship between UV exposure and KCs could explain the relatively higher incidence in populations with skin of color living in warmer climates, including Hispanic individuals.³⁴ Even so, the development of BCCs appears to correlate directly with the degree of pigmentation in the skin, as it is most common in individuals with lighter skin tones within the Hispanic population.^25,34,35 Other risk factors associated with BCC development include albinism, arsenic ingestion, chronic infections, immunosuppression, history of radiation treatment, and history of scars or ulcers due to physical/thermal trauma.^35-37

Squamous Cell Carcinoma—Squamous cell carcinoma is the second most common skin cancer among Latine/Hispanic patients. In contrast with NHW patients, evidence supporting the role of UV exposure as a primary risk factor for SCC in patients with skin of color remains limited.^25,38 Reports linking UV exposure and KCs in Hispanic and Black individuals predominantly include case series or population-based studies that do not consider levels of UV exposure.²⁵

More recently, genetic ancestry analyses of a large multiethnic cohort found an increased risk for cutaneous SCC among Latine/Hispanic individuals with European ancestry compared to those with Native American or African ancestry; however, these genetic ancestry associations were attenuated (although not eliminated) after considering skin pigmentation (using loci associated with skin pigmentation), history of sun exposure (using actinic keratoses as a covariate for chronic sun exposure), and sun-protected vs sun-exposed anatomic sites, supporting the role of other environmental or sociocultural factors in the development of SCC.³⁹ Similar to BCCs, immunosuppression, chronic scarring, skin irritation, and inflammatory disease also are documented risk factors.^9,32

Among NHW individuals with lighter skin tones, SCC characteristically manifests on sun-exposed areas of the skin such as the head and neck region. Typically, a lesion may appear as a scaly erythematous papule or plaque that may be verrucous in nature or a nonhealing bleeding ulcer. In patients with more deeply pigmented skin, SCC tends to develop in the perianal region and on the penis and lower legs; pigmented lesions also may be present (as commonly reported in BCCs).^9,32,36

Unfortunately, the lower incidence of KCs and lack of surveillance in populations with skin of color result in a low index of clinical suspicion, leading to delayed diagnoses and increased morbidity.⁴⁰ Keratinocyte carcinomas are more costly to treat and require more health care resources for Latine/Hispanic and Black patients compared to their NHW counterparts; for example, KCs are associated with more ambulatory visits, more prescription medications, and greater cost on a per-person, per-year basis in Latine/Hispanic and Black patients compared with NHW patients.⁴¹ Moreover, a recent multicenter retrospective study found Hispanic patients had 17% larger MMS defects following treatment for KCs compared to NHW patients after adjustment for age, sex, and insurance type.⁴²

Hispanic patients tend to present initially with SCCs in areas associated with advanced disease, such as the anogenital region, penis, and the lower extremities. Latine and Black men have the highest incidence of penile SCC, which is rare with high morbidity and mortality.^32,43,44 The higher incidence of penile SCC among Hispanic individuals living in southern states could correspond to circumcision or HPV infection rates,⁴⁴ ultimately impacting incidence.⁴⁵

Dermatofibrosarcoma Protuberans

Dermatofibrosarcoma protuberans (DFSP) is a rare locally aggressive cutaneous sarcoma. According to population studies, overall incidence of DFSP is around 4.1 to 4.2 per million in the United States. Population-based studies on DFSP are limited, but available data suggest that Black patients as well as women have the highest incidence.⁴⁶

Dermatofibrosarcoma protuberans is characterized by its capacity to invade surrounding tissues in a tentaclelike pattern.⁴⁷ This characteristic often leads to inadequate initial resection of the lesion as well as a high recurrence rate despite its low metastatic potential.⁴⁸ In early stages, DFSP typically manifests as an asymptomatic plaque with a slow growth rate. The color of the lesion ranges from reddish brown to flesh colored. The pigmented form of DFSP, known as Bednar tumor, is the most common among Black patients.⁴⁷ As the tumor grows, it tends to become firm and nodular. The most common location for DFSP is on the trunk or the upper and lower extremities.⁴⁷

Although current guidelines designate MMS as the first-line treatment for DFSP, the procedure may be inaccessible for certain populations.⁴⁹ Patients with skin of color are more likely to undergo wide local excision (WLE) than MMS; however, WLE is less effective, with a recurrence rate of 30% compared with 3% in those treated with MMS.⁵⁰ A retrospective cohort study of more than 2000 patients revealed that Hispanic and Black patients were less likely to undergo MMS. In addition, the authors noted that WLE recipients more commonly were deceased at the end of the study.⁵¹

Despite undergoing treatment for a primary DFSP, Hispanic patients also appear to be at increased risk for a second surgery.⁵² Additional studies are needed to elucidate the reasons behind higher recurrence rates in Latine/Hispanic patients compared to NHW individuals.

Factors Influencing Skin Cancer Outcomes

In recent years, racial and ethnic disparities in health care use, medical treatment, and quality of care among minoritized populations (including Latine/Hispanic groups) have been documented in the medical literature.^53,54 These systemic inequities, which are rooted in structural racism,⁵⁵ have contributed to poorer health outcomes, worse health status, and lower-quality care for minoritized patients living in the United States, including those impacted by dermatologic conditions.^8,43,55-57 Becoming familiar with the sociocultural factors influencing skin cancer outcomes in the Latine/Hispanic community (including the lack of or inadequate health insurance, medical mistrust, language, and other cultural elements) and the paucity of research in this domain could help eliminate existing health inequities in this population.

Health Insurance Coverage—Although the uninsured rates in the Latine population have decreased since the passage of the Affordable Care Act (from 30% in 2013 to a low of 19% in 2017),⁵⁸ inadequate health insurance coverage remains one of the largest barriers to health care access and a contributor to health disparities among the Latine community. Nearly 1 in 5 Latine individuals in the United States are uninsured compared to 8% of NHW individuals.⁵⁸ Even though Latine individuals are more likely than non-Latine individuals to be part of the workforce, Latine employees are less likely to receive employer-sponsored coverage (27% vs 53% for NHW individuals).⁵⁹

Not surprisingly, noncitizens are far less likely to be insured; this includes lawfully present immigrants (ie, permanent residents or green card holders, refugees, asylees, and others who are authorized to live in the United States temporarily or permanently) and undocumented immigrants (including individuals who entered the country without authorization and individuals who entered the country lawfully and stayed after their visa or status expired). The higher uninsured rate among noncitizens reflects not only limited access to employer-sponsored coverage but includes immigrant eligibility restrictions for federal programs such as Medicaid, the Children’s Health Insurance Program, and the Affordable Care Act Marketplace coverage.⁶⁰

With approximately 9 million Americans living in mixed-status families (and nearly 10% of babies born each year with at least one undocumented parent), restrictive federal or state health care policies may extend beyond their stated target and impact both Latine citizens and noncitizens.^61-65 For instance, Vargas et al⁶⁴ found that both Latine citizens and noncitizens who lived in states with a high number of immigration-related laws had decreased odds of reporting optimal health as compared to Latine respondents in states with fewer immigration-related laws.Other barriers to enrollment include fears and confusion about program qualification, even if eligible.⁵⁸

Medical Mistrust and Unfamiliarity—Mistrust of medical professionals has been shown to reduce patient adherence to treatment as prescribed by their medical provider and can negatively influence health outcomes.⁵³ For racial/ethnic minoritized groups (including Latine/Hispanic patients), medical mistrust may be rooted in patients’ experience of discrimination in the health care setting. In a recent cross-sectional study, results from a survey of California adults (including 704 non-Hispanic Black, 711 Hispanic, and 913 NHW adults) found links between levels of medical mistrust and perceived discrimination based on race/ethnicity and language as well as perceived discrimination due to income level and type or lack of insurance.⁵³ Interestingly, discrimination attributed to income level and insurance status remained after controlling for race/ethnicity and language. As expected, patients reliant on public insurance programs such as Medicare have been reported to have greater medical mistrust and suspicion compared with private insurance holders.⁶⁵ Together, these findings support the notion that individuals who have low socioeconomic status and lack insurance coverage—disproportionately historically marginalized populations—are more likely to perceive discrimination in health care settings, have greater medical mistrust, and experience poorer health outcomes.⁵³

It also is important for health care providers to consider that the US health care system is unfamiliar to many Latine/Hispanic individuals. Costs of medical services tend to be substantially higher in the United States, which can contribute to mistrust in the system.⁶⁶ In addition, unethical medical experimentations have negatively affected both Latine and especially non-Hispanic Black populations, with long-lasting perceptions of deception and exploitation.⁶⁷ These beliefs have undermined the trust that these populations have in clinicians and the health care system.^54,67

Language and Other Cultural Elements—The inability to effectively communicate with health care providers could contribute to disparities in access to and use of health care services among Latine/Hispanic individuals. In a Medical Expenditure Panel Survey analysis, half of Hispanic patients with limited comfort speaking English did not have a usual source of care, and almost 90% of those with a usual source of care had a provider who spoke Spanish or used interpreters—indicating that few Hispanic individuals with limited comfort speaking English selected a usual source of care without language assistance.^68,69 In other examples, language barriers ­contributed to disparities in cancer screening, and individuals with limited English proficiency were more likely to have difficulty understanding their physician due to language barriers.^68,70

Improving cultural misconceptions regarding skin conditions, especially skin cancer, is another important consideration in the Latine/Hispanic community. Many Latine/Hispanic individuals wrongly believe they cannot develop skin cancer due to their darker skin tones and lack of family history.²⁶ Moreover, multiple studies assessing melanoma knowledge and perception among participants with skin of color (including one with an equal number of Latine/Hispanic, Black/African American, and Asian individuals for a total of 120 participants) revealed that many were unaware of the risk for melanoma on acral sites.⁷¹ Participants expressed a need for more culturally relevant content from both clinicians and public materials (eg, images of acral melanoma in a person with skin of color).^71-73

Paucity of Research—There is limited research regarding skin cancer risks and methods of prevention for patients with skin of color, including the Latine/Hispanic population. Efforts to engage and include patients from these communities, as well as clinicians or investigators from similar backgrounds, in clinical studies are desperately needed. It also is important that clinical studies collect data beyond population descriptors to account for both clinical and genetic variations observed in the Latine/Hispanic population. 

Latine/Hispanic individuals are quite diverse with many variable factors that may influence skin cancer outcomes. Often, cancer surveillance data are available in aggregate only, which could mask this heterogeneity.⁷⁴ Rigorous studies that collect more granular data, including objective measures of skin pigmentation beyond self-reported Fitzpatrick skin type, culture/beliefs, lifestyle/behavior, geographic location, socioeconomic status, genetics, or epigenetics could help fully elucidate skin cancer risks and mitigate health disparities among individuals who identify as part of this population.

Final Thoughts

The Latine/Hispanic community—the largest ethnic minoritized group in the United States—is disproportionately affected by dermatologic health disparities. We hope this review helps to increase recognition of the clinical manifestations of skin cancer in Latine/Hispanic patients. Other factors that may impact skin cancer outcomes in this population include (but are not limited to) lack of or inadequate health insurance, medical mistrust, linguistic barriers and/or individual/cultural perspectives, along with limited research. Recognizing and addressing these (albeit complex) barriers that contribute to the inequitable access to health care in this population remains a critical step toward improving skin cancer outcomes.

Practice Gap

Verruca vulgaris is a common dermatologic challenge due to its high prevalence and tendency to recur following routinely employed destructive modalities (eg, cryotherapy, electrosurgery), which can incur a considerable amount of pain and some risk for scarring.^1,2 Other treatment methods for warts such as topical salicylic acid preparations, topical immunotherapy, or intralesional allergen injections often require multiple treatment sessions.^3,4 Furthermore, the financial burden of traditional wart treatment can be substantial.⁴ Better techniques are needed to improve the clinician’s approach to treating warts. We describe a home-based technique to treat common digital warts using pinto bean pressure wraps to induce ischemic changes in wart tissue with similar response rates to commonly used modalities.

Technique

Our technique utilizes a small, hard, convex object that is applied directly over the digital wart. A simple self-adhesive wrap is used to cover the object and maintain constant pressure on the wart overnight. We typically use a dried pinto bean (a variety of the common bean Phaseolus vulgaris) acquired from a local grocery store due to its ideal size, hard surface, and convex shape (Figure 1). The bean is taped in place directly overlying the wart and covered with a self-adhesive wrap overnight. The wrap is removed in the morning, and often no further treatment is needed. The ischemic wart tissue is allowed to slough spontaneously over 1 to 2 weeks. No wound care or dressing is necessary (Figure 2). Larger warts may require application of the pressure wraps for 2 to 3 additional nights. While most warts resolve with this technique, we have observed a recurrence rate similar to that for cryotherapy. Patients are advised that any recurrent warts can be re-treated monthly, if needed, until resolution.

What to Use and How to Prepare—Any small, hard, convex object can be used for the pressure wrap; we also have used appropriately sized and shaped plastic shirt buttons with similar results. Home kits can be assembled in advance and provided to patients at their initial visit along with appropriate instructions (Figure 1A).

Effects on the Skin and Distal Digit—Application of pressure wraps does not harm normal skin; however, care should be taken when the self-adherent wrap is applied so as not to induce ischemia of the distal digit. The wrap should be applied using gentle pressure with patients experiencing minimal discomfort from the overnight application.

Indications—This pressure wrap technique can be employed on most digital warts, including periungual warts, which can be difficult to treat by other means. However, in our experience this technique is not effective for nondigital warts, likely due to the inability to maintain adequate pressure with the overlying dressing. Patients at risk for compromised digital perfusion, such as those with Raynaud phenomenon or systemic sclerosis, should not be treated with pressure wraps due to possible digital ischemia.

Precautions—Patients should be advised that the pinto bean should only be used if dry and should not be ingested. The bean can be a choking hazard for small children, therefore appropriate precautions should be used. Allergic contact dermatitis to the materials used in this technique is possible, but we have never observed this. The pinto bean can be reused for future application as long as it remains dry and provides a hard convex surface.

Practice Implications

The probable mechanism of the ischemic changes to the wart tissue likely is the occlusion of tortuous blood vessels in the dermal papillae, which are intrinsic to wart tissue and absent in normal skin.¹ This pressure-induced ischemic injury allows for selective destruction of the wart tissue with sparing of the normal skin. Our technique is fairly novel, although at least one report in the literature has described the use of a mechanical device to induce ischemic changes in skin tags.⁵

The use of pinto bean pressure wraps to induce ischemic change in digital warts provides a low-risk and nearly pain-free alternative to more expensive and invasive treatment methods. Moreover, this technique allows for a low-cost home-based therapy that can be repeated easily for other digital sites or if recurrence is noted.

Practice Gap

Verruca vulgaris is a common dermatologic challenge due to its high prevalence and tendency to recur following routinely employed destructive modalities (eg, cryotherapy, electrosurgery), which can incur a considerable amount of pain and some risk for scarring.^1,2 Other treatment methods for warts such as topical salicylic acid preparations, topical immunotherapy, or intralesional allergen injections often require multiple treatment sessions.^3,4 Furthermore, the financial burden of traditional wart treatment can be substantial.⁴ Better techniques are needed to improve the clinician’s approach to treating warts. We describe a home-based technique to treat common digital warts using pinto bean pressure wraps to induce ischemic changes in wart tissue with similar response rates to commonly used modalities.

Technique

Our technique utilizes a small, hard, convex object that is applied directly over the digital wart. A simple self-adhesive wrap is used to cover the object and maintain constant pressure on the wart overnight. We typically use a dried pinto bean (a variety of the common bean Phaseolus vulgaris) acquired from a local grocery store due to its ideal size, hard surface, and convex shape (Figure 1). The bean is taped in place directly overlying the wart and covered with a self-adhesive wrap overnight. The wrap is removed in the morning, and often no further treatment is needed. The ischemic wart tissue is allowed to slough spontaneously over 1 to 2 weeks. No wound care or dressing is necessary (Figure 2). Larger warts may require application of the pressure wraps for 2 to 3 additional nights. While most warts resolve with this technique, we have observed a recurrence rate similar to that for cryotherapy. Patients are advised that any recurrent warts can be re-treated monthly, if needed, until resolution.

What to Use and How to Prepare—Any small, hard, convex object can be used for the pressure wrap; we also have used appropriately sized and shaped plastic shirt buttons with similar results. Home kits can be assembled in advance and provided to patients at their initial visit along with appropriate instructions (Figure 1A).

Effects on the Skin and Distal Digit—Application of pressure wraps does not harm normal skin; however, care should be taken when the self-adherent wrap is applied so as not to induce ischemia of the distal digit. The wrap should be applied using gentle pressure with patients experiencing minimal discomfort from the overnight application.

Indications—This pressure wrap technique can be employed on most digital warts, including periungual warts, which can be difficult to treat by other means. However, in our experience this technique is not effective for nondigital warts, likely due to the inability to maintain adequate pressure with the overlying dressing. Patients at risk for compromised digital perfusion, such as those with Raynaud phenomenon or systemic sclerosis, should not be treated with pressure wraps due to possible digital ischemia.

Precautions—Patients should be advised that the pinto bean should only be used if dry and should not be ingested. The bean can be a choking hazard for small children, therefore appropriate precautions should be used. Allergic contact dermatitis to the materials used in this technique is possible, but we have never observed this. The pinto bean can be reused for future application as long as it remains dry and provides a hard convex surface.

Practice Implications

The probable mechanism of the ischemic changes to the wart tissue likely is the occlusion of tortuous blood vessels in the dermal papillae, which are intrinsic to wart tissue and absent in normal skin.¹ This pressure-induced ischemic injury allows for selective destruction of the wart tissue with sparing of the normal skin. Our technique is fairly novel, although at least one report in the literature has described the use of a mechanical device to induce ischemic changes in skin tags.⁵

The use of pinto bean pressure wraps to induce ischemic change in digital warts provides a low-risk and nearly pain-free alternative to more expensive and invasive treatment methods. Moreover, this technique allows for a low-cost home-based therapy that can be repeated easily for other digital sites or if recurrence is noted.

Practice Gap

Verruca vulgaris is a common dermatologic challenge due to its high prevalence and tendency to recur following routinely employed destructive modalities (eg, cryotherapy, electrosurgery), which can incur a considerable amount of pain and some risk for scarring.^1,2 Other treatment methods for warts such as topical salicylic acid preparations, topical immunotherapy, or intralesional allergen injections often require multiple treatment sessions.^3,4 Furthermore, the financial burden of traditional wart treatment can be substantial.⁴ Better techniques are needed to improve the clinician’s approach to treating warts. We describe a home-based technique to treat common digital warts using pinto bean pressure wraps to induce ischemic changes in wart tissue with similar response rates to commonly used modalities.

Technique

Our technique utilizes a small, hard, convex object that is applied directly over the digital wart. A simple self-adhesive wrap is used to cover the object and maintain constant pressure on the wart overnight. We typically use a dried pinto bean (a variety of the common bean Phaseolus vulgaris) acquired from a local grocery store due to its ideal size, hard surface, and convex shape (Figure 1). The bean is taped in place directly overlying the wart and covered with a self-adhesive wrap overnight. The wrap is removed in the morning, and often no further treatment is needed. The ischemic wart tissue is allowed to slough spontaneously over 1 to 2 weeks. No wound care or dressing is necessary (Figure 2). Larger warts may require application of the pressure wraps for 2 to 3 additional nights. While most warts resolve with this technique, we have observed a recurrence rate similar to that for cryotherapy. Patients are advised that any recurrent warts can be re-treated monthly, if needed, until resolution.

What to Use and How to Prepare—Any small, hard, convex object can be used for the pressure wrap; we also have used appropriately sized and shaped plastic shirt buttons with similar results. Home kits can be assembled in advance and provided to patients at their initial visit along with appropriate instructions (Figure 1A).

Effects on the Skin and Distal Digit—Application of pressure wraps does not harm normal skin; however, care should be taken when the self-adherent wrap is applied so as not to induce ischemia of the distal digit. The wrap should be applied using gentle pressure with patients experiencing minimal discomfort from the overnight application.

Indications—This pressure wrap technique can be employed on most digital warts, including periungual warts, which can be difficult to treat by other means. However, in our experience this technique is not effective for nondigital warts, likely due to the inability to maintain adequate pressure with the overlying dressing. Patients at risk for compromised digital perfusion, such as those with Raynaud phenomenon or systemic sclerosis, should not be treated with pressure wraps due to possible digital ischemia.

Precautions—Patients should be advised that the pinto bean should only be used if dry and should not be ingested. The bean can be a choking hazard for small children, therefore appropriate precautions should be used. Allergic contact dermatitis to the materials used in this technique is possible, but we have never observed this. The pinto bean can be reused for future application as long as it remains dry and provides a hard convex surface.

Practice Implications

The probable mechanism of the ischemic changes to the wart tissue likely is the occlusion of tortuous blood vessels in the dermal papillae, which are intrinsic to wart tissue and absent in normal skin.¹ This pressure-induced ischemic injury allows for selective destruction of the wart tissue with sparing of the normal skin. Our technique is fairly novel, although at least one report in the literature has described the use of a mechanical device to induce ischemic changes in skin tags.⁵

The use of pinto bean pressure wraps to induce ischemic change in digital warts provides a low-risk and nearly pain-free alternative to more expensive and invasive treatment methods. Moreover, this technique allows for a low-cost home-based therapy that can be repeated easily for other digital sites or if recurrence is noted.

Cosmetic procedures carry inherent risks of adverse events. Transient and permanent alopecia are rare complications of these procedures. Although they have not been fully elucidated, several pathologic mechanisms for hair loss following cosmetic procedures have been proposed, including extravascular compression (a phenomenon that has been well documented in bed­ridden patients) as well as intravascular occlusion leading to inflammation and necrosis, which has been associated with hyaluronic acid (HA) fillers.¹ Cases of alopecia also have been reported following mesotherapy and calcium hydroxyapatite, deoxycholic acid, and botulinum toxin injections.² We report a case of alopecia resulting from poly-L-lactic acid (PLLA) injection in a 35-year-old woman with the intent to raise awareness of this rare adverse event.

Case Report

A healthy 35-year-old woman received aesthetic PLLA injections on the face and frontal hairline performed by an outside dermatologist using the vector technique. During the procedure, the patient experienced intense itchiness at the right temporal artery vascular territory and reported a substantial headache the next day. She also presented with erythema and edema of the frontal and right parietal scalp with a well-delimited livedoid vascular area along the temporal artery territory on the right side of the head 1 day after the procedure (Figure 1). These signs were reported to the outside dermatologist who performed the procedure, but they were not assumed to be adverse events at that time.

The condition persisted for 4 days followed by the development of an irregular 3×2-cm patch of alopecia on the right parietal scalp. A 3-day course of self-administered oral prednisolone 0.2 mg/kg/d was prescribed.

Twenty-seven days after the procedure, the patient presented to our trichology clinic for evaluation of a single patch of nonscarring alopecia on the right parietal scalp. Trichoscopy showed multiple yellow and black dots, broken hairs, pigment deposits, and an erythematous background mainly composed of linear telangiectatic vessels (Figure 2). Histopathologic analysis revealed a lymphocytic inflammatory infiltrate surrounding the follicular units that was compatible with an alopecia areata–like pattern as well as PLLA deposits in the subcutaneous tissue forming foreign body granulomas (Figure 3). The diagnosis of PLLA-induced alopecia was made based on the detection of PLLA at the biopsy site within the patchy alopecia.

Comment

Poly-L-lactic acid is a biostimulator synthesized from the α-hydroxy acid family in 1954 that has been safely used in suture materials, resorbable plates, and orthopedic screws.⁴ Alopecia has been reported as a systemic allergic reaction to biodegradable screws following an orthopedic procedure.⁵ Prior reports of embolization and retinal ischemia with PLLA have raised concerns regarding its occlusive potential.^6-9

Approved by the US Food and Drug Administration in 2004 for soft tissue restoration in HIV-related lipoatrophy, PLLA was expanded to cosmetic applications in 2009. As previously reported with HA fillers, we hypothesize that extravascular compression resulting from the placement of the filler material (due to the volume injected in the scalp area) contributes to the development of alopecia plus PLLA embolism–induced ischemic alopecia in the affected areas.¹⁰ In our case, the diagnosis of PLLA-induced alopecia was confirmed based on the finding of the filler material in the subcutaneous tissue on histopathology, probably due to embolization. Moreover, trichoscopic findings were all similar to those described after HA embolization.¹¹ The features found in our patient due to the PLLA local reaction were similar to those seen in other conditions such as alopecia areata, pressure alopecia, and chemotherapy-induced alopecia; therefore, histopathology confirmation is mandatory in cases of hair loss associated with PLLA.

The emergence of a secondary patch of alopecia prompts consideration of an intrinsic late inflammatory propensity of PLLA. Immune cells recognize PLLA as a foreign body, and subclinical inflammatory foreign body reactions can cause PLLA-induced collagen synthesis.¹² This phenomenon underscores the need for further investigation into the immunologic implications of PLLA in alopecia pathogenesis.

The angiogenic properties of the anagen phase require an adequate blood supply for effective hair growth; therefore, the lack of blood and nutrient supply to the hair bulb triggers miniaturization, a possible explanation for the hair thinning found in the alopecic patch.¹³

Conclusion

Alopecia as an adverse effect of cosmetic procedures can be distressing for patients, even when reversible. A detailed understanding of scalp anatomy is critical for satisfactory outcomes with aesthetic procedures. Physicians must pay attention to the amount and area of material injected in order to avoid possible mechanisms of ischemia—embolization and/or extravascular compression—especially in highly vascularized areas.

We present a rare report of alopecia as an adverse event of PLLA injection. Dermatologists must be aware of this rare condition, and trichoscopy combined with histopathologic analysis are encouraged for early recognition and proper management.

Cosmetic procedures carry inherent risks of adverse events. Transient and permanent alopecia are rare complications of these procedures. Although they have not been fully elucidated, several pathologic mechanisms for hair loss following cosmetic procedures have been proposed, including extravascular compression (a phenomenon that has been well documented in bed­ridden patients) as well as intravascular occlusion leading to inflammation and necrosis, which has been associated with hyaluronic acid (HA) fillers.¹ Cases of alopecia also have been reported following mesotherapy and calcium hydroxyapatite, deoxycholic acid, and botulinum toxin injections.² We report a case of alopecia resulting from poly-L-lactic acid (PLLA) injection in a 35-year-old woman with the intent to raise awareness of this rare adverse event.

Case Report

A healthy 35-year-old woman received aesthetic PLLA injections on the face and frontal hairline performed by an outside dermatologist using the vector technique. During the procedure, the patient experienced intense itchiness at the right temporal artery vascular territory and reported a substantial headache the next day. She also presented with erythema and edema of the frontal and right parietal scalp with a well-delimited livedoid vascular area along the temporal artery territory on the right side of the head 1 day after the procedure (Figure 1). These signs were reported to the outside dermatologist who performed the procedure, but they were not assumed to be adverse events at that time.

The condition persisted for 4 days followed by the development of an irregular 3×2-cm patch of alopecia on the right parietal scalp. A 3-day course of self-administered oral prednisolone 0.2 mg/kg/d was prescribed.

Twenty-seven days after the procedure, the patient presented to our trichology clinic for evaluation of a single patch of nonscarring alopecia on the right parietal scalp. Trichoscopy showed multiple yellow and black dots, broken hairs, pigment deposits, and an erythematous background mainly composed of linear telangiectatic vessels (Figure 2). Histopathologic analysis revealed a lymphocytic inflammatory infiltrate surrounding the follicular units that was compatible with an alopecia areata–like pattern as well as PLLA deposits in the subcutaneous tissue forming foreign body granulomas (Figure 3). The diagnosis of PLLA-induced alopecia was made based on the detection of PLLA at the biopsy site within the patchy alopecia.

Comment

Poly-L-lactic acid is a biostimulator synthesized from the α-hydroxy acid family in 1954 that has been safely used in suture materials, resorbable plates, and orthopedic screws.⁴ Alopecia has been reported as a systemic allergic reaction to biodegradable screws following an orthopedic procedure.⁵ Prior reports of embolization and retinal ischemia with PLLA have raised concerns regarding its occlusive potential.^6-9

Approved by the US Food and Drug Administration in 2004 for soft tissue restoration in HIV-related lipoatrophy, PLLA was expanded to cosmetic applications in 2009. As previously reported with HA fillers, we hypothesize that extravascular compression resulting from the placement of the filler material (due to the volume injected in the scalp area) contributes to the development of alopecia plus PLLA embolism–induced ischemic alopecia in the affected areas.¹⁰ In our case, the diagnosis of PLLA-induced alopecia was confirmed based on the finding of the filler material in the subcutaneous tissue on histopathology, probably due to embolization. Moreover, trichoscopic findings were all similar to those described after HA embolization.¹¹ The features found in our patient due to the PLLA local reaction were similar to those seen in other conditions such as alopecia areata, pressure alopecia, and chemotherapy-induced alopecia; therefore, histopathology confirmation is mandatory in cases of hair loss associated with PLLA.

The emergence of a secondary patch of alopecia prompts consideration of an intrinsic late inflammatory propensity of PLLA. Immune cells recognize PLLA as a foreign body, and subclinical inflammatory foreign body reactions can cause PLLA-induced collagen synthesis.¹² This phenomenon underscores the need for further investigation into the immunologic implications of PLLA in alopecia pathogenesis.

The angiogenic properties of the anagen phase require an adequate blood supply for effective hair growth; therefore, the lack of blood and nutrient supply to the hair bulb triggers miniaturization, a possible explanation for the hair thinning found in the alopecic patch.¹³

Conclusion

Alopecia as an adverse effect of cosmetic procedures can be distressing for patients, even when reversible. A detailed understanding of scalp anatomy is critical for satisfactory outcomes with aesthetic procedures. Physicians must pay attention to the amount and area of material injected in order to avoid possible mechanisms of ischemia—embolization and/or extravascular compression—especially in highly vascularized areas.

We present a rare report of alopecia as an adverse event of PLLA injection. Dermatologists must be aware of this rare condition, and trichoscopy combined with histopathologic analysis are encouraged for early recognition and proper management.

Cosmetic procedures carry inherent risks of adverse events. Transient and permanent alopecia are rare complications of these procedures. Although they have not been fully elucidated, several pathologic mechanisms for hair loss following cosmetic procedures have been proposed, including extravascular compression (a phenomenon that has been well documented in bed­ridden patients) as well as intravascular occlusion leading to inflammation and necrosis, which has been associated with hyaluronic acid (HA) fillers.¹ Cases of alopecia also have been reported following mesotherapy and calcium hydroxyapatite, deoxycholic acid, and botulinum toxin injections.² We report a case of alopecia resulting from poly-L-lactic acid (PLLA) injection in a 35-year-old woman with the intent to raise awareness of this rare adverse event.

Case Report

A healthy 35-year-old woman received aesthetic PLLA injections on the face and frontal hairline performed by an outside dermatologist using the vector technique. During the procedure, the patient experienced intense itchiness at the right temporal artery vascular territory and reported a substantial headache the next day. She also presented with erythema and edema of the frontal and right parietal scalp with a well-delimited livedoid vascular area along the temporal artery territory on the right side of the head 1 day after the procedure (Figure 1). These signs were reported to the outside dermatologist who performed the procedure, but they were not assumed to be adverse events at that time.

The condition persisted for 4 days followed by the development of an irregular 3×2-cm patch of alopecia on the right parietal scalp. A 3-day course of self-administered oral prednisolone 0.2 mg/kg/d was prescribed.

Twenty-seven days after the procedure, the patient presented to our trichology clinic for evaluation of a single patch of nonscarring alopecia on the right parietal scalp. Trichoscopy showed multiple yellow and black dots, broken hairs, pigment deposits, and an erythematous background mainly composed of linear telangiectatic vessels (Figure 2). Histopathologic analysis revealed a lymphocytic inflammatory infiltrate surrounding the follicular units that was compatible with an alopecia areata–like pattern as well as PLLA deposits in the subcutaneous tissue forming foreign body granulomas (Figure 3). The diagnosis of PLLA-induced alopecia was made based on the detection of PLLA at the biopsy site within the patchy alopecia.

Comment

Poly-L-lactic acid is a biostimulator synthesized from the α-hydroxy acid family in 1954 that has been safely used in suture materials, resorbable plates, and orthopedic screws.⁴ Alopecia has been reported as a systemic allergic reaction to biodegradable screws following an orthopedic procedure.⁵ Prior reports of embolization and retinal ischemia with PLLA have raised concerns regarding its occlusive potential.^6-9

Approved by the US Food and Drug Administration in 2004 for soft tissue restoration in HIV-related lipoatrophy, PLLA was expanded to cosmetic applications in 2009. As previously reported with HA fillers, we hypothesize that extravascular compression resulting from the placement of the filler material (due to the volume injected in the scalp area) contributes to the development of alopecia plus PLLA embolism–induced ischemic alopecia in the affected areas.¹⁰ In our case, the diagnosis of PLLA-induced alopecia was confirmed based on the finding of the filler material in the subcutaneous tissue on histopathology, probably due to embolization. Moreover, trichoscopic findings were all similar to those described after HA embolization.¹¹ The features found in our patient due to the PLLA local reaction were similar to those seen in other conditions such as alopecia areata, pressure alopecia, and chemotherapy-induced alopecia; therefore, histopathology confirmation is mandatory in cases of hair loss associated with PLLA.

The emergence of a secondary patch of alopecia prompts consideration of an intrinsic late inflammatory propensity of PLLA. Immune cells recognize PLLA as a foreign body, and subclinical inflammatory foreign body reactions can cause PLLA-induced collagen synthesis.¹² This phenomenon underscores the need for further investigation into the immunologic implications of PLLA in alopecia pathogenesis.

The angiogenic properties of the anagen phase require an adequate blood supply for effective hair growth; therefore, the lack of blood and nutrient supply to the hair bulb triggers miniaturization, a possible explanation for the hair thinning found in the alopecic patch.¹³

Conclusion

Alopecia as an adverse effect of cosmetic procedures can be distressing for patients, even when reversible. A detailed understanding of scalp anatomy is critical for satisfactory outcomes with aesthetic procedures. Physicians must pay attention to the amount and area of material injected in order to avoid possible mechanisms of ischemia—embolization and/or extravascular compression—especially in highly vascularized areas.

We present a rare report of alopecia as an adverse event of PLLA injection. Dermatologists must be aware of this rare condition, and trichoscopy combined with histopathologic analysis are encouraged for early recognition and proper management.

Inpatient consultative dermatology has advanced as a subspecialty and increasingly gained recognition in recent years. Since its founding in 2009, the Society of Dermatology Hospitalists has fostered research and education in hospital dermatology. Last year, we reviewed the 2022-2023 literature with a focus on developments in severe cutaneous adverse reactions, supportive oncodermatology, cost of inpatient services, and teledermatology.¹ In this review, we highlight 3 areas of interest from the 2023-2024 literature: severe cutaneous adverse drug reactions, skin and soft tissue infections, and autoimmune blistering diseases (AIBDs).

Severe Cutaneous Adverse Drug Reactions

Adverse drug reactions are among the most common diagnoses encountered by inpatient dermatology consultants.^2,3 Severe cutaneous adverse drug reactions are associated with substantial morbidity and mortality. Efforts to characterize these conditions and standardize their diagnosis and management continue to be a major focus of ongoing research.

A single-center retrospective analysis of 102 cases of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome evaluated differences in clinical manifestations depending on the culprit drug, offering insights into the heterogeneity of DRESS syndrome and the potential for diagnostic uncertainty.⁴ The shortest median latency was observed in a case caused by penicillin and cephalosporins (12 and 18 days, respectively), while DRESS syndrome secondary to allopurinol had the longest median latency (36 days). Nonsteroidal anti-inflammatory drug–induced DRESS syndrome was associated with the shortest hospital stay (6.5 days), while cephalosporin and vancomycin cases had the highest mortality rates.⁴

In the first international Delphi consensus study on the diagnostic workup, severity assessment, and management of DRESS syndrome, 54 dermatology and/or allergy experts reached consensus on 93 statements.⁵ Specific recommendations included basic evaluation with complete blood count with differential, kidney and liver function parameters, and electrocardiogram for all patients with suspected DRESS syndrome, with additional complementary workup considered in patients with evidence of specific organ damage and/or severe disease. In the proposed DRESS syndrome severity grading scheme, laboratory values that reached consensus for inclusion were hemoglobin, neutrophil, and platelet counts and creatinine, transaminases, and alkaline phosphatase levels. Although treatment of DRESS syndrome should be based on assessed disease severity, treatment with corticosteroids should be initiated in all patients with confirmed DRESS syndrome. Cyclosporine, antibodies interfering with the IL-5 axis, and intravenous immunoglobulins can be considered in patients with corticosteroid-refractory DRESS syndrome, and antiviral treatment can be considered in patients with a high serum cytomegalovirus viral load. Regularly following up with laboratory evaluation of involved organs; screening for autoantibodies, thyroid dysfunction, and steroid adverse effects; and offering of psychological support also were consensus recommendations.⁵

Identifying causative agents in drug hypersensitivity reactions remains challenging. A retrospective cohort study of 48 patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) highlighted the need for a systematic unbiased approach to identifying culprit drugs. Using the RegiSCAR database and algorithm for drug causality for epidermal necrolysis to analyze the cohort, more than half of causative agents were determined to be different from those initially identified by the treating physicians. Nine additional suspected culprit drugs were identified, while 43 drugs initially identified as allergens were exonerated.⁶

Etiology-associated definitions for blistering reactions in children have been proposed to replace the existing terms Stevens-Johnson syndrome, toxic epidermal necrolysis, and others.⁷ Investigators in a recent study reclassified cases of SJS and TEN as reactive infectious mucocutaneous eruption (RIME) or drug-induced epidermal necrolysis (DEN), respectively. In RIME cases, Mycoplasma pneumoniae was the most commonly identified trigger, and in DEN cases, anticonvulsants were the most common class of culprit medications. Cases of RIME were less severe and were most often treated with antibiotics, whereas patients with DEN were more likely to receive supportive care, corticosteroids, intravenous immunoglobulins, and other immunosuppressive therapies.⁷

In addition to causing acute devastating mucocutaneous complications, SJS and TEN have long-lasting effects that require ongoing care. In a cohort of 6552 incident SJS/TEN cases over an 11-year period, survivors of SJS/TEN endured a mean loss of 9.4 years in life expectancy and excess health care expenditures of $3752 per year compared with age- and sex-matched controls. Patients with more severe disease, comorbid malignancy, diabetes, end-stage renal disease, or SJS/TEN sequelae experienced greater loss in life expectancy and lifetime health care expenditures.⁸ Separately, a qualitative study investigating the psychological impact of SJS/TEN in pediatric patients described sequelae including night terrors, posttraumatic stress disorder, depression, and anxiety for many years after the acute phase. Many patients reported a desire for increased support for their physical and emotional needs following hospital discharge.⁹

Skin and Soft Tissue Infections: Diagnosis, Management, and Prevention

Dermatology consultation has been shown to be a cost-effective intervention to improve outcomes in hospitalized patients with skin and soft tissue infections.^10,11 In particular, cellulitis frequently is misdiagnosed, leading to unnecessary antibiotic use, hospitalizations, and major health care expenditures.¹² Recognizing this challenge, researchers have worked to develop objective tools to improve diagnostic accuracy. In a large prospective prognostic validation study, Pulia et al¹³ found that thermal imaging alone or in combination with the ALT-70 prediction model (asymmetry, leukocytosis, tachycardia, and age ≥70 years) could be used successfully to reduce overdiagnosis of cellulitis. Both thermal imaging and the ALT-70 prediction model demonstrated robust sensitivity (93.5% and 98.8%, respectively) but low specificity (38.4% and 22.0%, respectively, and 53.9% when combined).¹³

In a systematic review, Kovacs et al¹⁴ analyzed case reports of pseudocellulitis caused by chemotherapeutic medications. Of the 81 cases selected, 58 (71.6%) were associated with gemcitabine, with the remaining 23 (28.4%) attributed to pemetrexed. Within this group, two-thirds of the patients received antibiotic treatment prior to receiving the correct diagnosis, and 36% experienced interruptions to their oncologic therapies. In contrast to infectious cellulitis, which tends to be unilateral and associated with elevated erythrocyte sedimentation rate or C-reactive protein, most chemotherapy-induced pseudocellulitis cases occurred bilaterally on the lower extremities, while erythrocyte sedimentation rate and C-reactive protein seldom were elevated.¹⁴

Necrotizing soft tissue infections (NSTIs) are severe life-threatening conditions characterized by widespread tissue destruction, signs of systemic toxicity, hemodynamic collapse, organ failure, and high mortality. Surgical inspection along with intraoperative tissue culture is the gold standard for diagnosis. Early detection, prompt surgical intervention, and appropriate antibiotic treatment are essential to reduce mortality and improve outcomes.¹⁵ A retrospective study of patients with surgically confirmed NSTIs assessed the incidence and risk factors for recurrence within 1 year following an initial NSTI of the lower extremity. Among 93 included patients, 32 (34.4%) had recurrence within 1 year, and more than half of recurrences occurred in the first 3 months (median, 66 days). The comparison of patients with and without recurrence showed similar proportions of antibiotic prophylaxis use after the first NSTI. There was significantly less compression therapy use (33.3% vs 62.3%; P=.13) and more negative pressure wound therapy use (83.3% vs 63.3%; P=.03) in the recurrence group, though the authors acknowledged that factors such as severity of pain and size of soft tissue defect may have affected the decisions for compression and negative pressure wound therapy.¹⁶

Residents of nursing homes are a particularly vulnerable population at high risk for health care–associated infections due to older age and a higher likelihood of having wounds, indwelling medical devices, and/or coexisting conditions.¹⁷ One cluster-randomized trial compared universal decolonization with routine-care bathing practices in nursing homes (N=28,956 residents). Decolonization entailed the use of chlorhexidine for all routine bathing and showering and administration of nasal povidone-iodine twice daily for the first 5 days after admission and then twice daily for 5 days every other week. Transfer to a hospital due to infection decreased from 62.9% to 52.2% with decolonization, for a difference in risk ratio of 16.6% (P<.001) compared with routine care. Additionally, the difference in risk ratio of the secondary end point (transfer to a hospital for any reason) was 14.6%. The number needed to treat was 9.7 to prevent 1 infection-related hospitalization and 8.9 to prevent 1 hospitalization for any reason.¹⁷

Autoimmune Blistering Diseases

Although rare, AIBDs are potentially life-threatening cutaneous diseases that often require inpatient management. While corticosteroids remain the mainstay of initial AIBD management, rituximab is now well recognized as the steroid-sparing treatment of choice for patients with moderate to severe pemphigus. In a long-term follow-up study of Ritux 3¹⁸—the trial that led to the US Food and Drug Administration approval of rituximab in the treatment of moderate to severe pemphigus vulgaris—researchers assessed the long-term efficacy and safety of rituximab as a first-line treatment in patients with pemphigus.¹⁹ The 5- and 7-year disease-free survival rates without corticosteroid therapy for patients treated with rituximab were 76.7% and 72.1%, respectively, compared with 35.3% and 35.3% in those treated with prednisone alone (P<.001). Fewer serious adverse events were reported in those treated with rituximab plus prednisone compared with those treated with prednisone alone. None of the patients who maintained complete remission off corticosteroid therapy received any additional maintenance infusions of rituximab after the end of the Ritux 3 regimen (1 g of rituximab at day 0 and day 14, then 500 mg at months 12 and 18).¹⁹

By contrast, treatment of severe bullous pemphigoid (BP) often is less clear-cut, as no single therapeutic option has been shown to be superior to other immunomodulatory and immunosuppressive regimens, and the medical comorbidities of elderly patients with BP can be limiting. Fortunately, newer therapies with favorable safety profiles have emerged in recent years. In a multicenter retrospective study, 100 patients with BP received omalizumab after previously failing to respond to at least one alternative therapy. Disease control was obtained after a median of 10 days, and complete remission was achieved in 77% of patients in a median time of 3 months.²⁰ In a multicenter retrospective cohort study of 146 patients with BP treated with dupilumab following the atopic dermatitis dosing schedule (one 600-mg dose followed by 300 mg every 2 weeks), disease control was achieved in a median of 14 days, while complete remission was achieved in 35.6% of patients, with 8.9% relapsing during the observation period.²¹ A retrospective case series of 30 patients with BP treated with dupilumab with maintenance dosing frequency tailored to individual patient response showed complete remission or marked response in 76.7% (23/30) of patients.²² A phase 2/3 randomized controlled trial of dupilumab in BP is currently ongoing (ClinicalTrials.gov identifier NCT04206553).

Pemphigoid gestationis is a rare autoimmune subepidermal bullous dermatosis of pregnancy that may be difficult to distinguish clinically from polymorphic eruption of pregnancy but confers notably different maternal and fetal risks. Researchers developed and validated a scoring system using clinical factors—history of pemphigoid gestationis, primigravidae, timing of rash onset, and specific clinical examination findings—that was able to differentiate between the 2 diseases with 79% sensitivity, 95% specificity, and an area under the curve of 0.93 without the need for advanced immunologic testing.²³

Final Thoughts

Highlights of the literature from 2023-2024 demonstrate advancements in hospital-based dermatology as well as ongoing challenges. This year’s review emphasizes key developments in severe cutaneous adverse drug reactions, skin and soft tissue infections, and AIBDs. Continued expansion of knowledge in these areas and others informs patient care and demonstrates the value of dermatologic expertise in the inpatient setting.

Inpatient consultative dermatology has advanced as a subspecialty and increasingly gained recognition in recent years. Since its founding in 2009, the Society of Dermatology Hospitalists has fostered research and education in hospital dermatology. Last year, we reviewed the 2022-2023 literature with a focus on developments in severe cutaneous adverse reactions, supportive oncodermatology, cost of inpatient services, and teledermatology.¹ In this review, we highlight 3 areas of interest from the 2023-2024 literature: severe cutaneous adverse drug reactions, skin and soft tissue infections, and autoimmune blistering diseases (AIBDs).

Severe Cutaneous Adverse Drug Reactions

Adverse drug reactions are among the most common diagnoses encountered by inpatient dermatology consultants.^2,3 Severe cutaneous adverse drug reactions are associated with substantial morbidity and mortality. Efforts to characterize these conditions and standardize their diagnosis and management continue to be a major focus of ongoing research.

A single-center retrospective analysis of 102 cases of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome evaluated differences in clinical manifestations depending on the culprit drug, offering insights into the heterogeneity of DRESS syndrome and the potential for diagnostic uncertainty.⁴ The shortest median latency was observed in a case caused by penicillin and cephalosporins (12 and 18 days, respectively), while DRESS syndrome secondary to allopurinol had the longest median latency (36 days). Nonsteroidal anti-inflammatory drug–induced DRESS syndrome was associated with the shortest hospital stay (6.5 days), while cephalosporin and vancomycin cases had the highest mortality rates.⁴

In the first international Delphi consensus study on the diagnostic workup, severity assessment, and management of DRESS syndrome, 54 dermatology and/or allergy experts reached consensus on 93 statements.⁵ Specific recommendations included basic evaluation with complete blood count with differential, kidney and liver function parameters, and electrocardiogram for all patients with suspected DRESS syndrome, with additional complementary workup considered in patients with evidence of specific organ damage and/or severe disease. In the proposed DRESS syndrome severity grading scheme, laboratory values that reached consensus for inclusion were hemoglobin, neutrophil, and platelet counts and creatinine, transaminases, and alkaline phosphatase levels. Although treatment of DRESS syndrome should be based on assessed disease severity, treatment with corticosteroids should be initiated in all patients with confirmed DRESS syndrome. Cyclosporine, antibodies interfering with the IL-5 axis, and intravenous immunoglobulins can be considered in patients with corticosteroid-refractory DRESS syndrome, and antiviral treatment can be considered in patients with a high serum cytomegalovirus viral load. Regularly following up with laboratory evaluation of involved organs; screening for autoantibodies, thyroid dysfunction, and steroid adverse effects; and offering of psychological support also were consensus recommendations.⁵

Identifying causative agents in drug hypersensitivity reactions remains challenging. A retrospective cohort study of 48 patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) highlighted the need for a systematic unbiased approach to identifying culprit drugs. Using the RegiSCAR database and algorithm for drug causality for epidermal necrolysis to analyze the cohort, more than half of causative agents were determined to be different from those initially identified by the treating physicians. Nine additional suspected culprit drugs were identified, while 43 drugs initially identified as allergens were exonerated.⁶

Etiology-associated definitions for blistering reactions in children have been proposed to replace the existing terms Stevens-Johnson syndrome, toxic epidermal necrolysis, and others.⁷ Investigators in a recent study reclassified cases of SJS and TEN as reactive infectious mucocutaneous eruption (RIME) or drug-induced epidermal necrolysis (DEN), respectively. In RIME cases, Mycoplasma pneumoniae was the most commonly identified trigger, and in DEN cases, anticonvulsants were the most common class of culprit medications. Cases of RIME were less severe and were most often treated with antibiotics, whereas patients with DEN were more likely to receive supportive care, corticosteroids, intravenous immunoglobulins, and other immunosuppressive therapies.⁷

In addition to causing acute devastating mucocutaneous complications, SJS and TEN have long-lasting effects that require ongoing care. In a cohort of 6552 incident SJS/TEN cases over an 11-year period, survivors of SJS/TEN endured a mean loss of 9.4 years in life expectancy and excess health care expenditures of $3752 per year compared with age- and sex-matched controls. Patients with more severe disease, comorbid malignancy, diabetes, end-stage renal disease, or SJS/TEN sequelae experienced greater loss in life expectancy and lifetime health care expenditures.⁸ Separately, a qualitative study investigating the psychological impact of SJS/TEN in pediatric patients described sequelae including night terrors, posttraumatic stress disorder, depression, and anxiety for many years after the acute phase. Many patients reported a desire for increased support for their physical and emotional needs following hospital discharge.⁹

Skin and Soft Tissue Infections: Diagnosis, Management, and Prevention

Dermatology consultation has been shown to be a cost-effective intervention to improve outcomes in hospitalized patients with skin and soft tissue infections.^10,11 In particular, cellulitis frequently is misdiagnosed, leading to unnecessary antibiotic use, hospitalizations, and major health care expenditures.¹² Recognizing this challenge, researchers have worked to develop objective tools to improve diagnostic accuracy. In a large prospective prognostic validation study, Pulia et al¹³ found that thermal imaging alone or in combination with the ALT-70 prediction model (asymmetry, leukocytosis, tachycardia, and age ≥70 years) could be used successfully to reduce overdiagnosis of cellulitis. Both thermal imaging and the ALT-70 prediction model demonstrated robust sensitivity (93.5% and 98.8%, respectively) but low specificity (38.4% and 22.0%, respectively, and 53.9% when combined).¹³

In a systematic review, Kovacs et al¹⁴ analyzed case reports of pseudocellulitis caused by chemotherapeutic medications. Of the 81 cases selected, 58 (71.6%) were associated with gemcitabine, with the remaining 23 (28.4%) attributed to pemetrexed. Within this group, two-thirds of the patients received antibiotic treatment prior to receiving the correct diagnosis, and 36% experienced interruptions to their oncologic therapies. In contrast to infectious cellulitis, which tends to be unilateral and associated with elevated erythrocyte sedimentation rate or C-reactive protein, most chemotherapy-induced pseudocellulitis cases occurred bilaterally on the lower extremities, while erythrocyte sedimentation rate and C-reactive protein seldom were elevated.¹⁴

Necrotizing soft tissue infections (NSTIs) are severe life-threatening conditions characterized by widespread tissue destruction, signs of systemic toxicity, hemodynamic collapse, organ failure, and high mortality. Surgical inspection along with intraoperative tissue culture is the gold standard for diagnosis. Early detection, prompt surgical intervention, and appropriate antibiotic treatment are essential to reduce mortality and improve outcomes.¹⁵ A retrospective study of patients with surgically confirmed NSTIs assessed the incidence and risk factors for recurrence within 1 year following an initial NSTI of the lower extremity. Among 93 included patients, 32 (34.4%) had recurrence within 1 year, and more than half of recurrences occurred in the first 3 months (median, 66 days). The comparison of patients with and without recurrence showed similar proportions of antibiotic prophylaxis use after the first NSTI. There was significantly less compression therapy use (33.3% vs 62.3%; P=.13) and more negative pressure wound therapy use (83.3% vs 63.3%; P=.03) in the recurrence group, though the authors acknowledged that factors such as severity of pain and size of soft tissue defect may have affected the decisions for compression and negative pressure wound therapy.¹⁶

Residents of nursing homes are a particularly vulnerable population at high risk for health care–associated infections due to older age and a higher likelihood of having wounds, indwelling medical devices, and/or coexisting conditions.¹⁷ One cluster-randomized trial compared universal decolonization with routine-care bathing practices in nursing homes (N=28,956 residents). Decolonization entailed the use of chlorhexidine for all routine bathing and showering and administration of nasal povidone-iodine twice daily for the first 5 days after admission and then twice daily for 5 days every other week. Transfer to a hospital due to infection decreased from 62.9% to 52.2% with decolonization, for a difference in risk ratio of 16.6% (P<.001) compared with routine care. Additionally, the difference in risk ratio of the secondary end point (transfer to a hospital for any reason) was 14.6%. The number needed to treat was 9.7 to prevent 1 infection-related hospitalization and 8.9 to prevent 1 hospitalization for any reason.¹⁷

Autoimmune Blistering Diseases

Although rare, AIBDs are potentially life-threatening cutaneous diseases that often require inpatient management. While corticosteroids remain the mainstay of initial AIBD management, rituximab is now well recognized as the steroid-sparing treatment of choice for patients with moderate to severe pemphigus. In a long-term follow-up study of Ritux 3¹⁸—the trial that led to the US Food and Drug Administration approval of rituximab in the treatment of moderate to severe pemphigus vulgaris—researchers assessed the long-term efficacy and safety of rituximab as a first-line treatment in patients with pemphigus.¹⁹ The 5- and 7-year disease-free survival rates without corticosteroid therapy for patients treated with rituximab were 76.7% and 72.1%, respectively, compared with 35.3% and 35.3% in those treated with prednisone alone (P<.001). Fewer serious adverse events were reported in those treated with rituximab plus prednisone compared with those treated with prednisone alone. None of the patients who maintained complete remission off corticosteroid therapy received any additional maintenance infusions of rituximab after the end of the Ritux 3 regimen (1 g of rituximab at day 0 and day 14, then 500 mg at months 12 and 18).¹⁹

By contrast, treatment of severe bullous pemphigoid (BP) often is less clear-cut, as no single therapeutic option has been shown to be superior to other immunomodulatory and immunosuppressive regimens, and the medical comorbidities of elderly patients with BP can be limiting. Fortunately, newer therapies with favorable safety profiles have emerged in recent years. In a multicenter retrospective study, 100 patients with BP received omalizumab after previously failing to respond to at least one alternative therapy. Disease control was obtained after a median of 10 days, and complete remission was achieved in 77% of patients in a median time of 3 months.²⁰ In a multicenter retrospective cohort study of 146 patients with BP treated with dupilumab following the atopic dermatitis dosing schedule (one 600-mg dose followed by 300 mg every 2 weeks), disease control was achieved in a median of 14 days, while complete remission was achieved in 35.6% of patients, with 8.9% relapsing during the observation period.²¹ A retrospective case series of 30 patients with BP treated with dupilumab with maintenance dosing frequency tailored to individual patient response showed complete remission or marked response in 76.7% (23/30) of patients.²² A phase 2/3 randomized controlled trial of dupilumab in BP is currently ongoing (ClinicalTrials.gov identifier NCT04206553).

Pemphigoid gestationis is a rare autoimmune subepidermal bullous dermatosis of pregnancy that may be difficult to distinguish clinically from polymorphic eruption of pregnancy but confers notably different maternal and fetal risks. Researchers developed and validated a scoring system using clinical factors—history of pemphigoid gestationis, primigravidae, timing of rash onset, and specific clinical examination findings—that was able to differentiate between the 2 diseases with 79% sensitivity, 95% specificity, and an area under the curve of 0.93 without the need for advanced immunologic testing.²³

Final Thoughts

Highlights of the literature from 2023-2024 demonstrate advancements in hospital-based dermatology as well as ongoing challenges. This year’s review emphasizes key developments in severe cutaneous adverse drug reactions, skin and soft tissue infections, and AIBDs. Continued expansion of knowledge in these areas and others informs patient care and demonstrates the value of dermatologic expertise in the inpatient setting.

Inpatient consultative dermatology has advanced as a subspecialty and increasingly gained recognition in recent years. Since its founding in 2009, the Society of Dermatology Hospitalists has fostered research and education in hospital dermatology. Last year, we reviewed the 2022-2023 literature with a focus on developments in severe cutaneous adverse reactions, supportive oncodermatology, cost of inpatient services, and teledermatology.¹ In this review, we highlight 3 areas of interest from the 2023-2024 literature: severe cutaneous adverse drug reactions, skin and soft tissue infections, and autoimmune blistering diseases (AIBDs).

Severe Cutaneous Adverse Drug Reactions

Adverse drug reactions are among the most common diagnoses encountered by inpatient dermatology consultants.^2,3 Severe cutaneous adverse drug reactions are associated with substantial morbidity and mortality. Efforts to characterize these conditions and standardize their diagnosis and management continue to be a major focus of ongoing research.

A single-center retrospective analysis of 102 cases of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome evaluated differences in clinical manifestations depending on the culprit drug, offering insights into the heterogeneity of DRESS syndrome and the potential for diagnostic uncertainty.⁴ The shortest median latency was observed in a case caused by penicillin and cephalosporins (12 and 18 days, respectively), while DRESS syndrome secondary to allopurinol had the longest median latency (36 days). Nonsteroidal anti-inflammatory drug–induced DRESS syndrome was associated with the shortest hospital stay (6.5 days), while cephalosporin and vancomycin cases had the highest mortality rates.⁴

In the first international Delphi consensus study on the diagnostic workup, severity assessment, and management of DRESS syndrome, 54 dermatology and/or allergy experts reached consensus on 93 statements.⁵ Specific recommendations included basic evaluation with complete blood count with differential, kidney and liver function parameters, and electrocardiogram for all patients with suspected DRESS syndrome, with additional complementary workup considered in patients with evidence of specific organ damage and/or severe disease. In the proposed DRESS syndrome severity grading scheme, laboratory values that reached consensus for inclusion were hemoglobin, neutrophil, and platelet counts and creatinine, transaminases, and alkaline phosphatase levels. Although treatment of DRESS syndrome should be based on assessed disease severity, treatment with corticosteroids should be initiated in all patients with confirmed DRESS syndrome. Cyclosporine, antibodies interfering with the IL-5 axis, and intravenous immunoglobulins can be considered in patients with corticosteroid-refractory DRESS syndrome, and antiviral treatment can be considered in patients with a high serum cytomegalovirus viral load. Regularly following up with laboratory evaluation of involved organs; screening for autoantibodies, thyroid dysfunction, and steroid adverse effects; and offering of psychological support also were consensus recommendations.⁵

Identifying causative agents in drug hypersensitivity reactions remains challenging. A retrospective cohort study of 48 patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) highlighted the need for a systematic unbiased approach to identifying culprit drugs. Using the RegiSCAR database and algorithm for drug causality for epidermal necrolysis to analyze the cohort, more than half of causative agents were determined to be different from those initially identified by the treating physicians. Nine additional suspected culprit drugs were identified, while 43 drugs initially identified as allergens were exonerated.⁶

Etiology-associated definitions for blistering reactions in children have been proposed to replace the existing terms Stevens-Johnson syndrome, toxic epidermal necrolysis, and others.⁷ Investigators in a recent study reclassified cases of SJS and TEN as reactive infectious mucocutaneous eruption (RIME) or drug-induced epidermal necrolysis (DEN), respectively. In RIME cases, Mycoplasma pneumoniae was the most commonly identified trigger, and in DEN cases, anticonvulsants were the most common class of culprit medications. Cases of RIME were less severe and were most often treated with antibiotics, whereas patients with DEN were more likely to receive supportive care, corticosteroids, intravenous immunoglobulins, and other immunosuppressive therapies.⁷

In addition to causing acute devastating mucocutaneous complications, SJS and TEN have long-lasting effects that require ongoing care. In a cohort of 6552 incident SJS/TEN cases over an 11-year period, survivors of SJS/TEN endured a mean loss of 9.4 years in life expectancy and excess health care expenditures of $3752 per year compared with age- and sex-matched controls. Patients with more severe disease, comorbid malignancy, diabetes, end-stage renal disease, or SJS/TEN sequelae experienced greater loss in life expectancy and lifetime health care expenditures.⁸ Separately, a qualitative study investigating the psychological impact of SJS/TEN in pediatric patients described sequelae including night terrors, posttraumatic stress disorder, depression, and anxiety for many years after the acute phase. Many patients reported a desire for increased support for their physical and emotional needs following hospital discharge.⁹

Skin and Soft Tissue Infections: Diagnosis, Management, and Prevention

Dermatology consultation has been shown to be a cost-effective intervention to improve outcomes in hospitalized patients with skin and soft tissue infections.^10,11 In particular, cellulitis frequently is misdiagnosed, leading to unnecessary antibiotic use, hospitalizations, and major health care expenditures.¹² Recognizing this challenge, researchers have worked to develop objective tools to improve diagnostic accuracy. In a large prospective prognostic validation study, Pulia et al¹³ found that thermal imaging alone or in combination with the ALT-70 prediction model (asymmetry, leukocytosis, tachycardia, and age ≥70 years) could be used successfully to reduce overdiagnosis of cellulitis. Both thermal imaging and the ALT-70 prediction model demonstrated robust sensitivity (93.5% and 98.8%, respectively) but low specificity (38.4% and 22.0%, respectively, and 53.9% when combined).¹³

In a systematic review, Kovacs et al¹⁴ analyzed case reports of pseudocellulitis caused by chemotherapeutic medications. Of the 81 cases selected, 58 (71.6%) were associated with gemcitabine, with the remaining 23 (28.4%) attributed to pemetrexed. Within this group, two-thirds of the patients received antibiotic treatment prior to receiving the correct diagnosis, and 36% experienced interruptions to their oncologic therapies. In contrast to infectious cellulitis, which tends to be unilateral and associated with elevated erythrocyte sedimentation rate or C-reactive protein, most chemotherapy-induced pseudocellulitis cases occurred bilaterally on the lower extremities, while erythrocyte sedimentation rate and C-reactive protein seldom were elevated.¹⁴

Necrotizing soft tissue infections (NSTIs) are severe life-threatening conditions characterized by widespread tissue destruction, signs of systemic toxicity, hemodynamic collapse, organ failure, and high mortality. Surgical inspection along with intraoperative tissue culture is the gold standard for diagnosis. Early detection, prompt surgical intervention, and appropriate antibiotic treatment are essential to reduce mortality and improve outcomes.¹⁵ A retrospective study of patients with surgically confirmed NSTIs assessed the incidence and risk factors for recurrence within 1 year following an initial NSTI of the lower extremity. Among 93 included patients, 32 (34.4%) had recurrence within 1 year, and more than half of recurrences occurred in the first 3 months (median, 66 days). The comparison of patients with and without recurrence showed similar proportions of antibiotic prophylaxis use after the first NSTI. There was significantly less compression therapy use (33.3% vs 62.3%; P=.13) and more negative pressure wound therapy use (83.3% vs 63.3%; P=.03) in the recurrence group, though the authors acknowledged that factors such as severity of pain and size of soft tissue defect may have affected the decisions for compression and negative pressure wound therapy.¹⁶

Residents of nursing homes are a particularly vulnerable population at high risk for health care–associated infections due to older age and a higher likelihood of having wounds, indwelling medical devices, and/or coexisting conditions.¹⁷ One cluster-randomized trial compared universal decolonization with routine-care bathing practices in nursing homes (N=28,956 residents). Decolonization entailed the use of chlorhexidine for all routine bathing and showering and administration of nasal povidone-iodine twice daily for the first 5 days after admission and then twice daily for 5 days every other week. Transfer to a hospital due to infection decreased from 62.9% to 52.2% with decolonization, for a difference in risk ratio of 16.6% (P<.001) compared with routine care. Additionally, the difference in risk ratio of the secondary end point (transfer to a hospital for any reason) was 14.6%. The number needed to treat was 9.7 to prevent 1 infection-related hospitalization and 8.9 to prevent 1 hospitalization for any reason.¹⁷

Autoimmune Blistering Diseases

Although rare, AIBDs are potentially life-threatening cutaneous diseases that often require inpatient management. While corticosteroids remain the mainstay of initial AIBD management, rituximab is now well recognized as the steroid-sparing treatment of choice for patients with moderate to severe pemphigus. In a long-term follow-up study of Ritux 3¹⁸—the trial that led to the US Food and Drug Administration approval of rituximab in the treatment of moderate to severe pemphigus vulgaris—researchers assessed the long-term efficacy and safety of rituximab as a first-line treatment in patients with pemphigus.¹⁹ The 5- and 7-year disease-free survival rates without corticosteroid therapy for patients treated with rituximab were 76.7% and 72.1%, respectively, compared with 35.3% and 35.3% in those treated with prednisone alone (P<.001). Fewer serious adverse events were reported in those treated with rituximab plus prednisone compared with those treated with prednisone alone. None of the patients who maintained complete remission off corticosteroid therapy received any additional maintenance infusions of rituximab after the end of the Ritux 3 regimen (1 g of rituximab at day 0 and day 14, then 500 mg at months 12 and 18).¹⁹

By contrast, treatment of severe bullous pemphigoid (BP) often is less clear-cut, as no single therapeutic option has been shown to be superior to other immunomodulatory and immunosuppressive regimens, and the medical comorbidities of elderly patients with BP can be limiting. Fortunately, newer therapies with favorable safety profiles have emerged in recent years. In a multicenter retrospective study, 100 patients with BP received omalizumab after previously failing to respond to at least one alternative therapy. Disease control was obtained after a median of 10 days, and complete remission was achieved in 77% of patients in a median time of 3 months.²⁰ In a multicenter retrospective cohort study of 146 patients with BP treated with dupilumab following the atopic dermatitis dosing schedule (one 600-mg dose followed by 300 mg every 2 weeks), disease control was achieved in a median of 14 days, while complete remission was achieved in 35.6% of patients, with 8.9% relapsing during the observation period.²¹ A retrospective case series of 30 patients with BP treated with dupilumab with maintenance dosing frequency tailored to individual patient response showed complete remission or marked response in 76.7% (23/30) of patients.²² A phase 2/3 randomized controlled trial of dupilumab in BP is currently ongoing (ClinicalTrials.gov identifier NCT04206553).

Pemphigoid gestationis is a rare autoimmune subepidermal bullous dermatosis of pregnancy that may be difficult to distinguish clinically from polymorphic eruption of pregnancy but confers notably different maternal and fetal risks. Researchers developed and validated a scoring system using clinical factors—history of pemphigoid gestationis, primigravidae, timing of rash onset, and specific clinical examination findings—that was able to differentiate between the 2 diseases with 79% sensitivity, 95% specificity, and an area under the curve of 0.93 without the need for advanced immunologic testing.²³

Final Thoughts

Highlights of the literature from 2023-2024 demonstrate advancements in hospital-based dermatology as well as ongoing challenges. This year’s review emphasizes key developments in severe cutaneous adverse drug reactions, skin and soft tissue infections, and AIBDs. Continued expansion of knowledge in these areas and others informs patient care and demonstrates the value of dermatologic expertise in the inpatient setting.

Keloids are fibroproliferative lesions caused by aberrant wound healing in predisposed individuals.¹ While keloids have been reported in patients of all races and ethnicities, they most commonly develop in individuals of African or Asian descent.² Often associated with symptoms such as pain and itching, keloids can be disfiguring and result in poorer quality of life.³ There is a paucity of research on keloid pathogenesis and efficacious therapeutics, particularly in patients with skin of color (SOC). Herein, we outline the current research on keloid treatment and highlight promising new therapies ranging from innovative intralesional techniques to advanced laser-based and biologic therapies.

Deficiencies in Skin of Color Research

Although keloids are 17 times more prevalent in patients with SOC,⁴ there is a considerable lack of focus on this population in the literature.⁵ Studies on keloids that include individuals with SOC often group patients of all skin types together, and subgroup analyses are not always performed.^6,7 As a result, dermatologists may face considerable challenges in providing effective treatments for keloids in patients with SOC. With few evidence-based options available, patients with SOC who have keloids continue to experience impairments in quality of life.

Common Keloid Therapies

There currently is no gold-standard treatment for keloids. Common therapeutic modalities include intralesional corticosteroids (ILCs), antineoplastic agents and neuromodulators, laser-based devices, and surgical therapies (eg, excision), as well as combined medical and surgical techniques.⁸

Intralesional Corticosteroids—Minimally invasive ILCs are the first-line treatment in all patients with keloids, regardless of skin phototype. Because keloid formation results from trauma to the skin, ILCs often are recommended to minimize further skin damage.⁵ One meta-analysis found that ILCs have demonstrated success rates of 50% to 100%⁹; however, these studies frequently combine ILCs with other treatment modalities, and few studies have focused on the efficacy of ILC monotherapy in patients with SOC.^6,10-13

Antineoplastic Agents and Neuromodulators—Certain antineoplastic agents (eg, 5-fluorouracil [5-FU] and bleomycin) and neuromodulators (eg, botulinum toxin A [BTA]) also have been studied in keloid management.⁸

5-Fluorouracil frequently is combined with ILCs such as triamcinolone (TAC). Combined therapy is more effective than TAC monotherapy in scar height reduction.^14,15 Rates of adverse events such as dyspigmentation, atrophy, and telangiectasias also were lower in patients who received combined therapy.^14,15 A systematic review found that intralesional bleomycin may be more effective than TAC alone, 5-FU alone, TAC combined with 5-FU, and TAC combined with cryotherapy; however, hyperpigmentation was a common adverse event, occurring in roughly 70% (42/60) of patients.^16,17 Additionally, a 2024 meta-analysis evaluated 20 randomized controlled trials comprising 1114 patients treated with intralesional TAC, 5-FU, BTA, verapamil, and/or bleomycin. Botulinum toxin A and TAC plus 5-FU were found to have outstanding therapeutic efficacy for keloids, and rates of adverse events were similar among users of TAC, 5-FU, BTA, and TAC plus 5-FU.¹⁸

While antineoplastic agents and BTA may be promising keloid therapies, further studies demonstrating their efficacy and safety profiles are necessary, particularly regarding dyspigmentation as a potential adverse event, as this may be of concern in patients with darker phototypes.

Laser Therapies—Of all treatment modalities, laser-based keloid therapies have been the most robustly studied in SOC. The 2 main types are ablative (eg, CO₂, Er:YAG) and nonablative (eg, pulsed dye, Nd:YAG) lasers. Ablative lasers rapidly heat water molecules within the skin, thereby vaporizing the skin cells in a controlled precise process that reduces scar tissue by removing layers of skin. Nonablative lasers target hemoglobin in blood vessels, reducing oxygen supply and inducing collagen remodeling without damaging the epidermis.¹⁹

For patients with SOC, lasers carry a risk for postinflammatory hyperpigmentation.²⁰ To address this risk, recent advancements in laser technology and procedural protocols have aimed to minimize the number of passes and utilize cooling devices²¹; however, many of these recommendations are based on retrospective reviews and small case series. A 2024 meta-analysis comprising 550 patients found that the combination of fractional CO₂ laser therapy and 5-FU was the most effective intervention, markedly reducing Vancouver Scar Scale and pliability scores as well as keloid thickness.²² Conversely, pulsed dye lasers were the least effective in terms of improving scar thickness, pigmentation, and pliability when compared to other treatments.

Randomized controlled trials of laser-based therapies in patients with SOC are lacking in the literature. Future studies should focus on calibrating laser-based therapies for those with darker skin tones and examine the efficacy and adverse effects of ablative and nonablative lasers in patients with SOC.

Promising New Keloid Therapies

Keloid disease pathogenesis is incompletely understood, but several new therapeutic targets have been highlighted in the literature, including dupilumab, pentoxifylline, sirtuin 6 (SIRT6) modulators, remdesivir, and needle-assisted electrocoagulation plus pharmacotherapy.

Dupilumab—An anti–IL-4 and IL-13 monoclonal antibody, dupilumab was first approved for the treatment of severe atopic dermatitis. Its use has broadened since its approval, and keloids have been identified as a potential therapeutic target. A 2019 case study described a 53-year-old Black man with severe atopic dermatitis and chronic keloids that regressed with systemic dupilumab therapy.²³ This prompted a follow-up case-control study using real-time polymerase chain reaction testing to evaluate Th2 gene expression (IL-4R, IL-13, and CCL18) of lesional and nonlesional tissue in 3 Black patients with chronic keloids and no concurrent atopic dermatitis vs 5 healthy Black controls.Despite the limited sample size, a significant increase in IL-13 and the Th2 chemokine CCL18 was found in patients with keloids compared to controls (P<.05), suggesting that the entire integument of patients with severe keloids is abnormal.²³ This finding supports the use of systemic treatments for chronic and multifocal keloid disease. Several subsequent case reports have corroborated the efficacy of systemic and/or intralesional dupilumab.^24,25 However, some studies have reported contradictory findings, suggesting the need for high-quality clinical trials.^26,27

Pentoxifylline—Pentoxifylline is a methylated xanthine derivative and a nonspecific phosphodiesterase ­inhibitor used to treat claudication from peripheral artery disease. It also inhibits the proliferation and rate of collagen synthesis of fibroblasts from keloids in vitro.^28,29 A 2019 retrospective, open-label pilot study analyzed postsurgical keloid recurrence in 45 patients with 67 unique keloids that were stratified into low- and high-risk groups based on clinical factors including multiple symptomatic keloids, history of recurrence, and family history.³⁰ Both the low- and the high-risk groups were treated with 40 mg/mL intralesional triamcinolone acetonide monthly for 6 months; however, some of the high-risk keloids also received pentoxifylline 300 mg 3 times daily for 6 months. There was a statistically significant decrease in keloid recurrence rate between the high-risk group treated with pentoxifylline and the low-risk group for whom pentoxifylline was not prescribed (P=.015).

Similarly, a randomized clinical trial comparing the efficacy of combination intralesional pentoxifylline and intralesional triamcinolone vs monotherapy with pentoxifylline or triamcinolone found the most significant improvement in the combination cohort with reduction in keloid height (P=.04), pliability (P=.003), and vascularity (P=.05).³¹ These findings highlight the need for supplementary studies on the use of pentoxifylline for keloid therapy.

SIRT6 Modulators—SIRT6 modulators are an exciting future therapeutic target. In a recent case-control study evaluating the histologic milieu of keloid tissue vs normal skin specimens, the researchers found that selective overexpression of SIRT6 via the use of a recombinant adenovirus in keloid fibroblasts attenuated proliferation, invasion, and collagen synthesis while fostering apoptosis, likely through the suppression of MAPK/ERK pathway activity.³²

Remdesivir—The antiviral drug remdesivir has been reported to have pharmacologic activities in a wide range of fibrotic diseases, including keloids. A 2024 study explored the potential effect and mechanisms of remdesivir on skin fibrosis both in vitro and in rodents.³³ Remdesivir was found to decrease skin fibrosis and attenuate the gross weight of keloid tissues in vivo, suppress fibroblast activation and autophagy both in vivo and in vitro, dampen fibroblast activation by the TGF-β1/Smad signaling pathway, and inhibit fibroblasts autophagy by the PI3K/Akt/mTOR signaling pathway. These results demonstrate the therapeutic potential of remdesivir for keloid management.

Needle-Assisted Electrocoagulation Plus Pharmacotherapy—A novel needle-assisted electrocoagulation technique combined with pharmacotherapy (corticosteroid and 5-FU injections) was effective in a Chinese clinical trial involving 6 patients with keloids.³⁴ Investigators used Vancouver Scar Scale and both Patient and Observer Scar Assessment Scale scores to grade patients’ scars before treatment and 1 month after the first treatment cycle. They found that ablation combined with pharmacotherapy significantly reduced all 3 scores without any obvious adverse events (P=.004, P=.006, and P=.017, respectively). This novel combination treatment may serve as a safe and effective therapeutic approach for keloid removal.

Final Thoughts

Emerging treatments offer promising new horizons in keloid management; however, the lack of robust, high-quality clinical trials, especially those focusing on SOC, underscores a pressing need for comprehensive and inclusive studies. There is much work to be done to close the existing knowledge gap, and future studies must be more intentional with recruitment, assuring that the patients who are disproportionately affected by these lesions are represented in study populations.

Keloids are fibroproliferative lesions caused by aberrant wound healing in predisposed individuals.¹ While keloids have been reported in patients of all races and ethnicities, they most commonly develop in individuals of African or Asian descent.² Often associated with symptoms such as pain and itching, keloids can be disfiguring and result in poorer quality of life.³ There is a paucity of research on keloid pathogenesis and efficacious therapeutics, particularly in patients with skin of color (SOC). Herein, we outline the current research on keloid treatment and highlight promising new therapies ranging from innovative intralesional techniques to advanced laser-based and biologic therapies.

Deficiencies in Skin of Color Research

Although keloids are 17 times more prevalent in patients with SOC,⁴ there is a considerable lack of focus on this population in the literature.⁵ Studies on keloids that include individuals with SOC often group patients of all skin types together, and subgroup analyses are not always performed.^6,7 As a result, dermatologists may face considerable challenges in providing effective treatments for keloids in patients with SOC. With few evidence-based options available, patients with SOC who have keloids continue to experience impairments in quality of life.

Common Keloid Therapies

There currently is no gold-standard treatment for keloids. Common therapeutic modalities include intralesional corticosteroids (ILCs), antineoplastic agents and neuromodulators, laser-based devices, and surgical therapies (eg, excision), as well as combined medical and surgical techniques.⁸

Intralesional Corticosteroids—Minimally invasive ILCs are the first-line treatment in all patients with keloids, regardless of skin phototype. Because keloid formation results from trauma to the skin, ILCs often are recommended to minimize further skin damage.⁵ One meta-analysis found that ILCs have demonstrated success rates of 50% to 100%⁹; however, these studies frequently combine ILCs with other treatment modalities, and few studies have focused on the efficacy of ILC monotherapy in patients with SOC.^6,10-13

Antineoplastic Agents and Neuromodulators—Certain antineoplastic agents (eg, 5-fluorouracil [5-FU] and bleomycin) and neuromodulators (eg, botulinum toxin A [BTA]) also have been studied in keloid management.⁸

5-Fluorouracil frequently is combined with ILCs such as triamcinolone (TAC). Combined therapy is more effective than TAC monotherapy in scar height reduction.^14,15 Rates of adverse events such as dyspigmentation, atrophy, and telangiectasias also were lower in patients who received combined therapy.^14,15 A systematic review found that intralesional bleomycin may be more effective than TAC alone, 5-FU alone, TAC combined with 5-FU, and TAC combined with cryotherapy; however, hyperpigmentation was a common adverse event, occurring in roughly 70% (42/60) of patients.^16,17 Additionally, a 2024 meta-analysis evaluated 20 randomized controlled trials comprising 1114 patients treated with intralesional TAC, 5-FU, BTA, verapamil, and/or bleomycin. Botulinum toxin A and TAC plus 5-FU were found to have outstanding therapeutic efficacy for keloids, and rates of adverse events were similar among users of TAC, 5-FU, BTA, and TAC plus 5-FU.¹⁸

While antineoplastic agents and BTA may be promising keloid therapies, further studies demonstrating their efficacy and safety profiles are necessary, particularly regarding dyspigmentation as a potential adverse event, as this may be of concern in patients with darker phototypes.

Laser Therapies—Of all treatment modalities, laser-based keloid therapies have been the most robustly studied in SOC. The 2 main types are ablative (eg, CO₂, Er:YAG) and nonablative (eg, pulsed dye, Nd:YAG) lasers. Ablative lasers rapidly heat water molecules within the skin, thereby vaporizing the skin cells in a controlled precise process that reduces scar tissue by removing layers of skin. Nonablative lasers target hemoglobin in blood vessels, reducing oxygen supply and inducing collagen remodeling without damaging the epidermis.¹⁹

For patients with SOC, lasers carry a risk for postinflammatory hyperpigmentation.²⁰ To address this risk, recent advancements in laser technology and procedural protocols have aimed to minimize the number of passes and utilize cooling devices²¹; however, many of these recommendations are based on retrospective reviews and small case series. A 2024 meta-analysis comprising 550 patients found that the combination of fractional CO₂ laser therapy and 5-FU was the most effective intervention, markedly reducing Vancouver Scar Scale and pliability scores as well as keloid thickness.²² Conversely, pulsed dye lasers were the least effective in terms of improving scar thickness, pigmentation, and pliability when compared to other treatments.

Randomized controlled trials of laser-based therapies in patients with SOC are lacking in the literature. Future studies should focus on calibrating laser-based therapies for those with darker skin tones and examine the efficacy and adverse effects of ablative and nonablative lasers in patients with SOC.

Promising New Keloid Therapies

Keloid disease pathogenesis is incompletely understood, but several new therapeutic targets have been highlighted in the literature, including dupilumab, pentoxifylline, sirtuin 6 (SIRT6) modulators, remdesivir, and needle-assisted electrocoagulation plus pharmacotherapy.

Dupilumab—An anti–IL-4 and IL-13 monoclonal antibody, dupilumab was first approved for the treatment of severe atopic dermatitis. Its use has broadened since its approval, and keloids have been identified as a potential therapeutic target. A 2019 case study described a 53-year-old Black man with severe atopic dermatitis and chronic keloids that regressed with systemic dupilumab therapy.²³ This prompted a follow-up case-control study using real-time polymerase chain reaction testing to evaluate Th2 gene expression (IL-4R, IL-13, and CCL18) of lesional and nonlesional tissue in 3 Black patients with chronic keloids and no concurrent atopic dermatitis vs 5 healthy Black controls.Despite the limited sample size, a significant increase in IL-13 and the Th2 chemokine CCL18 was found in patients with keloids compared to controls (P<.05), suggesting that the entire integument of patients with severe keloids is abnormal.²³ This finding supports the use of systemic treatments for chronic and multifocal keloid disease. Several subsequent case reports have corroborated the efficacy of systemic and/or intralesional dupilumab.^24,25 However, some studies have reported contradictory findings, suggesting the need for high-quality clinical trials.^26,27

Pentoxifylline—Pentoxifylline is a methylated xanthine derivative and a nonspecific phosphodiesterase ­inhibitor used to treat claudication from peripheral artery disease. It also inhibits the proliferation and rate of collagen synthesis of fibroblasts from keloids in vitro.^28,29 A 2019 retrospective, open-label pilot study analyzed postsurgical keloid recurrence in 45 patients with 67 unique keloids that were stratified into low- and high-risk groups based on clinical factors including multiple symptomatic keloids, history of recurrence, and family history.³⁰ Both the low- and the high-risk groups were treated with 40 mg/mL intralesional triamcinolone acetonide monthly for 6 months; however, some of the high-risk keloids also received pentoxifylline 300 mg 3 times daily for 6 months. There was a statistically significant decrease in keloid recurrence rate between the high-risk group treated with pentoxifylline and the low-risk group for whom pentoxifylline was not prescribed (P=.015).

Similarly, a randomized clinical trial comparing the efficacy of combination intralesional pentoxifylline and intralesional triamcinolone vs monotherapy with pentoxifylline or triamcinolone found the most significant improvement in the combination cohort with reduction in keloid height (P=.04), pliability (P=.003), and vascularity (P=.05).³¹ These findings highlight the need for supplementary studies on the use of pentoxifylline for keloid therapy.

SIRT6 Modulators—SIRT6 modulators are an exciting future therapeutic target. In a recent case-control study evaluating the histologic milieu of keloid tissue vs normal skin specimens, the researchers found that selective overexpression of SIRT6 via the use of a recombinant adenovirus in keloid fibroblasts attenuated proliferation, invasion, and collagen synthesis while fostering apoptosis, likely through the suppression of MAPK/ERK pathway activity.³²

Remdesivir—The antiviral drug remdesivir has been reported to have pharmacologic activities in a wide range of fibrotic diseases, including keloids. A 2024 study explored the potential effect and mechanisms of remdesivir on skin fibrosis both in vitro and in rodents.³³ Remdesivir was found to decrease skin fibrosis and attenuate the gross weight of keloid tissues in vivo, suppress fibroblast activation and autophagy both in vivo and in vitro, dampen fibroblast activation by the TGF-β1/Smad signaling pathway, and inhibit fibroblasts autophagy by the PI3K/Akt/mTOR signaling pathway. These results demonstrate the therapeutic potential of remdesivir for keloid management.

Needle-Assisted Electrocoagulation Plus Pharmacotherapy—A novel needle-assisted electrocoagulation technique combined with pharmacotherapy (corticosteroid and 5-FU injections) was effective in a Chinese clinical trial involving 6 patients with keloids.³⁴ Investigators used Vancouver Scar Scale and both Patient and Observer Scar Assessment Scale scores to grade patients’ scars before treatment and 1 month after the first treatment cycle. They found that ablation combined with pharmacotherapy significantly reduced all 3 scores without any obvious adverse events (P=.004, P=.006, and P=.017, respectively). This novel combination treatment may serve as a safe and effective therapeutic approach for keloid removal.

Final Thoughts

Emerging treatments offer promising new horizons in keloid management; however, the lack of robust, high-quality clinical trials, especially those focusing on SOC, underscores a pressing need for comprehensive and inclusive studies. There is much work to be done to close the existing knowledge gap, and future studies must be more intentional with recruitment, assuring that the patients who are disproportionately affected by these lesions are represented in study populations.

Keloids are fibroproliferative lesions caused by aberrant wound healing in predisposed individuals.¹ While keloids have been reported in patients of all races and ethnicities, they most commonly develop in individuals of African or Asian descent.² Often associated with symptoms such as pain and itching, keloids can be disfiguring and result in poorer quality of life.³ There is a paucity of research on keloid pathogenesis and efficacious therapeutics, particularly in patients with skin of color (SOC). Herein, we outline the current research on keloid treatment and highlight promising new therapies ranging from innovative intralesional techniques to advanced laser-based and biologic therapies.

Deficiencies in Skin of Color Research

Although keloids are 17 times more prevalent in patients with SOC,⁴ there is a considerable lack of focus on this population in the literature.⁵ Studies on keloids that include individuals with SOC often group patients of all skin types together, and subgroup analyses are not always performed.^6,7 As a result, dermatologists may face considerable challenges in providing effective treatments for keloids in patients with SOC. With few evidence-based options available, patients with SOC who have keloids continue to experience impairments in quality of life.

Common Keloid Therapies

There currently is no gold-standard treatment for keloids. Common therapeutic modalities include intralesional corticosteroids (ILCs), antineoplastic agents and neuromodulators, laser-based devices, and surgical therapies (eg, excision), as well as combined medical and surgical techniques.⁸

Intralesional Corticosteroids—Minimally invasive ILCs are the first-line treatment in all patients with keloids, regardless of skin phototype. Because keloid formation results from trauma to the skin, ILCs often are recommended to minimize further skin damage.⁵ One meta-analysis found that ILCs have demonstrated success rates of 50% to 100%⁹; however, these studies frequently combine ILCs with other treatment modalities, and few studies have focused on the efficacy of ILC monotherapy in patients with SOC.^6,10-13

Antineoplastic Agents and Neuromodulators—Certain antineoplastic agents (eg, 5-fluorouracil [5-FU] and bleomycin) and neuromodulators (eg, botulinum toxin A [BTA]) also have been studied in keloid management.⁸

5-Fluorouracil frequently is combined with ILCs such as triamcinolone (TAC). Combined therapy is more effective than TAC monotherapy in scar height reduction.^14,15 Rates of adverse events such as dyspigmentation, atrophy, and telangiectasias also were lower in patients who received combined therapy.^14,15 A systematic review found that intralesional bleomycin may be more effective than TAC alone, 5-FU alone, TAC combined with 5-FU, and TAC combined with cryotherapy; however, hyperpigmentation was a common adverse event, occurring in roughly 70% (42/60) of patients.^16,17 Additionally, a 2024 meta-analysis evaluated 20 randomized controlled trials comprising 1114 patients treated with intralesional TAC, 5-FU, BTA, verapamil, and/or bleomycin. Botulinum toxin A and TAC plus 5-FU were found to have outstanding therapeutic efficacy for keloids, and rates of adverse events were similar among users of TAC, 5-FU, BTA, and TAC plus 5-FU.¹⁸

While antineoplastic agents and BTA may be promising keloid therapies, further studies demonstrating their efficacy and safety profiles are necessary, particularly regarding dyspigmentation as a potential adverse event, as this may be of concern in patients with darker phototypes.

Laser Therapies—Of all treatment modalities, laser-based keloid therapies have been the most robustly studied in SOC. The 2 main types are ablative (eg, CO₂, Er:YAG) and nonablative (eg, pulsed dye, Nd:YAG) lasers. Ablative lasers rapidly heat water molecules within the skin, thereby vaporizing the skin cells in a controlled precise process that reduces scar tissue by removing layers of skin. Nonablative lasers target hemoglobin in blood vessels, reducing oxygen supply and inducing collagen remodeling without damaging the epidermis.¹⁹

For patients with SOC, lasers carry a risk for postinflammatory hyperpigmentation.²⁰ To address this risk, recent advancements in laser technology and procedural protocols have aimed to minimize the number of passes and utilize cooling devices²¹; however, many of these recommendations are based on retrospective reviews and small case series. A 2024 meta-analysis comprising 550 patients found that the combination of fractional CO₂ laser therapy and 5-FU was the most effective intervention, markedly reducing Vancouver Scar Scale and pliability scores as well as keloid thickness.²² Conversely, pulsed dye lasers were the least effective in terms of improving scar thickness, pigmentation, and pliability when compared to other treatments.

Randomized controlled trials of laser-based therapies in patients with SOC are lacking in the literature. Future studies should focus on calibrating laser-based therapies for those with darker skin tones and examine the efficacy and adverse effects of ablative and nonablative lasers in patients with SOC.

Promising New Keloid Therapies

Keloid disease pathogenesis is incompletely understood, but several new therapeutic targets have been highlighted in the literature, including dupilumab, pentoxifylline, sirtuin 6 (SIRT6) modulators, remdesivir, and needle-assisted electrocoagulation plus pharmacotherapy.

Dupilumab—An anti–IL-4 and IL-13 monoclonal antibody, dupilumab was first approved for the treatment of severe atopic dermatitis. Its use has broadened since its approval, and keloids have been identified as a potential therapeutic target. A 2019 case study described a 53-year-old Black man with severe atopic dermatitis and chronic keloids that regressed with systemic dupilumab therapy.²³ This prompted a follow-up case-control study using real-time polymerase chain reaction testing to evaluate Th2 gene expression (IL-4R, IL-13, and CCL18) of lesional and nonlesional tissue in 3 Black patients with chronic keloids and no concurrent atopic dermatitis vs 5 healthy Black controls.Despite the limited sample size, a significant increase in IL-13 and the Th2 chemokine CCL18 was found in patients with keloids compared to controls (P<.05), suggesting that the entire integument of patients with severe keloids is abnormal.²³ This finding supports the use of systemic treatments for chronic and multifocal keloid disease. Several subsequent case reports have corroborated the efficacy of systemic and/or intralesional dupilumab.^24,25 However, some studies have reported contradictory findings, suggesting the need for high-quality clinical trials.^26,27

Pentoxifylline—Pentoxifylline is a methylated xanthine derivative and a nonspecific phosphodiesterase ­inhibitor used to treat claudication from peripheral artery disease. It also inhibits the proliferation and rate of collagen synthesis of fibroblasts from keloids in vitro.^28,29 A 2019 retrospective, open-label pilot study analyzed postsurgical keloid recurrence in 45 patients with 67 unique keloids that were stratified into low- and high-risk groups based on clinical factors including multiple symptomatic keloids, history of recurrence, and family history.³⁰ Both the low- and the high-risk groups were treated with 40 mg/mL intralesional triamcinolone acetonide monthly for 6 months; however, some of the high-risk keloids also received pentoxifylline 300 mg 3 times daily for 6 months. There was a statistically significant decrease in keloid recurrence rate between the high-risk group treated with pentoxifylline and the low-risk group for whom pentoxifylline was not prescribed (P=.015).

Similarly, a randomized clinical trial comparing the efficacy of combination intralesional pentoxifylline and intralesional triamcinolone vs monotherapy with pentoxifylline or triamcinolone found the most significant improvement in the combination cohort with reduction in keloid height (P=.04), pliability (P=.003), and vascularity (P=.05).³¹ These findings highlight the need for supplementary studies on the use of pentoxifylline for keloid therapy.

SIRT6 Modulators—SIRT6 modulators are an exciting future therapeutic target. In a recent case-control study evaluating the histologic milieu of keloid tissue vs normal skin specimens, the researchers found that selective overexpression of SIRT6 via the use of a recombinant adenovirus in keloid fibroblasts attenuated proliferation, invasion, and collagen synthesis while fostering apoptosis, likely through the suppression of MAPK/ERK pathway activity.³²

Remdesivir—The antiviral drug remdesivir has been reported to have pharmacologic activities in a wide range of fibrotic diseases, including keloids. A 2024 study explored the potential effect and mechanisms of remdesivir on skin fibrosis both in vitro and in rodents.³³ Remdesivir was found to decrease skin fibrosis and attenuate the gross weight of keloid tissues in vivo, suppress fibroblast activation and autophagy both in vivo and in vitro, dampen fibroblast activation by the TGF-β1/Smad signaling pathway, and inhibit fibroblasts autophagy by the PI3K/Akt/mTOR signaling pathway. These results demonstrate the therapeutic potential of remdesivir for keloid management.

Needle-Assisted Electrocoagulation Plus Pharmacotherapy—A novel needle-assisted electrocoagulation technique combined with pharmacotherapy (corticosteroid and 5-FU injections) was effective in a Chinese clinical trial involving 6 patients with keloids.³⁴ Investigators used Vancouver Scar Scale and both Patient and Observer Scar Assessment Scale scores to grade patients’ scars before treatment and 1 month after the first treatment cycle. They found that ablation combined with pharmacotherapy significantly reduced all 3 scores without any obvious adverse events (P=.004, P=.006, and P=.017, respectively). This novel combination treatment may serve as a safe and effective therapeutic approach for keloid removal.

Final Thoughts

Emerging treatments offer promising new horizons in keloid management; however, the lack of robust, high-quality clinical trials, especially those focusing on SOC, underscores a pressing need for comprehensive and inclusive studies. There is much work to be done to close the existing knowledge gap, and future studies must be more intentional with recruitment, assuring that the patients who are disproportionately affected by these lesions are represented in study populations.

The American Contact Dermatitis Society (ACDS) selected sulfites as the 2024 Allergen of the Year.¹ Due to their preservative and antioxidant properties, sulfites are prevalent in a variety of foods, beverages, medications, and personal care products; however, sulfites also have been implicated as a potential contact allergen. In this article, we review common sources of sulfite exposure, clinical manifestations of allergic contact dermatitis (ACD) to sulfites, and patch testing considerations for this emerging allergen.

What Are Sulfites?

Sulfiting agents are compounds that contain the sulfite ion SO₃^2-, including sulfur dioxide, sodium disulfite (sodium metabisulfite), and potassium metabisulfite.² Sulfites occur naturally in the environment and commonly are used as preservatives, antibrowning agents, and antioxidants in various foods, beverages, medications, cosmetics, and skin care products. As antibrowning agents and antioxidants, sulfites help maintain the natural appearance of foods and other products and prevent premature spoiling by inactivating oxidative enzymes.³ It should be noted that sulfites and sulfates are distinct and unrelated compounds that do not cross-react.¹

Common Sources of Sulfite Exposure

From a morning glass of juice to an evening shower, in the pharmacy and at the hair salon, sulfite exposure is ubiquitous in most daily routines. Sulfites are present in many foods and beverages, either as a byproduct of natural fermentation or as an additive to prevent spoiling and color change. The Table provides examples of foods with high sulfite content.^1,4-6 In particular, dried fruit, bottled lemon juice, wine, grape juice, sauerkraut juice, and pickled onions have high sulfite content.

Topical medications and personal care products represent other potential sources of sulfite exposure. A number of reports have shown that sulfites may be included in topical steroids,⁷ antibiotics,⁸ antifungals,⁹ hemorrhoidal preparations,¹⁰ local anesthetics,¹¹ and urinary catheterization gel,¹² highlighting their many potential applications. In addition, a comprehensive ingredient analysis of 264 ophthalmic medications found that 3.8% of the products contained sodium disulfite.¹³ Sulfites may be found in personal care products, including facial and hand cleansers, shampoos, moisturizers, and toothpastes. Hair dyes also commonly contain sulfites,⁷ which are listed in as many as 90% of hair dye kits in the ACDS Contact Allergen Management Program database.¹

Occupational exposures also are widespread, as sulfites are extensively utilized across diverse industries such as pharmaceuticals, health care, leather manufacturing, mineral extraction, food preparation, chemical manufacturing, textiles, alcohol brewing, and wine production.¹

Sulfites also are used in the rubber industry—­particularly in gloves—due to their anticoagulant and preservative properties.⁴ This is relevant to health care providers, who may use dozens of disposable gloves in a single day. In an experimental pilot study, ­researchers detected sulfites in 83% (5/6) of natural rubber latex gloves, 96% (23/24) of synthetic (nitrile) gloves, and 0% (0/5) of polyvinyl chloride gloves.¹⁴ While this study was limited to a small sample size, it demonstrates the common use of sulfites in certain rubber gloves and encourages future studies to determine whether there is a quantitative threshold to elicit allergic reactions.

Sulfite Allergy

In 1968, an early case report of ACD to sulfites was published involving a pharmaceutical worker who developed hand eczema after working at a factory for 3 months and had a positive patch test to potassium metabisulfite.¹⁵ There have been other cases published in the literature since then, including localized ACD as well as less common cases of systemic contact dermatitis following oral, injectable, and rectal sulfite exposures.¹⁶

The North American Contact Dermatitis Group found that, among 132 (2.7%) of 4885 patients with positive patch tests to sodium disulfite from 2017 to 2018, the most commonly involved body sites were the face (28.8%) and hands (20.5%) followed by a scattered/generalized distribution (13.6%). Involvement of the face and hands may correlate with the most frequent sources of exposure that were identified, including personal care products (particularly hair dyes)(18.9%), medications (9.1%), and foods (7.6%).¹⁷ A multicenter analysis of patch test results from Germany, Austria, and Switzerland from 1999 to 2013 showed that 357 (2.9%) of 12,156 patients had positive reactions to sodium disulfite, with the most commonly identified exposure sources being topical pharmaceutical agents (59.3%); cosmetics, creams, and sunscreens (13.6%); and systemic drugs (6.8%).¹⁸ However, it is not always possible to determine the clinical relevance of a positive patch test to sulfites.¹

Other than the face and hands, there have been other unexpected anatomic locations for sulfite ACD (eg, the lower back), and systemic contact dermatitis has manifested with widespread rashes due to oral, rectal, and parenteral exposure.^4,16,19 There is no definitive link between sulfite contact allergy and patient sex, but there seems to be a higher prevalence in patients older than 40 years, perhaps related to overall lifetime exposure.¹

Immediate hypersensitivity reactions to sulfites also have been reported, including urticaria, angioedema, and anaphylaxis.⁴ Due to multiple cases of severe dermatologic and respiratory reactions to food products containing sulfites,²⁰ the US Food and Drug Administration prohibited their use in fresh fruit and vegetables as antibrowning agents in 1986 and required labels on packaged foods that contained sulfites at more than 10 parts per million.²¹ However, food and drinks produced in restaurants, bakeries, and cafes as well as those that are distributed directly to consumers from the preparation site are exempt from these rules.¹⁷

In addition, consuming high amounts of dietary sulfites has been linked to headaches through unclear (ie, not necessarily allergic) mechanisms.^4,22 One study found that wine with a higher sulfite concentration was associated with increased risk for headaches in participants who had a history of headaches related to wine consumption.²²

Patch Testing to Sulfites

The North American Contact Dermatitis Group has tested sodium disulfite since 2017 and found an increased frequency of positive patch tests from 2.7% (N=4885) in 2017 and 2018¹⁷ to 3.3% (N=4115) in 2019 and 2020²³ among patients referred for testing. Similarly, patch testing to sodium disulfite in nearly 40,000 patients in 9 European countries showed a pooled prevalence of reactions of 3.1%.¹⁷ However, this contact allergy may go unrecognized, as sulfites are not included in common patch test series, including the thin-layer rapid use epicutaneous test and the ACDS Core Allergen Series.^24,25 The relatively high patch test positivity to sulfites along with the prevalence of daily exposures supports the addition of sulfites to more patch test screening series.

The recommended patch test concentration for sodium disulfite is 1% in petrolatum.⁵ Testing in aqueous solutions is not recommended because they can cause sulfites to break down, potentially producing false-positive or irritant patch test reactions.^7,26,27

Recommendations for Patients With Sulfite Allergies

Individuals with contact allergies to sulfites should be counseled on exposure sources and should be given resources providing a list of safe products, such as the ACDS Contact Allergen Management Program (https://www.acdscamp.org/login) or SkinSAFE ­(https://www.skinsafeproducts.com/). Prescribers should be cognizant of sulfites that are present in prescription medications. Just because a patient has a positive patch test to sulfites does not automatically imply that they will need to modify their diet to avoid sulfite-containing foods; in the absence of cheilitis or a distribution suggestive of systemic contact dermatitis (eg, vesicular hand/foot dermatitis, intertriginous eruptions), this step may be unnecessary. On the other hand, individuals who have experienced immediate hypersensitivity reactions to sulfites should avoid sulfite-containing foods and carry an epinephrine autoinjector.

Final Interpretation

Sulfites are ubiquitous compounds found in various foods, beverages, medications, and personal care products in addition to a range of occupational exposures. The face and hands are the most common sites of sulfite ACD. Despite patch test positivity in as many as 3% of tested patients,^17,23 sulfite allergy may be missed due to lack of routine testing on standard screening series.

The American Contact Dermatitis Society (ACDS) selected sulfites as the 2024 Allergen of the Year.¹ Due to their preservative and antioxidant properties, sulfites are prevalent in a variety of foods, beverages, medications, and personal care products; however, sulfites also have been implicated as a potential contact allergen. In this article, we review common sources of sulfite exposure, clinical manifestations of allergic contact dermatitis (ACD) to sulfites, and patch testing considerations for this emerging allergen.

What Are Sulfites?

Sulfiting agents are compounds that contain the sulfite ion SO₃^2-, including sulfur dioxide, sodium disulfite (sodium metabisulfite), and potassium metabisulfite.² Sulfites occur naturally in the environment and commonly are used as preservatives, antibrowning agents, and antioxidants in various foods, beverages, medications, cosmetics, and skin care products. As antibrowning agents and antioxidants, sulfites help maintain the natural appearance of foods and other products and prevent premature spoiling by inactivating oxidative enzymes.³ It should be noted that sulfites and sulfates are distinct and unrelated compounds that do not cross-react.¹

Common Sources of Sulfite Exposure

From a morning glass of juice to an evening shower, in the pharmacy and at the hair salon, sulfite exposure is ubiquitous in most daily routines. Sulfites are present in many foods and beverages, either as a byproduct of natural fermentation or as an additive to prevent spoiling and color change. The Table provides examples of foods with high sulfite content.^1,4-6 In particular, dried fruit, bottled lemon juice, wine, grape juice, sauerkraut juice, and pickled onions have high sulfite content.

Topical medications and personal care products represent other potential sources of sulfite exposure. A number of reports have shown that sulfites may be included in topical steroids,⁷ antibiotics,⁸ antifungals,⁹ hemorrhoidal preparations,¹⁰ local anesthetics,¹¹ and urinary catheterization gel,¹² highlighting their many potential applications. In addition, a comprehensive ingredient analysis of 264 ophthalmic medications found that 3.8% of the products contained sodium disulfite.¹³ Sulfites may be found in personal care products, including facial and hand cleansers, shampoos, moisturizers, and toothpastes. Hair dyes also commonly contain sulfites,⁷ which are listed in as many as 90% of hair dye kits in the ACDS Contact Allergen Management Program database.¹

Occupational exposures also are widespread, as sulfites are extensively utilized across diverse industries such as pharmaceuticals, health care, leather manufacturing, mineral extraction, food preparation, chemical manufacturing, textiles, alcohol brewing, and wine production.¹

Sulfites also are used in the rubber industry—­particularly in gloves—due to their anticoagulant and preservative properties.⁴ This is relevant to health care providers, who may use dozens of disposable gloves in a single day. In an experimental pilot study, ­researchers detected sulfites in 83% (5/6) of natural rubber latex gloves, 96% (23/24) of synthetic (nitrile) gloves, and 0% (0/5) of polyvinyl chloride gloves.¹⁴ While this study was limited to a small sample size, it demonstrates the common use of sulfites in certain rubber gloves and encourages future studies to determine whether there is a quantitative threshold to elicit allergic reactions.

Sulfite Allergy

In 1968, an early case report of ACD to sulfites was published involving a pharmaceutical worker who developed hand eczema after working at a factory for 3 months and had a positive patch test to potassium metabisulfite.¹⁵ There have been other cases published in the literature since then, including localized ACD as well as less common cases of systemic contact dermatitis following oral, injectable, and rectal sulfite exposures.¹⁶

The North American Contact Dermatitis Group found that, among 132 (2.7%) of 4885 patients with positive patch tests to sodium disulfite from 2017 to 2018, the most commonly involved body sites were the face (28.8%) and hands (20.5%) followed by a scattered/generalized distribution (13.6%). Involvement of the face and hands may correlate with the most frequent sources of exposure that were identified, including personal care products (particularly hair dyes)(18.9%), medications (9.1%), and foods (7.6%).¹⁷ A multicenter analysis of patch test results from Germany, Austria, and Switzerland from 1999 to 2013 showed that 357 (2.9%) of 12,156 patients had positive reactions to sodium disulfite, with the most commonly identified exposure sources being topical pharmaceutical agents (59.3%); cosmetics, creams, and sunscreens (13.6%); and systemic drugs (6.8%).¹⁸ However, it is not always possible to determine the clinical relevance of a positive patch test to sulfites.¹

Other than the face and hands, there have been other unexpected anatomic locations for sulfite ACD (eg, the lower back), and systemic contact dermatitis has manifested with widespread rashes due to oral, rectal, and parenteral exposure.^4,16,19 There is no definitive link between sulfite contact allergy and patient sex, but there seems to be a higher prevalence in patients older than 40 years, perhaps related to overall lifetime exposure.¹

Immediate hypersensitivity reactions to sulfites also have been reported, including urticaria, angioedema, and anaphylaxis.⁴ Due to multiple cases of severe dermatologic and respiratory reactions to food products containing sulfites,²⁰ the US Food and Drug Administration prohibited their use in fresh fruit and vegetables as antibrowning agents in 1986 and required labels on packaged foods that contained sulfites at more than 10 parts per million.²¹ However, food and drinks produced in restaurants, bakeries, and cafes as well as those that are distributed directly to consumers from the preparation site are exempt from these rules.¹⁷

In addition, consuming high amounts of dietary sulfites has been linked to headaches through unclear (ie, not necessarily allergic) mechanisms.^4,22 One study found that wine with a higher sulfite concentration was associated with increased risk for headaches in participants who had a history of headaches related to wine consumption.²²

Patch Testing to Sulfites

The North American Contact Dermatitis Group has tested sodium disulfite since 2017 and found an increased frequency of positive patch tests from 2.7% (N=4885) in 2017 and 2018¹⁷ to 3.3% (N=4115) in 2019 and 2020²³ among patients referred for testing. Similarly, patch testing to sodium disulfite in nearly 40,000 patients in 9 European countries showed a pooled prevalence of reactions of 3.1%.¹⁷ However, this contact allergy may go unrecognized, as sulfites are not included in common patch test series, including the thin-layer rapid use epicutaneous test and the ACDS Core Allergen Series.^24,25 The relatively high patch test positivity to sulfites along with the prevalence of daily exposures supports the addition of sulfites to more patch test screening series.

The recommended patch test concentration for sodium disulfite is 1% in petrolatum.⁵ Testing in aqueous solutions is not recommended because they can cause sulfites to break down, potentially producing false-positive or irritant patch test reactions.^7,26,27

Recommendations for Patients With Sulfite Allergies

Individuals with contact allergies to sulfites should be counseled on exposure sources and should be given resources providing a list of safe products, such as the ACDS Contact Allergen Management Program (https://www.acdscamp.org/login) or SkinSAFE ­(https://www.skinsafeproducts.com/). Prescribers should be cognizant of sulfites that are present in prescription medications. Just because a patient has a positive patch test to sulfites does not automatically imply that they will need to modify their diet to avoid sulfite-containing foods; in the absence of cheilitis or a distribution suggestive of systemic contact dermatitis (eg, vesicular hand/foot dermatitis, intertriginous eruptions), this step may be unnecessary. On the other hand, individuals who have experienced immediate hypersensitivity reactions to sulfites should avoid sulfite-containing foods and carry an epinephrine autoinjector.

Final Interpretation

Sulfites are ubiquitous compounds found in various foods, beverages, medications, and personal care products in addition to a range of occupational exposures. The face and hands are the most common sites of sulfite ACD. Despite patch test positivity in as many as 3% of tested patients,^17,23 sulfite allergy may be missed due to lack of routine testing on standard screening series.

The American Contact Dermatitis Society (ACDS) selected sulfites as the 2024 Allergen of the Year.¹ Due to their preservative and antioxidant properties, sulfites are prevalent in a variety of foods, beverages, medications, and personal care products; however, sulfites also have been implicated as a potential contact allergen. In this article, we review common sources of sulfite exposure, clinical manifestations of allergic contact dermatitis (ACD) to sulfites, and patch testing considerations for this emerging allergen.

What Are Sulfites?

Sulfiting agents are compounds that contain the sulfite ion SO₃^2-, including sulfur dioxide, sodium disulfite (sodium metabisulfite), and potassium metabisulfite.² Sulfites occur naturally in the environment and commonly are used as preservatives, antibrowning agents, and antioxidants in various foods, beverages, medications, cosmetics, and skin care products. As antibrowning agents and antioxidants, sulfites help maintain the natural appearance of foods and other products and prevent premature spoiling by inactivating oxidative enzymes.³ It should be noted that sulfites and sulfates are distinct and unrelated compounds that do not cross-react.¹

Common Sources of Sulfite Exposure

From a morning glass of juice to an evening shower, in the pharmacy and at the hair salon, sulfite exposure is ubiquitous in most daily routines. Sulfites are present in many foods and beverages, either as a byproduct of natural fermentation or as an additive to prevent spoiling and color change. The Table provides examples of foods with high sulfite content.^1,4-6 In particular, dried fruit, bottled lemon juice, wine, grape juice, sauerkraut juice, and pickled onions have high sulfite content.

Topical medications and personal care products represent other potential sources of sulfite exposure. A number of reports have shown that sulfites may be included in topical steroids,⁷ antibiotics,⁸ antifungals,⁹ hemorrhoidal preparations,¹⁰ local anesthetics,¹¹ and urinary catheterization gel,¹² highlighting their many potential applications. In addition, a comprehensive ingredient analysis of 264 ophthalmic medications found that 3.8% of the products contained sodium disulfite.¹³ Sulfites may be found in personal care products, including facial and hand cleansers, shampoos, moisturizers, and toothpastes. Hair dyes also commonly contain sulfites,⁷ which are listed in as many as 90% of hair dye kits in the ACDS Contact Allergen Management Program database.¹

Occupational exposures also are widespread, as sulfites are extensively utilized across diverse industries such as pharmaceuticals, health care, leather manufacturing, mineral extraction, food preparation, chemical manufacturing, textiles, alcohol brewing, and wine production.¹

Sulfites also are used in the rubber industry—­particularly in gloves—due to their anticoagulant and preservative properties.⁴ This is relevant to health care providers, who may use dozens of disposable gloves in a single day. In an experimental pilot study, ­researchers detected sulfites in 83% (5/6) of natural rubber latex gloves, 96% (23/24) of synthetic (nitrile) gloves, and 0% (0/5) of polyvinyl chloride gloves.¹⁴ While this study was limited to a small sample size, it demonstrates the common use of sulfites in certain rubber gloves and encourages future studies to determine whether there is a quantitative threshold to elicit allergic reactions.

Sulfite Allergy

In 1968, an early case report of ACD to sulfites was published involving a pharmaceutical worker who developed hand eczema after working at a factory for 3 months and had a positive patch test to potassium metabisulfite.¹⁵ There have been other cases published in the literature since then, including localized ACD as well as less common cases of systemic contact dermatitis following oral, injectable, and rectal sulfite exposures.¹⁶

The North American Contact Dermatitis Group found that, among 132 (2.7%) of 4885 patients with positive patch tests to sodium disulfite from 2017 to 2018, the most commonly involved body sites were the face (28.8%) and hands (20.5%) followed by a scattered/generalized distribution (13.6%). Involvement of the face and hands may correlate with the most frequent sources of exposure that were identified, including personal care products (particularly hair dyes)(18.9%), medications (9.1%), and foods (7.6%).¹⁷ A multicenter analysis of patch test results from Germany, Austria, and Switzerland from 1999 to 2013 showed that 357 (2.9%) of 12,156 patients had positive reactions to sodium disulfite, with the most commonly identified exposure sources being topical pharmaceutical agents (59.3%); cosmetics, creams, and sunscreens (13.6%); and systemic drugs (6.8%).¹⁸ However, it is not always possible to determine the clinical relevance of a positive patch test to sulfites.¹

Other than the face and hands, there have been other unexpected anatomic locations for sulfite ACD (eg, the lower back), and systemic contact dermatitis has manifested with widespread rashes due to oral, rectal, and parenteral exposure.^4,16,19 There is no definitive link between sulfite contact allergy and patient sex, but there seems to be a higher prevalence in patients older than 40 years, perhaps related to overall lifetime exposure.¹

Immediate hypersensitivity reactions to sulfites also have been reported, including urticaria, angioedema, and anaphylaxis.⁴ Due to multiple cases of severe dermatologic and respiratory reactions to food products containing sulfites,²⁰ the US Food and Drug Administration prohibited their use in fresh fruit and vegetables as antibrowning agents in 1986 and required labels on packaged foods that contained sulfites at more than 10 parts per million.²¹ However, food and drinks produced in restaurants, bakeries, and cafes as well as those that are distributed directly to consumers from the preparation site are exempt from these rules.¹⁷

In addition, consuming high amounts of dietary sulfites has been linked to headaches through unclear (ie, not necessarily allergic) mechanisms.^4,22 One study found that wine with a higher sulfite concentration was associated with increased risk for headaches in participants who had a history of headaches related to wine consumption.²²

Patch Testing to Sulfites

The North American Contact Dermatitis Group has tested sodium disulfite since 2017 and found an increased frequency of positive patch tests from 2.7% (N=4885) in 2017 and 2018¹⁷ to 3.3% (N=4115) in 2019 and 2020²³ among patients referred for testing. Similarly, patch testing to sodium disulfite in nearly 40,000 patients in 9 European countries showed a pooled prevalence of reactions of 3.1%.¹⁷ However, this contact allergy may go unrecognized, as sulfites are not included in common patch test series, including the thin-layer rapid use epicutaneous test and the ACDS Core Allergen Series.^24,25 The relatively high patch test positivity to sulfites along with the prevalence of daily exposures supports the addition of sulfites to more patch test screening series.

The recommended patch test concentration for sodium disulfite is 1% in petrolatum.⁵ Testing in aqueous solutions is not recommended because they can cause sulfites to break down, potentially producing false-positive or irritant patch test reactions.^7,26,27

Recommendations for Patients With Sulfite Allergies

Individuals with contact allergies to sulfites should be counseled on exposure sources and should be given resources providing a list of safe products, such as the ACDS Contact Allergen Management Program (https://www.acdscamp.org/login) or SkinSAFE ­(https://www.skinsafeproducts.com/). Prescribers should be cognizant of sulfites that are present in prescription medications. Just because a patient has a positive patch test to sulfites does not automatically imply that they will need to modify their diet to avoid sulfite-containing foods; in the absence of cheilitis or a distribution suggestive of systemic contact dermatitis (eg, vesicular hand/foot dermatitis, intertriginous eruptions), this step may be unnecessary. On the other hand, individuals who have experienced immediate hypersensitivity reactions to sulfites should avoid sulfite-containing foods and carry an epinephrine autoinjector.

Final Interpretation

Sulfites are ubiquitous compounds found in various foods, beverages, medications, and personal care products in addition to a range of occupational exposures. The face and hands are the most common sites of sulfite ACD. Despite patch test positivity in as many as 3% of tested patients,^17,23 sulfite allergy may be missed due to lack of routine testing on standard screening series.

THE DIAGNOSIS: Habit-Tic Deformity

Habit-tic deformity is a cause of nail dystrophy that commonly arises in children and adults due to subconscious repetitive and self-injurious manipulation of the nail bed or cuticle, which ultimately damages the nail matrix.^1,2 It can be considered a variant of onychotillomania.¹

Characteristic features of habit-tic deformity include a longitudinal depression on the central nail plate with transverse ridges,¹ which can be more prominent on the dominant hand.³ Patients typically note a long duration of nail deformity, often without insight into its etiology.² Diagnosis relies on careful assessment of the clinical presentation and the patient’s history to rule out other differential diagnoses. Based on our patient’s clinical presentation and history, we excluded wart, squamous cell carcinoma, eczema, psoriasis, lichen planus, autoimmune connective tissue disease, onychomycosis, paronychia, pincer nail deformity, and Beau line as potential diagnoses. Biopsy also can be performed to exclude these diagnoses from the differential if the cause is unclear following clinical examination.

Treatment for habit-tic deformity involves identifying and addressing the underlying habit. Barrier methods such as bandages and cyanoacrylate adhesives that prevent further manipulation of the nail matrix are effective treatments for habit-tic deformity.² A multidisciplinary approach with psychiatry may be optimal to identify underlying psychological comorbidities and break the habit through behavior interventions and medications.⁴ Nail dystrophy generally improves once the habit is disrupted; however, a younger age of onset may carry a worse prognosis.³ Patients should be counseled that the affected nail may never grow normally.

Our patient was advised to use fluocinonide ointment 0.05% to reduce inflammation of the proximal nail fold and to cover the thumbnail with a bandage to prevent picking. He also was counseled that the nail may show ongoing abnormal growth. Minimal improvement was noted after 6 months.

THE DIAGNOSIS: Habit-Tic Deformity

Habit-tic deformity is a cause of nail dystrophy that commonly arises in children and adults due to subconscious repetitive and self-injurious manipulation of the nail bed or cuticle, which ultimately damages the nail matrix.^1,2 It can be considered a variant of onychotillomania.¹

Characteristic features of habit-tic deformity include a longitudinal depression on the central nail plate with transverse ridges,¹ which can be more prominent on the dominant hand.³ Patients typically note a long duration of nail deformity, often without insight into its etiology.² Diagnosis relies on careful assessment of the clinical presentation and the patient’s history to rule out other differential diagnoses. Based on our patient’s clinical presentation and history, we excluded wart, squamous cell carcinoma, eczema, psoriasis, lichen planus, autoimmune connective tissue disease, onychomycosis, paronychia, pincer nail deformity, and Beau line as potential diagnoses. Biopsy also can be performed to exclude these diagnoses from the differential if the cause is unclear following clinical examination.

Treatment for habit-tic deformity involves identifying and addressing the underlying habit. Barrier methods such as bandages and cyanoacrylate adhesives that prevent further manipulation of the nail matrix are effective treatments for habit-tic deformity.² A multidisciplinary approach with psychiatry may be optimal to identify underlying psychological comorbidities and break the habit through behavior interventions and medications.⁴ Nail dystrophy generally improves once the habit is disrupted; however, a younger age of onset may carry a worse prognosis.³ Patients should be counseled that the affected nail may never grow normally.

Our patient was advised to use fluocinonide ointment 0.05% to reduce inflammation of the proximal nail fold and to cover the thumbnail with a bandage to prevent picking. He also was counseled that the nail may show ongoing abnormal growth. Minimal improvement was noted after 6 months.

THE DIAGNOSIS: Habit-Tic Deformity

Habit-tic deformity is a cause of nail dystrophy that commonly arises in children and adults due to subconscious repetitive and self-injurious manipulation of the nail bed or cuticle, which ultimately damages the nail matrix.^1,2 It can be considered a variant of onychotillomania.¹

Characteristic features of habit-tic deformity include a longitudinal depression on the central nail plate with transverse ridges,¹ which can be more prominent on the dominant hand.³ Patients typically note a long duration of nail deformity, often without insight into its etiology.² Diagnosis relies on careful assessment of the clinical presentation and the patient’s history to rule out other differential diagnoses. Based on our patient’s clinical presentation and history, we excluded wart, squamous cell carcinoma, eczema, psoriasis, lichen planus, autoimmune connective tissue disease, onychomycosis, paronychia, pincer nail deformity, and Beau line as potential diagnoses. Biopsy also can be performed to exclude these diagnoses from the differential if the cause is unclear following clinical examination.

Treatment for habit-tic deformity involves identifying and addressing the underlying habit. Barrier methods such as bandages and cyanoacrylate adhesives that prevent further manipulation of the nail matrix are effective treatments for habit-tic deformity.² A multidisciplinary approach with psychiatry may be optimal to identify underlying psychological comorbidities and break the habit through behavior interventions and medications.⁴ Nail dystrophy generally improves once the habit is disrupted; however, a younger age of onset may carry a worse prognosis.³ Patients should be counseled that the affected nail may never grow normally.

Our patient was advised to use fluocinonide ointment 0.05% to reduce inflammation of the proximal nail fold and to cover the thumbnail with a bandage to prevent picking. He also was counseled that the nail may show ongoing abnormal growth. Minimal improvement was noted after 6 months.

To the Editor:

Lichenoid drug eruptions are lichen planus–like hypersensitivity reactions induced by medications. These reactions are rare but cause irritation to the skin, as extreme pruritus is common. One review of 300 consecutive cases of drug eruptions submitted to dermatopathology revealed that 12% of cases were classified as lichenoid drug reactions.¹ Lichenoid dermatitis is characterized by extremely pruritic, scaly, eczematous or psoriasiform papules, often along the extensor surfaces and trunk.² The pruritic nature of the rash can negatively impact quality of life. Treatment typically involves discontinuation of the offending medication, although complete resolution can take months, even after the drug is stopped. Although there have been some data suggesting that topical and/or oral corticosteroids can help with resolution, the rash can persist even with steroid treatment.²

The histopathologic findings of lichenoid drug eruptions show lichen planus–like changes such as hyperkeratosis, irregular acanthosis, and lichenoid interface dermatitis. Accordingly, idiopathic lichen planus is an important differential diagnosis for lichenoid drug eruptions; however, compared to idiopathic lichen planus, lichenoid drug eruptions are more likely to be associated with eosinophils and parakeratosis.^1,3 In some cases, the histopathologic distinction between the 2 conditions is impossible, and clinical history needs to be considered to make a diagnosis.¹ Drugs known to cause lichenoid drug reactions more commonly include angiotensin-converting enzyme inhibitors, beta blockers, thiazides, gold, penicillamine, and antimalarials.² Lichenoid drug eruptions also have been documented in patients taking the second-generation nonsteroidal androgen receptor antagonist enzalutamide, which is used for the treatment of prostate cancer.⁴ More recently, the newer second-generation nonsteroidal androgen receptor antagonist apalutamide has been implicated in several cases of lichenoid drug eruptions.^5,6

We present a case of an apalutamide-induced lichenoid drug eruption that was resistant to dose reduction and required discontinuation of treatment due to the negative impact on the patient’s quality of life. Once the rash resolved, the patient transitioned to enzalutamide without any adverse events (AEs).

A 72-year-old man with a history of metastatic prostate cancer (stage IVB) presented to the dermatology clinic with a 4-month history of a dry itchy rash on the face, chest, back, and legs that had developed 2 to 3 months after oncology started him on apalutamide. The patient initially received apalutamide 240 mg/d, which was reduced by his oncologist 3 months later to 180 mg/d following the appearance of the rash. Then apalutamide was held as he awaited improvement of the rash.

One week after the apalutamide was held, the patient presented to dermatology. He reported that he had tried over-the-counter ammonium lactate 12% lotion twice daily when the rash first developed without improvement. When the apalutamide was held, oncology prescribed mupirocin ointment 2% 3 times daily which yielded minimal relief. On physical examination, widespread lichenified papules and plaques were noted on the face, chest, back, and legs (Figure 1). Dermatology initially prescribed triamcinolone ointment 0.1% twice daily. A 4-mm punch biopsy specimen of the upper back revealed a lichenoid interface dermatitis with numerous eosinophils compatible with a lichenoid hypersensitivity reaction (Figure 2). Considering the clinical and histologic findings, a diagnosis of lichenoid drug eruption secondary to apalutamide treatment was made.

To the Editor:

Lichenoid drug eruptions are lichen planus–like hypersensitivity reactions induced by medications. These reactions are rare but cause irritation to the skin, as extreme pruritus is common. One review of 300 consecutive cases of drug eruptions submitted to dermatopathology revealed that 12% of cases were classified as lichenoid drug reactions.¹ Lichenoid dermatitis is characterized by extremely pruritic, scaly, eczematous or psoriasiform papules, often along the extensor surfaces and trunk.² The pruritic nature of the rash can negatively impact quality of life. Treatment typically involves discontinuation of the offending medication, although complete resolution can take months, even after the drug is stopped. Although there have been some data suggesting that topical and/or oral corticosteroids can help with resolution, the rash can persist even with steroid treatment.²

The histopathologic findings of lichenoid drug eruptions show lichen planus–like changes such as hyperkeratosis, irregular acanthosis, and lichenoid interface dermatitis. Accordingly, idiopathic lichen planus is an important differential diagnosis for lichenoid drug eruptions; however, compared to idiopathic lichen planus, lichenoid drug eruptions are more likely to be associated with eosinophils and parakeratosis.^1,3 In some cases, the histopathologic distinction between the 2 conditions is impossible, and clinical history needs to be considered to make a diagnosis.¹ Drugs known to cause lichenoid drug reactions more commonly include angiotensin-converting enzyme inhibitors, beta blockers, thiazides, gold, penicillamine, and antimalarials.² Lichenoid drug eruptions also have been documented in patients taking the second-generation nonsteroidal androgen receptor antagonist enzalutamide, which is used for the treatment of prostate cancer.⁴ More recently, the newer second-generation nonsteroidal androgen receptor antagonist apalutamide has been implicated in several cases of lichenoid drug eruptions.^5,6

We present a case of an apalutamide-induced lichenoid drug eruption that was resistant to dose reduction and required discontinuation of treatment due to the negative impact on the patient’s quality of life. Once the rash resolved, the patient transitioned to enzalutamide without any adverse events (AEs).

A 72-year-old man with a history of metastatic prostate cancer (stage IVB) presented to the dermatology clinic with a 4-month history of a dry itchy rash on the face, chest, back, and legs that had developed 2 to 3 months after oncology started him on apalutamide. The patient initially received apalutamide 240 mg/d, which was reduced by his oncologist 3 months later to 180 mg/d following the appearance of the rash. Then apalutamide was held as he awaited improvement of the rash.

One week after the apalutamide was held, the patient presented to dermatology. He reported that he had tried over-the-counter ammonium lactate 12% lotion twice daily when the rash first developed without improvement. When the apalutamide was held, oncology prescribed mupirocin ointment 2% 3 times daily which yielded minimal relief. On physical examination, widespread lichenified papules and plaques were noted on the face, chest, back, and legs (Figure 1). Dermatology initially prescribed triamcinolone ointment 0.1% twice daily. A 4-mm punch biopsy specimen of the upper back revealed a lichenoid interface dermatitis with numerous eosinophils compatible with a lichenoid hypersensitivity reaction (Figure 2). Considering the clinical and histologic findings, a diagnosis of lichenoid drug eruption secondary to apalutamide treatment was made.

To the Editor:

Lichenoid drug eruptions are lichen planus–like hypersensitivity reactions induced by medications. These reactions are rare but cause irritation to the skin, as extreme pruritus is common. One review of 300 consecutive cases of drug eruptions submitted to dermatopathology revealed that 12% of cases were classified as lichenoid drug reactions.¹ Lichenoid dermatitis is characterized by extremely pruritic, scaly, eczematous or psoriasiform papules, often along the extensor surfaces and trunk.² The pruritic nature of the rash can negatively impact quality of life. Treatment typically involves discontinuation of the offending medication, although complete resolution can take months, even after the drug is stopped. Although there have been some data suggesting that topical and/or oral corticosteroids can help with resolution, the rash can persist even with steroid treatment.²

The histopathologic findings of lichenoid drug eruptions show lichen planus–like changes such as hyperkeratosis, irregular acanthosis, and lichenoid interface dermatitis. Accordingly, idiopathic lichen planus is an important differential diagnosis for lichenoid drug eruptions; however, compared to idiopathic lichen planus, lichenoid drug eruptions are more likely to be associated with eosinophils and parakeratosis.^1,3 In some cases, the histopathologic distinction between the 2 conditions is impossible, and clinical history needs to be considered to make a diagnosis.¹ Drugs known to cause lichenoid drug reactions more commonly include angiotensin-converting enzyme inhibitors, beta blockers, thiazides, gold, penicillamine, and antimalarials.² Lichenoid drug eruptions also have been documented in patients taking the second-generation nonsteroidal androgen receptor antagonist enzalutamide, which is used for the treatment of prostate cancer.⁴ More recently, the newer second-generation nonsteroidal androgen receptor antagonist apalutamide has been implicated in several cases of lichenoid drug eruptions.^5,6

We present a case of an apalutamide-induced lichenoid drug eruption that was resistant to dose reduction and required discontinuation of treatment due to the negative impact on the patient’s quality of life. Once the rash resolved, the patient transitioned to enzalutamide without any adverse events (AEs).

A 72-year-old man with a history of metastatic prostate cancer (stage IVB) presented to the dermatology clinic with a 4-month history of a dry itchy rash on the face, chest, back, and legs that had developed 2 to 3 months after oncology started him on apalutamide. The patient initially received apalutamide 240 mg/d, which was reduced by his oncologist 3 months later to 180 mg/d following the appearance of the rash. Then apalutamide was held as he awaited improvement of the rash.

One week after the apalutamide was held, the patient presented to dermatology. He reported that he had tried over-the-counter ammonium lactate 12% lotion twice daily when the rash first developed without improvement. When the apalutamide was held, oncology prescribed mupirocin ointment 2% 3 times daily which yielded minimal relief. On physical examination, widespread lichenified papules and plaques were noted on the face, chest, back, and legs (Figure 1). Dermatology initially prescribed triamcinolone ointment 0.1% twice daily. A 4-mm punch biopsy specimen of the upper back revealed a lichenoid interface dermatitis with numerous eosinophils compatible with a lichenoid hypersensitivity reaction (Figure 2). Considering the clinical and histologic findings, a diagnosis of lichenoid drug eruption secondary to apalutamide treatment was made.