Article

THE DIAGNOSIS: Borderline-Borderline Leprosy With Type 1 Lepra Reaction

Punch biopsies from plaques on the right elbow and right shin revealed diffuse granulomatous dermatitis (Figure 1) with a narrow Grenz zone in the superficial dermis. The upper dermis contained a dense bandlike infiltrate of histiocytes with abundant foamy-gray cytoplasm and a moderate admixture of lymphocytes. The mid and deep dermis contained a nodular, perivascular, periadnexal, and perineural infiltrate of histiocytes and a dense admixture of lymphocytes. Periodic acid-Schiff and Gram stains were negative for microorganisms. Fite stain was positive for numerous organisms in histiocytes and small dermal nerves (Figure 2). These findings and the clinical examination confirmed a diagnosis of borderline-borderline leprosy with type 1 lepra reaction. The patient was started on dapsone 100 mg, rifampin 600 mg, and clofazimine 100 mg once daily and experienced clinical improvement within 6 months.

The World Health Organization reported more than 200,000 new leprosy cases globally in 2019, with most occurring in India, Brazil, and Indonesia.¹ About 150 to 250 new cases are detected in the United States annually.¹ The Ridley-Jopling classification of leprosy divides the condition into 5 categories: tuberculoid, borderline tuberculoid, borderline-borderline (BB), borderline lepromatous, and lepromatous. At one end of the spectrum, tuberculoid leprosy—a predominant Th1 immune response mediated by CD4 lymphocytes, interleukin (IL) 2, and interferon gamma²—is characterized by sharply demarcated erythematous and hypopigmented plaques with raised borders and an annular appearance.^2,3 Lesions typically have atrophic and hypopigmented centers that often appear in an asymmetric distribution on the arms and legs.^2,3 Histologic features include dermal tuberculoid granulomas with epithelioid cells—some located directly beneath the epidermis and others around deep vessels and nerves³—multinucleated Langerhans giant cells, thickened peripheral nerves with intraneural lymphocytic infiltrates, and granulomas with central necrosis. Fite-Faraco staining exhibits few bacteria.²

Lepromatous leprosy occurs in individuals with impaired T-cell immunity, leading to multiple red-brown nodular infiltrates in the skin and mucous membranes.^2,3 Lesions typically are symmetric and favor the face and auricle of the ear.^2,3 Histologically, there are bluish-gray foamy macrophages that form diffuse or nodular infiltrates with few lymphocytes,² with a Grenz zone between the epidermis and dermis. Nerves may show lamination of the perineurium resembling an onion skin.^2,3 Immunohistochemistry shows predominant CD8-positive infiltrates with a Th2 response and positive IL-4 and IL-10. Fite-Faraco stain shows numerous mycobacteria arranged in clusters and in histiocytes.²

Tuberculoid leprosy is treated with dapsone 100 mg and rifampin 600 mg once daily for 6 months,⁴ and lepromatous leprosy is treated with dapsone 100 mg, rifampin 600 mg, and clofazimine 50 mg once daily for 12 months.⁴ The prognosis for both is good with treatment; erythema and induration of skin lesions may improve within a few months, but residual nerve damage is common, especially in those with advanced disease prior to treatment.² For direct contacts, a single dose of rifampin may be given.⁴

Borderline-borderline leprosy manifests with numerous asymmetric annular plaques, as seen in our patient (Figure 3). Histology findings can be variable and often overlap with other forms of leprosy. There can be epithelioid granulomas and only a few acid-fast bacilli (AFB) or diffuse histiocytic aggregates with foamy histiocytes containing large numbers of AFB.³ Nerve involvement is variable but can be severe in the setting of type 1 lepra reaction, which was present in our patient. Type 1 lepra reaction—a type IV cell-mediated allergic hypersensitivity reaction to Mycobacterium leprae antigens—manifests clinically with hyperesthesia, erythema, edema, and subsequent scaling.² It occurs in up to 30% of patients with borderline leprosy, usually within 12 months of treatment initiation.² Our patient had considerable edema and erythema of the hands and feet (Figure 4) along with extensive polyneuropathy prior to starting therapy.

Lucio phenomenon is a rare leprosy reaction found in patients with untreated lepromatous leprosy characterized by erythematous to violaceous macules that lead to ulceronecrotic lesions.⁵ Histologically, there are many AFB in the vascular endothelium, leukocytoclastic vasculitis, and ischemic epidermal necrosis.⁵ Our patient did not have ulcerative or necrotic lesions.

The classic skin lesions of psoriasis vulgaris can be described as well-demarcated pink plaques with white or silvery scales that usually are distributed symmetrically and often are found on extensor surfaces.⁶ Rapidly progressive lesions can be annular with normal skin in the center, mimicking the lesions seen in tuberculoid leprosy. Clinically, both psoriasis and tuberculoid forms of leprosy are sharply demarcated; however, psoriatic lesions often have micaceous overlying scale that is not present in leprosy. Characteristic histologic findings of psoriasis are hyperkeratosis, parakeratosis, and acanthosis of the epidermis with dilated blood vessels and a lymphocytic infiltrate, predominantly into the dermis.⁷ Psoriatic arthritis has a variable clinical course but tends to emerge 5 to 12 years after initial skin manifestation.⁸ Classic clinical symptoms include swelling, tenderness, stiffness, and pain in joints and surrounding tissues.⁸ Other than edema, our patient did not exhibit signs of psoriatic arthritis.

Sarcoidosis is a systemic autoimmune disease characterized by noncaseating epithelioid granulomas affecting various organs, with cutaneous manifestations present in approximately 30% of all cases. Cutaneous manifestations can be variable, including maculopapular lesions, plaques, and nodules.⁹ Differentiating between cutaneous sarcoidosis and tuberculoid leprosy can be challenging, as both are granulomatous processes; however, histology of sarcoidosis demonstrates noncaseating granulomas in the dermis and/or subcutaneous tissues without AFB9 compared to granulomas with necrotic centers in tuberculoid leprosy.

Cutaneous tuberculosis has variable morphologies. One subtype, lupus vulgaris, can manifest with violaceous, scaly, eroded plaques that could be confused for leprosy. Lupus vulgaris usually results from hematogenous or lymphatic seeding in individuals with high or moderate immunity to M tuberculosis.¹⁰

Histologically, the dermis has tuberculoid granulomas containing multinucleated giant cells,¹⁰ which can mimic those seen in BB leprosy. Tuberculin skin test results often are positive¹⁰; while this test was not performed in our patient, chest radiography was unremarkable, making this diagnosis less likely.

Mycobacterium leprae infections should be considered in a patient with a worsening rash and progressive polyneuropathy. Clinical diagnosis can be challenging due to similarities with other diseases; however, histopathologic findings can help differentiate M leprae from other conditions. This infection is treatable, and early detection can minimize long-term patient morbidity.

THE DIAGNOSIS: Borderline-Borderline Leprosy With Type 1 Lepra Reaction

Punch biopsies from plaques on the right elbow and right shin revealed diffuse granulomatous dermatitis (Figure 1) with a narrow Grenz zone in the superficial dermis. The upper dermis contained a dense bandlike infiltrate of histiocytes with abundant foamy-gray cytoplasm and a moderate admixture of lymphocytes. The mid and deep dermis contained a nodular, perivascular, periadnexal, and perineural infiltrate of histiocytes and a dense admixture of lymphocytes. Periodic acid-Schiff and Gram stains were negative for microorganisms. Fite stain was positive for numerous organisms in histiocytes and small dermal nerves (Figure 2). These findings and the clinical examination confirmed a diagnosis of borderline-borderline leprosy with type 1 lepra reaction. The patient was started on dapsone 100 mg, rifampin 600 mg, and clofazimine 100 mg once daily and experienced clinical improvement within 6 months.

The World Health Organization reported more than 200,000 new leprosy cases globally in 2019, with most occurring in India, Brazil, and Indonesia.¹ About 150 to 250 new cases are detected in the United States annually.¹ The Ridley-Jopling classification of leprosy divides the condition into 5 categories: tuberculoid, borderline tuberculoid, borderline-borderline (BB), borderline lepromatous, and lepromatous. At one end of the spectrum, tuberculoid leprosy—a predominant Th1 immune response mediated by CD4 lymphocytes, interleukin (IL) 2, and interferon gamma²—is characterized by sharply demarcated erythematous and hypopigmented plaques with raised borders and an annular appearance.^2,3 Lesions typically have atrophic and hypopigmented centers that often appear in an asymmetric distribution on the arms and legs.^2,3 Histologic features include dermal tuberculoid granulomas with epithelioid cells—some located directly beneath the epidermis and others around deep vessels and nerves³—multinucleated Langerhans giant cells, thickened peripheral nerves with intraneural lymphocytic infiltrates, and granulomas with central necrosis. Fite-Faraco staining exhibits few bacteria.²

Lepromatous leprosy occurs in individuals with impaired T-cell immunity, leading to multiple red-brown nodular infiltrates in the skin and mucous membranes.^2,3 Lesions typically are symmetric and favor the face and auricle of the ear.^2,3 Histologically, there are bluish-gray foamy macrophages that form diffuse or nodular infiltrates with few lymphocytes,² with a Grenz zone between the epidermis and dermis. Nerves may show lamination of the perineurium resembling an onion skin.^2,3 Immunohistochemistry shows predominant CD8-positive infiltrates with a Th2 response and positive IL-4 and IL-10. Fite-Faraco stain shows numerous mycobacteria arranged in clusters and in histiocytes.²

Tuberculoid leprosy is treated with dapsone 100 mg and rifampin 600 mg once daily for 6 months,⁴ and lepromatous leprosy is treated with dapsone 100 mg, rifampin 600 mg, and clofazimine 50 mg once daily for 12 months.⁴ The prognosis for both is good with treatment; erythema and induration of skin lesions may improve within a few months, but residual nerve damage is common, especially in those with advanced disease prior to treatment.² For direct contacts, a single dose of rifampin may be given.⁴

Borderline-borderline leprosy manifests with numerous asymmetric annular plaques, as seen in our patient (Figure 3). Histology findings can be variable and often overlap with other forms of leprosy. There can be epithelioid granulomas and only a few acid-fast bacilli (AFB) or diffuse histiocytic aggregates with foamy histiocytes containing large numbers of AFB.³ Nerve involvement is variable but can be severe in the setting of type 1 lepra reaction, which was present in our patient. Type 1 lepra reaction—a type IV cell-mediated allergic hypersensitivity reaction to Mycobacterium leprae antigens—manifests clinically with hyperesthesia, erythema, edema, and subsequent scaling.² It occurs in up to 30% of patients with borderline leprosy, usually within 12 months of treatment initiation.² Our patient had considerable edema and erythema of the hands and feet (Figure 4) along with extensive polyneuropathy prior to starting therapy.

Lucio phenomenon is a rare leprosy reaction found in patients with untreated lepromatous leprosy characterized by erythematous to violaceous macules that lead to ulceronecrotic lesions.⁵ Histologically, there are many AFB in the vascular endothelium, leukocytoclastic vasculitis, and ischemic epidermal necrosis.⁵ Our patient did not have ulcerative or necrotic lesions.

The classic skin lesions of psoriasis vulgaris can be described as well-demarcated pink plaques with white or silvery scales that usually are distributed symmetrically and often are found on extensor surfaces.⁶ Rapidly progressive lesions can be annular with normal skin in the center, mimicking the lesions seen in tuberculoid leprosy. Clinically, both psoriasis and tuberculoid forms of leprosy are sharply demarcated; however, psoriatic lesions often have micaceous overlying scale that is not present in leprosy. Characteristic histologic findings of psoriasis are hyperkeratosis, parakeratosis, and acanthosis of the epidermis with dilated blood vessels and a lymphocytic infiltrate, predominantly into the dermis.⁷ Psoriatic arthritis has a variable clinical course but tends to emerge 5 to 12 years after initial skin manifestation.⁸ Classic clinical symptoms include swelling, tenderness, stiffness, and pain in joints and surrounding tissues.⁸ Other than edema, our patient did not exhibit signs of psoriatic arthritis.

Sarcoidosis is a systemic autoimmune disease characterized by noncaseating epithelioid granulomas affecting various organs, with cutaneous manifestations present in approximately 30% of all cases. Cutaneous manifestations can be variable, including maculopapular lesions, plaques, and nodules.⁹ Differentiating between cutaneous sarcoidosis and tuberculoid leprosy can be challenging, as both are granulomatous processes; however, histology of sarcoidosis demonstrates noncaseating granulomas in the dermis and/or subcutaneous tissues without AFB9 compared to granulomas with necrotic centers in tuberculoid leprosy.

Cutaneous tuberculosis has variable morphologies. One subtype, lupus vulgaris, can manifest with violaceous, scaly, eroded plaques that could be confused for leprosy. Lupus vulgaris usually results from hematogenous or lymphatic seeding in individuals with high or moderate immunity to M tuberculosis.¹⁰

Histologically, the dermis has tuberculoid granulomas containing multinucleated giant cells,¹⁰ which can mimic those seen in BB leprosy. Tuberculin skin test results often are positive¹⁰; while this test was not performed in our patient, chest radiography was unremarkable, making this diagnosis less likely.

Mycobacterium leprae infections should be considered in a patient with a worsening rash and progressive polyneuropathy. Clinical diagnosis can be challenging due to similarities with other diseases; however, histopathologic findings can help differentiate M leprae from other conditions. This infection is treatable, and early detection can minimize long-term patient morbidity.

THE DIAGNOSIS: Borderline-Borderline Leprosy With Type 1 Lepra Reaction

Punch biopsies from plaques on the right elbow and right shin revealed diffuse granulomatous dermatitis (Figure 1) with a narrow Grenz zone in the superficial dermis. The upper dermis contained a dense bandlike infiltrate of histiocytes with abundant foamy-gray cytoplasm and a moderate admixture of lymphocytes. The mid and deep dermis contained a nodular, perivascular, periadnexal, and perineural infiltrate of histiocytes and a dense admixture of lymphocytes. Periodic acid-Schiff and Gram stains were negative for microorganisms. Fite stain was positive for numerous organisms in histiocytes and small dermal nerves (Figure 2). These findings and the clinical examination confirmed a diagnosis of borderline-borderline leprosy with type 1 lepra reaction. The patient was started on dapsone 100 mg, rifampin 600 mg, and clofazimine 100 mg once daily and experienced clinical improvement within 6 months.

The World Health Organization reported more than 200,000 new leprosy cases globally in 2019, with most occurring in India, Brazil, and Indonesia.¹ About 150 to 250 new cases are detected in the United States annually.¹ The Ridley-Jopling classification of leprosy divides the condition into 5 categories: tuberculoid, borderline tuberculoid, borderline-borderline (BB), borderline lepromatous, and lepromatous. At one end of the spectrum, tuberculoid leprosy—a predominant Th1 immune response mediated by CD4 lymphocytes, interleukin (IL) 2, and interferon gamma²—is characterized by sharply demarcated erythematous and hypopigmented plaques with raised borders and an annular appearance.^2,3 Lesions typically have atrophic and hypopigmented centers that often appear in an asymmetric distribution on the arms and legs.^2,3 Histologic features include dermal tuberculoid granulomas with epithelioid cells—some located directly beneath the epidermis and others around deep vessels and nerves³—multinucleated Langerhans giant cells, thickened peripheral nerves with intraneural lymphocytic infiltrates, and granulomas with central necrosis. Fite-Faraco staining exhibits few bacteria.²

Lepromatous leprosy occurs in individuals with impaired T-cell immunity, leading to multiple red-brown nodular infiltrates in the skin and mucous membranes.^2,3 Lesions typically are symmetric and favor the face and auricle of the ear.^2,3 Histologically, there are bluish-gray foamy macrophages that form diffuse or nodular infiltrates with few lymphocytes,² with a Grenz zone between the epidermis and dermis. Nerves may show lamination of the perineurium resembling an onion skin.^2,3 Immunohistochemistry shows predominant CD8-positive infiltrates with a Th2 response and positive IL-4 and IL-10. Fite-Faraco stain shows numerous mycobacteria arranged in clusters and in histiocytes.²

Tuberculoid leprosy is treated with dapsone 100 mg and rifampin 600 mg once daily for 6 months,⁴ and lepromatous leprosy is treated with dapsone 100 mg, rifampin 600 mg, and clofazimine 50 mg once daily for 12 months.⁴ The prognosis for both is good with treatment; erythema and induration of skin lesions may improve within a few months, but residual nerve damage is common, especially in those with advanced disease prior to treatment.² For direct contacts, a single dose of rifampin may be given.⁴

Borderline-borderline leprosy manifests with numerous asymmetric annular plaques, as seen in our patient (Figure 3). Histology findings can be variable and often overlap with other forms of leprosy. There can be epithelioid granulomas and only a few acid-fast bacilli (AFB) or diffuse histiocytic aggregates with foamy histiocytes containing large numbers of AFB.³ Nerve involvement is variable but can be severe in the setting of type 1 lepra reaction, which was present in our patient. Type 1 lepra reaction—a type IV cell-mediated allergic hypersensitivity reaction to Mycobacterium leprae antigens—manifests clinically with hyperesthesia, erythema, edema, and subsequent scaling.² It occurs in up to 30% of patients with borderline leprosy, usually within 12 months of treatment initiation.² Our patient had considerable edema and erythema of the hands and feet (Figure 4) along with extensive polyneuropathy prior to starting therapy.

Lucio phenomenon is a rare leprosy reaction found in patients with untreated lepromatous leprosy characterized by erythematous to violaceous macules that lead to ulceronecrotic lesions.⁵ Histologically, there are many AFB in the vascular endothelium, leukocytoclastic vasculitis, and ischemic epidermal necrosis.⁵ Our patient did not have ulcerative or necrotic lesions.

The classic skin lesions of psoriasis vulgaris can be described as well-demarcated pink plaques with white or silvery scales that usually are distributed symmetrically and often are found on extensor surfaces.⁶ Rapidly progressive lesions can be annular with normal skin in the center, mimicking the lesions seen in tuberculoid leprosy. Clinically, both psoriasis and tuberculoid forms of leprosy are sharply demarcated; however, psoriatic lesions often have micaceous overlying scale that is not present in leprosy. Characteristic histologic findings of psoriasis are hyperkeratosis, parakeratosis, and acanthosis of the epidermis with dilated blood vessels and a lymphocytic infiltrate, predominantly into the dermis.⁷ Psoriatic arthritis has a variable clinical course but tends to emerge 5 to 12 years after initial skin manifestation.⁸ Classic clinical symptoms include swelling, tenderness, stiffness, and pain in joints and surrounding tissues.⁸ Other than edema, our patient did not exhibit signs of psoriatic arthritis.

Sarcoidosis is a systemic autoimmune disease characterized by noncaseating epithelioid granulomas affecting various organs, with cutaneous manifestations present in approximately 30% of all cases. Cutaneous manifestations can be variable, including maculopapular lesions, plaques, and nodules.⁹ Differentiating between cutaneous sarcoidosis and tuberculoid leprosy can be challenging, as both are granulomatous processes; however, histology of sarcoidosis demonstrates noncaseating granulomas in the dermis and/or subcutaneous tissues without AFB9 compared to granulomas with necrotic centers in tuberculoid leprosy.

Cutaneous tuberculosis has variable morphologies. One subtype, lupus vulgaris, can manifest with violaceous, scaly, eroded plaques that could be confused for leprosy. Lupus vulgaris usually results from hematogenous or lymphatic seeding in individuals with high or moderate immunity to M tuberculosis.¹⁰

Histologically, the dermis has tuberculoid granulomas containing multinucleated giant cells,¹⁰ which can mimic those seen in BB leprosy. Tuberculin skin test results often are positive¹⁰; while this test was not performed in our patient, chest radiography was unremarkable, making this diagnosis less likely.

Mycobacterium leprae infections should be considered in a patient with a worsening rash and progressive polyneuropathy. Clinical diagnosis can be challenging due to similarities with other diseases; however, histopathologic findings can help differentiate M leprae from other conditions. This infection is treatable, and early detection can minimize long-term patient morbidity.

To the Editor:

Psoriasis is a chronic inflammatory condition that affects individuals in various extracutaneous ways.¹ Prior studies have documented a decrease in exercise intensity among patients with psoriasis²; however, few studies have specifically investigated baseline mobility in this population. Baseline mobility denotes an individual’s fundamental ability to walk or move around without assistance of any kind. Impaired mobility—when baseline mobility is compromised—is an aspect of the wider diversity, equity, and inclusion framework that underscores the significance of recognizing challenges and promoting inclusive measures, both at the point of care and in research.³ study sought to analyze the relationship between psoriasis and baseline mobility among US adults (aged 45 to 80 years) utilizing the latest data from the National Health and Nutrition Examination Survey (NHANES) database for psoriasis.⁴ We used three 2-year cycles of NHANES data to create a 2009-2014 dataset.

The overall NHANES response rate among adults aged 45 to 80 years between 2009 and 2014 was 67.9%. Patients were categorized as having impaired mobility if they responded “yes” to the following question: “Because of a health problem, do you have difficulty walking without using any special equipment?” Psoriasis status was assessed by the following question: “Have you ever been told by a doctor or other health professional that you had psoriasis?” Multivariable logistic regression analyses were performed using Stata/SE 18.0 software (StataCorp LLC) to assess the relationship between psoriasis and impaired mobility. Age, income, education, sex, race, tobacco use, diabetes status, body mass index, and arthritis status were controlled for in our models.

Our analysis initially included 9982 participants; 14 did not respond to questions assessing psoriasis and impaired mobility and were excluded. The prevalence of impaired mobility in patients with psoriasis was 17.1% compared with 10.9% among those without psoriasis (Table 1). There was a significant association between psoriasis and impaired mobility among patients aged 45 to 80 years after adjusting for potential confounding variables (adjusted odds ratio [AOR], 1.54; 95% CI, 1.04- 2.29; P=.032)(Table 2). Analyses of subgroups yielded no statistically significant results.

Our study demonstrated a statistically significant difference in mobility between individuals with psoriasis compared with the general population, which remained significant when controlling for arthritis, obesity, and diabetes (P=.032). This may be the result of several influences. First, the location of the psoriasis may impact mobility. Plantar psoriasis—a manifestation on the soles of the feet—can cause discomfort and pain, which can hinder walking and standing.⁵ Second, a study by Lasselin et al⁶ found that systemic inflammation contributes to mobility impairment through alterations in gait and posture, which suggests that the inflammatory processes inherent in psoriasis could intrinsically modify walking speed and stride, potentially exacerbating mobility difficulties independent of other comorbid conditions. These findings suggest that psoriasis may disproportionately affect individuals with impaired mobility, independent of comorbid arthritis, obesity, and diabetes.

These findings have broad implications for diversity, equity, and inclusion. They should prompt us to consider the practical challenges faced by this patient population and the ways that we can address barriers to care. Offering telehealth appointments, making primary care referrals for impaired mobility workups, and advising patients of direct-to-home delivery of prescriptions are good places to start.

Limitations to our study include the lack of specificity in the survey question, self-reporting bias, and the inability to control for the psoriasis location. Further investigations are warranted in large, representative US adult populations to assess the implications of impaired mobility in patients with psoriasis.

To the Editor:

Psoriasis is a chronic inflammatory condition that affects individuals in various extracutaneous ways.¹ Prior studies have documented a decrease in exercise intensity among patients with psoriasis²; however, few studies have specifically investigated baseline mobility in this population. Baseline mobility denotes an individual’s fundamental ability to walk or move around without assistance of any kind. Impaired mobility—when baseline mobility is compromised—is an aspect of the wider diversity, equity, and inclusion framework that underscores the significance of recognizing challenges and promoting inclusive measures, both at the point of care and in research.³ study sought to analyze the relationship between psoriasis and baseline mobility among US adults (aged 45 to 80 years) utilizing the latest data from the National Health and Nutrition Examination Survey (NHANES) database for psoriasis.⁴ We used three 2-year cycles of NHANES data to create a 2009-2014 dataset.

The overall NHANES response rate among adults aged 45 to 80 years between 2009 and 2014 was 67.9%. Patients were categorized as having impaired mobility if they responded “yes” to the following question: “Because of a health problem, do you have difficulty walking without using any special equipment?” Psoriasis status was assessed by the following question: “Have you ever been told by a doctor or other health professional that you had psoriasis?” Multivariable logistic regression analyses were performed using Stata/SE 18.0 software (StataCorp LLC) to assess the relationship between psoriasis and impaired mobility. Age, income, education, sex, race, tobacco use, diabetes status, body mass index, and arthritis status were controlled for in our models.

Our analysis initially included 9982 participants; 14 did not respond to questions assessing psoriasis and impaired mobility and were excluded. The prevalence of impaired mobility in patients with psoriasis was 17.1% compared with 10.9% among those without psoriasis (Table 1). There was a significant association between psoriasis and impaired mobility among patients aged 45 to 80 years after adjusting for potential confounding variables (adjusted odds ratio [AOR], 1.54; 95% CI, 1.04- 2.29; P=.032)(Table 2). Analyses of subgroups yielded no statistically significant results.

Our study demonstrated a statistically significant difference in mobility between individuals with psoriasis compared with the general population, which remained significant when controlling for arthritis, obesity, and diabetes (P=.032). This may be the result of several influences. First, the location of the psoriasis may impact mobility. Plantar psoriasis—a manifestation on the soles of the feet—can cause discomfort and pain, which can hinder walking and standing.⁵ Second, a study by Lasselin et al⁶ found that systemic inflammation contributes to mobility impairment through alterations in gait and posture, which suggests that the inflammatory processes inherent in psoriasis could intrinsically modify walking speed and stride, potentially exacerbating mobility difficulties independent of other comorbid conditions. These findings suggest that psoriasis may disproportionately affect individuals with impaired mobility, independent of comorbid arthritis, obesity, and diabetes.

These findings have broad implications for diversity, equity, and inclusion. They should prompt us to consider the practical challenges faced by this patient population and the ways that we can address barriers to care. Offering telehealth appointments, making primary care referrals for impaired mobility workups, and advising patients of direct-to-home delivery of prescriptions are good places to start.

Limitations to our study include the lack of specificity in the survey question, self-reporting bias, and the inability to control for the psoriasis location. Further investigations are warranted in large, representative US adult populations to assess the implications of impaired mobility in patients with psoriasis.

To the Editor:

Psoriasis is a chronic inflammatory condition that affects individuals in various extracutaneous ways.¹ Prior studies have documented a decrease in exercise intensity among patients with psoriasis²; however, few studies have specifically investigated baseline mobility in this population. Baseline mobility denotes an individual’s fundamental ability to walk or move around without assistance of any kind. Impaired mobility—when baseline mobility is compromised—is an aspect of the wider diversity, equity, and inclusion framework that underscores the significance of recognizing challenges and promoting inclusive measures, both at the point of care and in research.³ study sought to analyze the relationship between psoriasis and baseline mobility among US adults (aged 45 to 80 years) utilizing the latest data from the National Health and Nutrition Examination Survey (NHANES) database for psoriasis.⁴ We used three 2-year cycles of NHANES data to create a 2009-2014 dataset.

The overall NHANES response rate among adults aged 45 to 80 years between 2009 and 2014 was 67.9%. Patients were categorized as having impaired mobility if they responded “yes” to the following question: “Because of a health problem, do you have difficulty walking without using any special equipment?” Psoriasis status was assessed by the following question: “Have you ever been told by a doctor or other health professional that you had psoriasis?” Multivariable logistic regression analyses were performed using Stata/SE 18.0 software (StataCorp LLC) to assess the relationship between psoriasis and impaired mobility. Age, income, education, sex, race, tobacco use, diabetes status, body mass index, and arthritis status were controlled for in our models.

Our analysis initially included 9982 participants; 14 did not respond to questions assessing psoriasis and impaired mobility and were excluded. The prevalence of impaired mobility in patients with psoriasis was 17.1% compared with 10.9% among those without psoriasis (Table 1). There was a significant association between psoriasis and impaired mobility among patients aged 45 to 80 years after adjusting for potential confounding variables (adjusted odds ratio [AOR], 1.54; 95% CI, 1.04- 2.29; P=.032)(Table 2). Analyses of subgroups yielded no statistically significant results.

Our study demonstrated a statistically significant difference in mobility between individuals with psoriasis compared with the general population, which remained significant when controlling for arthritis, obesity, and diabetes (P=.032). This may be the result of several influences. First, the location of the psoriasis may impact mobility. Plantar psoriasis—a manifestation on the soles of the feet—can cause discomfort and pain, which can hinder walking and standing.⁵ Second, a study by Lasselin et al⁶ found that systemic inflammation contributes to mobility impairment through alterations in gait and posture, which suggests that the inflammatory processes inherent in psoriasis could intrinsically modify walking speed and stride, potentially exacerbating mobility difficulties independent of other comorbid conditions. These findings suggest that psoriasis may disproportionately affect individuals with impaired mobility, independent of comorbid arthritis, obesity, and diabetes.

These findings have broad implications for diversity, equity, and inclusion. They should prompt us to consider the practical challenges faced by this patient population and the ways that we can address barriers to care. Offering telehealth appointments, making primary care referrals for impaired mobility workups, and advising patients of direct-to-home delivery of prescriptions are good places to start.

Limitations to our study include the lack of specificity in the survey question, self-reporting bias, and the inability to control for the psoriasis location. Further investigations are warranted in large, representative US adult populations to assess the implications of impaired mobility in patients with psoriasis.

To the Editor:

Cutaneous medical conditions can have a substantial impact on patients’ functioning and quality of life. Many patients with severe skin disease are eligible to receive disability assistance that can provide them with essential income and health care. Previous research has highlighted disability assessment as one of the most important ways physicians can help mitigate the health consequences of poverty.¹ Dermatologists can play an important role in the disability assessment process by documenting the facts associated with patients’ skin conditions.

Although skin conditions have a relatively high prevalence, they remain underrepresented in disability claims. Between 1997 and 2004, occupational skin diseases accounted for 12% to 17% of nonfatal work-related illnesses; however, during that same period, skin conditions comprised only 0.21% of disability claims in the United States.^2,3 Historically, there has been hesitancy among dermatologists to complete disability paperwork; a 1976 survey of dermatologists cited extensive paperwork, “troublesome patients,” and fee schedule issues as reasons.⁴ The lack of training regarding disability assessment in medical school and residency also has been noted.⁵

To characterize modern attitudes toward disability assessments, we conducted a survey of dermatologists across the United States. Our study was reviewed and declared exempt by the institutional review board of the Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center (Torrance, California)(approval #18CR-32242-01). Using convenience sampling, we emailed dermatologists from the Association of Professors of Dermatology and dermatology state societies in all 50 states inviting them to participate in our voluntary and anonymous survey, which was administered using SurveyMonkey. The use of all society mailing lists was approved by the respective owners. The 15-question survey included multiple choice, Likert scale, and free response sections. Summary and descriptive statistics were used to describe respondent demographics and identify any patterns in responses.

For each Likert-based question, participants ranked their degree of agreement with a statement as: 1=strongly disagree, 2=somewhat disagree, 3=neither agree nor disagree/neutral, 4=somewhat agree, and 5=strongly agree. The mean response and standard deviation were reported for each Likert scale prompt. Preplanned 1-sample t testing was used to analyze Likert scale data, in which the mean response for each prompt was compared to a baseline response of 3 (neutral). A P value <.05 was considered statistically significant. Statistical analyses were performed using SPSS Statistics for MacOS, version 27 (IBM).

Seventy-eight dermatologists agreed to participate, and 70 completed the survey, for a response rate of 89.7% (Table 1). The dermatologists we surveyed practiced in a variety of clinical settings, including academic public hospitals (46.2% [36/78]), academic private hospitals (33.3% [26/78]), and private practices (32.1% [25/78]), and 60.3% (47/78) reported providing disability documentation at some point. Most of the respondents (64.3% [45/70]) did not perform assessments in an average month (Table 2). Medical assessment documentation was provided most frequently for workers’ compensation (50.0% [35/70]), private insurance (27.1% [19/70]), and Social Security Disability Insurance (25.7% [18/70]). Dermatologists overwhelmingly reported no formal training for disability assessment in medical school (94.3% [66/70]), residency (97.1% [68/70]), or clinical practice (81.4% [57/70]).

In the Likert scale prompts, respondents agreed that they were uncertain of their role in disability assessment (mean response, 3.6; P<.001). Moreover, they were uncomfortable providing assessments (mean response, 3.5; P<.001) and felt that they did not have sufficient time to perform them (mean response, 3.6; P<.001). Dermatologists disagreed that they received adequate compensation for performing assessments (mean response, 2.2; P<.001) and felt that they did not have enough time to participate in assessments (mean response, 3.6; P<.001). Respondents generally did not feel distrustful of patients seeking disability assessment (mean response, 2.8; P=.043). Dermatologists neither agreed nor disagreed when asked if they thought that physicians can determine disability status (mean response, 3.2; P=.118). The details of the Likert scale responses are described in Table 3. Respondents also were uncertain as to which dermatologic conditions were eligible for disability. When asked to select which conditions from a list of 10 were eligible per the Social Security Administration listing of disability impairments, only 15.4% (12/70) of respondents correctly identified that all the conditions qualified; these included ichthyosis, pemphigus vulgaris, allergic contact dermatitis, hidradenitis suppurativa, systemic lupus erythematosus, chromoblastomycosis, xeroderma pigmentosum, burns, malignant melanoma, and scleroderma.⁶

In the free-response prompts, respondents frequently described extensive paperwork, inadequate time, and lack of reimbursement as barriers to providing documentation. Often, dermatologists found that the forms were not well matched to the skin conditions they were evaluating and rather had a musculoskeletal focus. Multiple individuals commented on the challenge in assessing the percentage of disability and functional/psychosocial impairment in skin conditions. One respondent noted that workers’ compensation forms ask if the patient is “…permanent and stationary…for most conditions this has no meaning in dermatology.” Some felt hesitant to provide documentation because they had insufficient patient history, especially regarding employment, and opted to defer to primary care providers who might be more familiar with the full patient history.

A dermatologist described their perspective as follows:

“…As a specialist I feel that I don’t have a complete look into all the factors that could contribute to a patient[’]s need to go on disability, and I don’t have experience with filling out disability requests. That being said, if a patient[’]s request for disability was due to a skin disease that I know way more about than [a] primary care [physician] would, I would do the disability assessment.”

Another respondent noted the complexity in “establishing causality” for workers’ compensation. Another dermatologist reported,

“The most frequent challenging situation I encounter is being asked to evaluate for maximum medical improvement after patch testing. If the patient is not fully avoiding contact allergens either at home or at work, then I typically document that they are not at [maximum medical improvement]. The reality is that most frequently it is due to exposure to allergens at home so the line between what is a legitimate worker’s comp[ensation] issue and what is a home life choice is blurry.”

Nevertheless, respondents expressed interest in learning more about disability assessment procedures. Summary guides, lectures, and prefilled paperwork were the most popular initiatives that respondents agreed would be beneficial toward becoming educated regarding disability assessment (78.6%, 58.6%, and 58.6%, respectively)(Table 2). One respondent noted that “previous [internal medicine] history help[ed]” them in performing cutaneous disability assessments.

As with any survey, our study did have some inherent limitations. Only a relatively small sample size was willing to complete the survey. There was a predominance of respondents from California (34.6% [27/78]), as well as those practicing for less than 15 years (58.9% [46/78])(Figure). This could limit generalizability to the national population of dermatologists. In addition, there was potential for recall bias and errors in responding given the self-reported nature of the study. Different individuals may interpret the Likert scale options in various ways, which could skew results unintentionally. However, the survey was largely qualitative in nature, making it a legitimate tool for answering our research questions. Moreover, we were able to hear the perspectives of dermatologists across diverse practice settings, with free response prompts to increase the depth of the survey.

Almost 50 years later, our survey echoes common themes from Adams’ 1976 survey.⁴ Inadequate compensation, limited time, and burdensome paperwork all continue to hinder dermatologists’ ability to perform disability assessments. Our participants frequently commented that the current disability forms are not congruent with the nature of skin conditions, making it challenging to accurately document the facts.

Moreover, respondents felt uncertain in their role in disability assessment and occasionally noted distrust of patients or insufficient patient history as barriers to completing assessments. They also were unsure if physicians can grant disability status. This is a common misconception among physicians that leads to discomfort in helping with disability assessment.⁷ The role of physicians in disability assessment is to document the facts of a patient’s illness, not to determine whether they are eligible for benefits. We discovered uncertainty in our respondents’ ability to identify conditions eligible for disability, highlighting an area in need of greater education for physicians.

Despite these obstacles, respondents were interested in learning more about disability assessment and highlighted several practical approaches that could help them better perform this task. As skin specialists, dermatologists are the best-equipped physicians to assess cutaneous conditions and should play a greater role in performing disability assessments, which could be achieved through increased educational initiatives and individual physician motivation.⁷ We call for greater collaboration and reflection on the importance of disability assistance among dermatologists to increase participation in the disability-assessment process.

To the Editor:

Cutaneous medical conditions can have a substantial impact on patients’ functioning and quality of life. Many patients with severe skin disease are eligible to receive disability assistance that can provide them with essential income and health care. Previous research has highlighted disability assessment as one of the most important ways physicians can help mitigate the health consequences of poverty.¹ Dermatologists can play an important role in the disability assessment process by documenting the facts associated with patients’ skin conditions.

Although skin conditions have a relatively high prevalence, they remain underrepresented in disability claims. Between 1997 and 2004, occupational skin diseases accounted for 12% to 17% of nonfatal work-related illnesses; however, during that same period, skin conditions comprised only 0.21% of disability claims in the United States.^2,3 Historically, there has been hesitancy among dermatologists to complete disability paperwork; a 1976 survey of dermatologists cited extensive paperwork, “troublesome patients,” and fee schedule issues as reasons.⁴ The lack of training regarding disability assessment in medical school and residency also has been noted.⁵

To characterize modern attitudes toward disability assessments, we conducted a survey of dermatologists across the United States. Our study was reviewed and declared exempt by the institutional review board of the Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center (Torrance, California)(approval #18CR-32242-01). Using convenience sampling, we emailed dermatologists from the Association of Professors of Dermatology and dermatology state societies in all 50 states inviting them to participate in our voluntary and anonymous survey, which was administered using SurveyMonkey. The use of all society mailing lists was approved by the respective owners. The 15-question survey included multiple choice, Likert scale, and free response sections. Summary and descriptive statistics were used to describe respondent demographics and identify any patterns in responses.

For each Likert-based question, participants ranked their degree of agreement with a statement as: 1=strongly disagree, 2=somewhat disagree, 3=neither agree nor disagree/neutral, 4=somewhat agree, and 5=strongly agree. The mean response and standard deviation were reported for each Likert scale prompt. Preplanned 1-sample t testing was used to analyze Likert scale data, in which the mean response for each prompt was compared to a baseline response of 3 (neutral). A P value <.05 was considered statistically significant. Statistical analyses were performed using SPSS Statistics for MacOS, version 27 (IBM).

Seventy-eight dermatologists agreed to participate, and 70 completed the survey, for a response rate of 89.7% (Table 1). The dermatologists we surveyed practiced in a variety of clinical settings, including academic public hospitals (46.2% [36/78]), academic private hospitals (33.3% [26/78]), and private practices (32.1% [25/78]), and 60.3% (47/78) reported providing disability documentation at some point. Most of the respondents (64.3% [45/70]) did not perform assessments in an average month (Table 2). Medical assessment documentation was provided most frequently for workers’ compensation (50.0% [35/70]), private insurance (27.1% [19/70]), and Social Security Disability Insurance (25.7% [18/70]). Dermatologists overwhelmingly reported no formal training for disability assessment in medical school (94.3% [66/70]), residency (97.1% [68/70]), or clinical practice (81.4% [57/70]).

In the Likert scale prompts, respondents agreed that they were uncertain of their role in disability assessment (mean response, 3.6; P<.001). Moreover, they were uncomfortable providing assessments (mean response, 3.5; P<.001) and felt that they did not have sufficient time to perform them (mean response, 3.6; P<.001). Dermatologists disagreed that they received adequate compensation for performing assessments (mean response, 2.2; P<.001) and felt that they did not have enough time to participate in assessments (mean response, 3.6; P<.001). Respondents generally did not feel distrustful of patients seeking disability assessment (mean response, 2.8; P=.043). Dermatologists neither agreed nor disagreed when asked if they thought that physicians can determine disability status (mean response, 3.2; P=.118). The details of the Likert scale responses are described in Table 3. Respondents also were uncertain as to which dermatologic conditions were eligible for disability. When asked to select which conditions from a list of 10 were eligible per the Social Security Administration listing of disability impairments, only 15.4% (12/70) of respondents correctly identified that all the conditions qualified; these included ichthyosis, pemphigus vulgaris, allergic contact dermatitis, hidradenitis suppurativa, systemic lupus erythematosus, chromoblastomycosis, xeroderma pigmentosum, burns, malignant melanoma, and scleroderma.⁶

In the free-response prompts, respondents frequently described extensive paperwork, inadequate time, and lack of reimbursement as barriers to providing documentation. Often, dermatologists found that the forms were not well matched to the skin conditions they were evaluating and rather had a musculoskeletal focus. Multiple individuals commented on the challenge in assessing the percentage of disability and functional/psychosocial impairment in skin conditions. One respondent noted that workers’ compensation forms ask if the patient is “…permanent and stationary…for most conditions this has no meaning in dermatology.” Some felt hesitant to provide documentation because they had insufficient patient history, especially regarding employment, and opted to defer to primary care providers who might be more familiar with the full patient history.

A dermatologist described their perspective as follows:

“…As a specialist I feel that I don’t have a complete look into all the factors that could contribute to a patient[’]s need to go on disability, and I don’t have experience with filling out disability requests. That being said, if a patient[’]s request for disability was due to a skin disease that I know way more about than [a] primary care [physician] would, I would do the disability assessment.”

Another respondent noted the complexity in “establishing causality” for workers’ compensation. Another dermatologist reported,

“The most frequent challenging situation I encounter is being asked to evaluate for maximum medical improvement after patch testing. If the patient is not fully avoiding contact allergens either at home or at work, then I typically document that they are not at [maximum medical improvement]. The reality is that most frequently it is due to exposure to allergens at home so the line between what is a legitimate worker’s comp[ensation] issue and what is a home life choice is blurry.”

Nevertheless, respondents expressed interest in learning more about disability assessment procedures. Summary guides, lectures, and prefilled paperwork were the most popular initiatives that respondents agreed would be beneficial toward becoming educated regarding disability assessment (78.6%, 58.6%, and 58.6%, respectively)(Table 2). One respondent noted that “previous [internal medicine] history help[ed]” them in performing cutaneous disability assessments.

As with any survey, our study did have some inherent limitations. Only a relatively small sample size was willing to complete the survey. There was a predominance of respondents from California (34.6% [27/78]), as well as those practicing for less than 15 years (58.9% [46/78])(Figure). This could limit generalizability to the national population of dermatologists. In addition, there was potential for recall bias and errors in responding given the self-reported nature of the study. Different individuals may interpret the Likert scale options in various ways, which could skew results unintentionally. However, the survey was largely qualitative in nature, making it a legitimate tool for answering our research questions. Moreover, we were able to hear the perspectives of dermatologists across diverse practice settings, with free response prompts to increase the depth of the survey.

Almost 50 years later, our survey echoes common themes from Adams’ 1976 survey.⁴ Inadequate compensation, limited time, and burdensome paperwork all continue to hinder dermatologists’ ability to perform disability assessments. Our participants frequently commented that the current disability forms are not congruent with the nature of skin conditions, making it challenging to accurately document the facts.

Moreover, respondents felt uncertain in their role in disability assessment and occasionally noted distrust of patients or insufficient patient history as barriers to completing assessments. They also were unsure if physicians can grant disability status. This is a common misconception among physicians that leads to discomfort in helping with disability assessment.⁷ The role of physicians in disability assessment is to document the facts of a patient’s illness, not to determine whether they are eligible for benefits. We discovered uncertainty in our respondents’ ability to identify conditions eligible for disability, highlighting an area in need of greater education for physicians.

Despite these obstacles, respondents were interested in learning more about disability assessment and highlighted several practical approaches that could help them better perform this task. As skin specialists, dermatologists are the best-equipped physicians to assess cutaneous conditions and should play a greater role in performing disability assessments, which could be achieved through increased educational initiatives and individual physician motivation.⁷ We call for greater collaboration and reflection on the importance of disability assistance among dermatologists to increase participation in the disability-assessment process.

To the Editor:

Cutaneous medical conditions can have a substantial impact on patients’ functioning and quality of life. Many patients with severe skin disease are eligible to receive disability assistance that can provide them with essential income and health care. Previous research has highlighted disability assessment as one of the most important ways physicians can help mitigate the health consequences of poverty.¹ Dermatologists can play an important role in the disability assessment process by documenting the facts associated with patients’ skin conditions.

Although skin conditions have a relatively high prevalence, they remain underrepresented in disability claims. Between 1997 and 2004, occupational skin diseases accounted for 12% to 17% of nonfatal work-related illnesses; however, during that same period, skin conditions comprised only 0.21% of disability claims in the United States.^2,3 Historically, there has been hesitancy among dermatologists to complete disability paperwork; a 1976 survey of dermatologists cited extensive paperwork, “troublesome patients,” and fee schedule issues as reasons.⁴ The lack of training regarding disability assessment in medical school and residency also has been noted.⁵

To characterize modern attitudes toward disability assessments, we conducted a survey of dermatologists across the United States. Our study was reviewed and declared exempt by the institutional review board of the Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center (Torrance, California)(approval #18CR-32242-01). Using convenience sampling, we emailed dermatologists from the Association of Professors of Dermatology and dermatology state societies in all 50 states inviting them to participate in our voluntary and anonymous survey, which was administered using SurveyMonkey. The use of all society mailing lists was approved by the respective owners. The 15-question survey included multiple choice, Likert scale, and free response sections. Summary and descriptive statistics were used to describe respondent demographics and identify any patterns in responses.

For each Likert-based question, participants ranked their degree of agreement with a statement as: 1=strongly disagree, 2=somewhat disagree, 3=neither agree nor disagree/neutral, 4=somewhat agree, and 5=strongly agree. The mean response and standard deviation were reported for each Likert scale prompt. Preplanned 1-sample t testing was used to analyze Likert scale data, in which the mean response for each prompt was compared to a baseline response of 3 (neutral). A P value <.05 was considered statistically significant. Statistical analyses were performed using SPSS Statistics for MacOS, version 27 (IBM).

Seventy-eight dermatologists agreed to participate, and 70 completed the survey, for a response rate of 89.7% (Table 1). The dermatologists we surveyed practiced in a variety of clinical settings, including academic public hospitals (46.2% [36/78]), academic private hospitals (33.3% [26/78]), and private practices (32.1% [25/78]), and 60.3% (47/78) reported providing disability documentation at some point. Most of the respondents (64.3% [45/70]) did not perform assessments in an average month (Table 2). Medical assessment documentation was provided most frequently for workers’ compensation (50.0% [35/70]), private insurance (27.1% [19/70]), and Social Security Disability Insurance (25.7% [18/70]). Dermatologists overwhelmingly reported no formal training for disability assessment in medical school (94.3% [66/70]), residency (97.1% [68/70]), or clinical practice (81.4% [57/70]).

In the Likert scale prompts, respondents agreed that they were uncertain of their role in disability assessment (mean response, 3.6; P<.001). Moreover, they were uncomfortable providing assessments (mean response, 3.5; P<.001) and felt that they did not have sufficient time to perform them (mean response, 3.6; P<.001). Dermatologists disagreed that they received adequate compensation for performing assessments (mean response, 2.2; P<.001) and felt that they did not have enough time to participate in assessments (mean response, 3.6; P<.001). Respondents generally did not feel distrustful of patients seeking disability assessment (mean response, 2.8; P=.043). Dermatologists neither agreed nor disagreed when asked if they thought that physicians can determine disability status (mean response, 3.2; P=.118). The details of the Likert scale responses are described in Table 3. Respondents also were uncertain as to which dermatologic conditions were eligible for disability. When asked to select which conditions from a list of 10 were eligible per the Social Security Administration listing of disability impairments, only 15.4% (12/70) of respondents correctly identified that all the conditions qualified; these included ichthyosis, pemphigus vulgaris, allergic contact dermatitis, hidradenitis suppurativa, systemic lupus erythematosus, chromoblastomycosis, xeroderma pigmentosum, burns, malignant melanoma, and scleroderma.⁶

In the free-response prompts, respondents frequently described extensive paperwork, inadequate time, and lack of reimbursement as barriers to providing documentation. Often, dermatologists found that the forms were not well matched to the skin conditions they were evaluating and rather had a musculoskeletal focus. Multiple individuals commented on the challenge in assessing the percentage of disability and functional/psychosocial impairment in skin conditions. One respondent noted that workers’ compensation forms ask if the patient is “…permanent and stationary…for most conditions this has no meaning in dermatology.” Some felt hesitant to provide documentation because they had insufficient patient history, especially regarding employment, and opted to defer to primary care providers who might be more familiar with the full patient history.

A dermatologist described their perspective as follows:

“…As a specialist I feel that I don’t have a complete look into all the factors that could contribute to a patient[’]s need to go on disability, and I don’t have experience with filling out disability requests. That being said, if a patient[’]s request for disability was due to a skin disease that I know way more about than [a] primary care [physician] would, I would do the disability assessment.”

Another respondent noted the complexity in “establishing causality” for workers’ compensation. Another dermatologist reported,

“The most frequent challenging situation I encounter is being asked to evaluate for maximum medical improvement after patch testing. If the patient is not fully avoiding contact allergens either at home or at work, then I typically document that they are not at [maximum medical improvement]. The reality is that most frequently it is due to exposure to allergens at home so the line between what is a legitimate worker’s comp[ensation] issue and what is a home life choice is blurry.”

Nevertheless, respondents expressed interest in learning more about disability assessment procedures. Summary guides, lectures, and prefilled paperwork were the most popular initiatives that respondents agreed would be beneficial toward becoming educated regarding disability assessment (78.6%, 58.6%, and 58.6%, respectively)(Table 2). One respondent noted that “previous [internal medicine] history help[ed]” them in performing cutaneous disability assessments.

As with any survey, our study did have some inherent limitations. Only a relatively small sample size was willing to complete the survey. There was a predominance of respondents from California (34.6% [27/78]), as well as those practicing for less than 15 years (58.9% [46/78])(Figure). This could limit generalizability to the national population of dermatologists. In addition, there was potential for recall bias and errors in responding given the self-reported nature of the study. Different individuals may interpret the Likert scale options in various ways, which could skew results unintentionally. However, the survey was largely qualitative in nature, making it a legitimate tool for answering our research questions. Moreover, we were able to hear the perspectives of dermatologists across diverse practice settings, with free response prompts to increase the depth of the survey.

Almost 50 years later, our survey echoes common themes from Adams’ 1976 survey.⁴ Inadequate compensation, limited time, and burdensome paperwork all continue to hinder dermatologists’ ability to perform disability assessments. Our participants frequently commented that the current disability forms are not congruent with the nature of skin conditions, making it challenging to accurately document the facts.

Moreover, respondents felt uncertain in their role in disability assessment and occasionally noted distrust of patients or insufficient patient history as barriers to completing assessments. They also were unsure if physicians can grant disability status. This is a common misconception among physicians that leads to discomfort in helping with disability assessment.⁷ The role of physicians in disability assessment is to document the facts of a patient’s illness, not to determine whether they are eligible for benefits. We discovered uncertainty in our respondents’ ability to identify conditions eligible for disability, highlighting an area in need of greater education for physicians.

Despite these obstacles, respondents were interested in learning more about disability assessment and highlighted several practical approaches that could help them better perform this task. As skin specialists, dermatologists are the best-equipped physicians to assess cutaneous conditions and should play a greater role in performing disability assessments, which could be achieved through increased educational initiatives and individual physician motivation.⁷ We call for greater collaboration and reflection on the importance of disability assistance among dermatologists to increase participation in the disability-assessment process.

Humans are inherently prone to errors. The extent and consequences of medical errors were documented in the 2000 publication of To Err is Human: Building a Safer Health System.¹ Published research on medical errors in dermatology has emphasized the heuristic issues involved in diagnosis,^2-6 essentially approaching the “why?” and “how?” of such errors. By contrast, the current study aimed to elucidate the “what?”—what are the dermatologic conditions most prone to diagnostic and/or management errors? One study published in 1987 approached this question by analyzing patterns of errors for dermatologic conditions in patients referred for specialty care by primary care physicians.⁷ The current study aimed to update and expand on the findings of this 1987 report by comparing more recent data on the errors made by providers and patients regarding skin conditions.

Methods

Data were collected prospectively from March 18, 2021, through July 25, 2023. Prospective data were obtained by recording the nature of errors noted for all patients seen by a board-certified dermatologist (R.J.P.) during routine outpatient practice in Norfolk, Virginia. This practice is limited to medical dermatology and accepts patients of any age from any referral source, with or without medical insurance. Retrospective data were obtained by review of electronic medical records for all patients seen by the same board-certified dermatologist from June 5, 2020, through March 12, 2021, who previously had been seen by an outside provider or were self-referred. In this study, the term diagnosis is used to describe providers’ explicit or imputed conclusions as to the nature of a dermatosis, and the term interpretation is used to describe patients' conclusions about their own condition. For this study, the patients’ self-made interpretations of their dermatoses were deemed to be correct when they agreed with those made by the dermatologist using standard clinicopathologic criteria supplemented by rapid bedside diagnostic techniques, as detailed in the 1987 study.⁷

Cases in which diagnostic or therapeutic errors were noted were entered into a spreadsheet that excluded patients’ names or other identifiers. For each noted case of diagnostic or therapeutic error, the following data were entered: patient’s age and sex; the name of the incorrect diagnosis, interpretation, or treatment; and the name of the correct (missed) diagnosis, along with the source of the error (provider or patient). Provider diagnoses were determined from medical records or patient statements or were imputed from the generally accepted indications for prescribed treatments. A provider was deemed to be any practitioner with prescriptive authority. Patients’ interpretations of their conditions were determined by patient statements or were imputed based on the indications for treatments being used. A treatment error was recorded when a diagnosis or interpretation was deemed to be correct, but treatment was deemed to be inappropriate. The same dermatologist (R.J.P) made all determinations as to the nature of the errors and their source.

Diagnostic errors were determined in several situations: (1) if the interpretation made by the patient of their dermatosis differed from the correct diagnosis in the absence of any additional diagnostic documentation, the correct diagnosis was scored as a missed diagnosis and the incorrect interpretation was scored as such; (2) if the provider’s diagnosis in the patient’s medical record differed from the correct diagnosis, both the correct (missed) and incorrect diagnoses were recorded; and (3) if the indication(s) of the medication(s) prescribed by the provider or used by the patient for their condition differed from the correct diagnosis, an imputed diagnosis based on this indication was scored as the incorrect diagnosis and the correct (missed) diagnosis was recorded; for example, an error would be entered into the spreadsheet for a patient using terbinafine cream for what was actually psoriasis. For a medication with multiple active agents, an error would be entered into the spreadsheet only if none of its indications matched the correct diagnosis; for example, if the patient had been prescribed a betamethasone/clotrimazole product, no error would be scored if the correct diagnosis was a steroid-responsive dermatosis, dermatophytosis, candidiasis, or tinea versicolor. For a single medication with multiple indications, no error would be recorded if the correct diagnosis was any of these indications; for example, in a patient who had been prescribed topical ketoconazole, no error would be scored if the correct diagnosis was dermatophytosis, candidiasis, tinea versicolor, or seborrheic dermatitis. Additionally, no error would be recorded if the correct diagnosis was uncertain at the time of initial patient evaluation or during chart review.

Standard spreadsheet functions and the pandas package⁸ from the Python programming language⁹ were used to extract relevant data from the spreadsheet (Tables 1-4).

Results

A total of 446 patient visits (182 males, 264 females) were included in the study, in which a total of 486 errors were found in the combined prospective and retrospective portions of the study. These errors involved 1.4% of all patient visits for the study period—specifically, all in routine practice as well as all patient records retrospectively reviewed. The age of the patients ranged from 4 to 95 years; the mean age was 51.5 years for males and 50.8 years for females.

The study results are outlined in Tables 1 through 4. To minimize the amount of data provided with no appreciable effect on the results, cases in which an incorrect or missed diagnosis/interpretation occurred only once (ie, unique case errors) were excluded from the tables. Tables 1 and 2 indicate the numbers and types of incorrect and missed diagnoses.

In the combined patient and provider cases, there were 434 instances in which provider diagnoses and patient interpretations were incorrect, 320 (73.7%) of which involved infectious disorders. By contrast, of the 413 instances of provider and patient missed diagnoses 289 (70.0%) were inflammatory dermatoses. The pattern was similar for patients’ incorrect interpretations compared to the incorrect diagnoses of the medical providers. Patients incorrectly interpreted their dermatoses as infectious in 79.5% (101/127) of cases. Similarly, providers incorrectly diagnosed their patients’ dermatoses as infectious in 75.4% (211/280) of cases (Table 3). For patients’ missed diagnoses, 70.7% (82/116) involved inflammatory dermatoses. For providers’ missed diagnoses, 63.9% (179/280) involved inflammatory dermatoses (Table 4).

Treatment errors in the context of correct diagnoses were uncommon. Fifteen (3.4%) such cases were noted in the 446 error-containing patient visits. In 4 (26.7%) of the 15 cases, potent topical corticosteroids were used long term on inappropriate cutaneous sites (eg, genital, facial, or intertriginous areas). Another 4 (26.7%) cases involved fungal infections: nystatin used for tinea versicolor in 1 case and for dermatophytosis in another, widespread dermatophytosis treated topically, and use of a nonindicated topical antifungal for onychomycosis. Other examples involved inadequate dosing of systemic corticosteroids for extensive acute contact dermatitis, psoriasis treated with systemic corticosteroids, inadequate dosing of medication for seborrheic dermatitis, and treatment with valacyclovir based solely on serologic testing.

Comment

The results of our study indicate that errors in management of cutaneous disorders are overwhelmingly diagnostic in nature, while treatment errors appear to be unusual when the correct diagnosis is made. Both the current study and the 1987 study indicated a notable tendency of providers to incorrectly diagnose infectious disorders and to miss the diagnosis of inflammatory dermatoses.⁷ The current study extends this finding to include patients’ interpretive errors. 

It is notable that many of the incorrect and missed diagnoses can be confirmed or ruled out by rapid bedside techniques, namely potassium hydroxide (KOH) preparation for dermatophytes, candidiasis, and tinea versicolor; wet preparation for scabies and pediculosis; Tzanck preparation for herpes simplex and herpes zoster; and crush preparation for molluscum contagiosum. Notably, 57.8% (281/486) of cases in which error was noted involved disorders for which the use of one of these bedside diagnostic tests could have correctly established a diagnosis or ruled out an incorrect one; thus in an ideal world in which these tests were performed perfectly in all appropriate cases, more than half of the errors detected in this study could have been avoided. Dermatophytosis was involved in 35.8% (174/486) of the error-containing patient encounters in this study; therefore, if only the KOH preparation is considered, more than one-third of all errors documented in this study could have been avoided. Unfortunately, surveys have suggested that among dermatologists in the United States and some other countries, KOH preparations are used infrequently.^10-12

Certain limitations were inherent to this study. The data were derived from a single dermatology practice by one physician in one geographic region over a short period of time. These factors may limit the generalizability of the results. Although the goal was to identify all errors made for the patients seen, some errors likely were missed due to incomplete patient history or inaccurate medication listings. There is no absolute way to determine if the diagnoses or the treatments deemed correct by the dermatologist were, in fact, correct. For cases in which a patient’s interpretation or a provider’s diagnosis was imputed from the indication(s) associated with the medication(s) being used, one cannot exclude the possibility that a medication was used appropriately for a nonlabeled or nonstandard indication. The designation of treatment errors may be subject to different interpretations by different clinicians. Despite these limitations, it is likely that the results of this study can be extrapolated to reasonably similar dermatology practices. The apparently persistent and consistent tendency of clinicians to incorrectly diagnose infectious dermatoses and to miss inflammatory conditions has implications for teaching of medical dermatology in the academic and clinical settings. In particular, given that dermatophytosis is the diagnosis involved in the highest number of errors, special emphasis should be placed on this infection in clinician education.

Acknowledgement—The authors would like to acknowledge the essential contributions to this study by Urvi Jain (Virginia Beach, Virginia), particularly for analysis and interpretation of data and for suggestions to improve the manuscript.

Humans are inherently prone to errors. The extent and consequences of medical errors were documented in the 2000 publication of To Err is Human: Building a Safer Health System.¹ Published research on medical errors in dermatology has emphasized the heuristic issues involved in diagnosis,^2-6 essentially approaching the “why?” and “how?” of such errors. By contrast, the current study aimed to elucidate the “what?”—what are the dermatologic conditions most prone to diagnostic and/or management errors? One study published in 1987 approached this question by analyzing patterns of errors for dermatologic conditions in patients referred for specialty care by primary care physicians.⁷ The current study aimed to update and expand on the findings of this 1987 report by comparing more recent data on the errors made by providers and patients regarding skin conditions.

Methods

Data were collected prospectively from March 18, 2021, through July 25, 2023. Prospective data were obtained by recording the nature of errors noted for all patients seen by a board-certified dermatologist (R.J.P.) during routine outpatient practice in Norfolk, Virginia. This practice is limited to medical dermatology and accepts patients of any age from any referral source, with or without medical insurance. Retrospective data were obtained by review of electronic medical records for all patients seen by the same board-certified dermatologist from June 5, 2020, through March 12, 2021, who previously had been seen by an outside provider or were self-referred. In this study, the term diagnosis is used to describe providers’ explicit or imputed conclusions as to the nature of a dermatosis, and the term interpretation is used to describe patients' conclusions about their own condition. For this study, the patients’ self-made interpretations of their dermatoses were deemed to be correct when they agreed with those made by the dermatologist using standard clinicopathologic criteria supplemented by rapid bedside diagnostic techniques, as detailed in the 1987 study.⁷

Cases in which diagnostic or therapeutic errors were noted were entered into a spreadsheet that excluded patients’ names or other identifiers. For each noted case of diagnostic or therapeutic error, the following data were entered: patient’s age and sex; the name of the incorrect diagnosis, interpretation, or treatment; and the name of the correct (missed) diagnosis, along with the source of the error (provider or patient). Provider diagnoses were determined from medical records or patient statements or were imputed from the generally accepted indications for prescribed treatments. A provider was deemed to be any practitioner with prescriptive authority. Patients’ interpretations of their conditions were determined by patient statements or were imputed based on the indications for treatments being used. A treatment error was recorded when a diagnosis or interpretation was deemed to be correct, but treatment was deemed to be inappropriate. The same dermatologist (R.J.P) made all determinations as to the nature of the errors and their source.

Diagnostic errors were determined in several situations: (1) if the interpretation made by the patient of their dermatosis differed from the correct diagnosis in the absence of any additional diagnostic documentation, the correct diagnosis was scored as a missed diagnosis and the incorrect interpretation was scored as such; (2) if the provider’s diagnosis in the patient’s medical record differed from the correct diagnosis, both the correct (missed) and incorrect diagnoses were recorded; and (3) if the indication(s) of the medication(s) prescribed by the provider or used by the patient for their condition differed from the correct diagnosis, an imputed diagnosis based on this indication was scored as the incorrect diagnosis and the correct (missed) diagnosis was recorded; for example, an error would be entered into the spreadsheet for a patient using terbinafine cream for what was actually psoriasis. For a medication with multiple active agents, an error would be entered into the spreadsheet only if none of its indications matched the correct diagnosis; for example, if the patient had been prescribed a betamethasone/clotrimazole product, no error would be scored if the correct diagnosis was a steroid-responsive dermatosis, dermatophytosis, candidiasis, or tinea versicolor. For a single medication with multiple indications, no error would be recorded if the correct diagnosis was any of these indications; for example, in a patient who had been prescribed topical ketoconazole, no error would be scored if the correct diagnosis was dermatophytosis, candidiasis, tinea versicolor, or seborrheic dermatitis. Additionally, no error would be recorded if the correct diagnosis was uncertain at the time of initial patient evaluation or during chart review.

Standard spreadsheet functions and the pandas package⁸ from the Python programming language⁹ were used to extract relevant data from the spreadsheet (Tables 1-4).

Results

A total of 446 patient visits (182 males, 264 females) were included in the study, in which a total of 486 errors were found in the combined prospective and retrospective portions of the study. These errors involved 1.4% of all patient visits for the study period—specifically, all in routine practice as well as all patient records retrospectively reviewed. The age of the patients ranged from 4 to 95 years; the mean age was 51.5 years for males and 50.8 years for females.

The study results are outlined in Tables 1 through 4. To minimize the amount of data provided with no appreciable effect on the results, cases in which an incorrect or missed diagnosis/interpretation occurred only once (ie, unique case errors) were excluded from the tables. Tables 1 and 2 indicate the numbers and types of incorrect and missed diagnoses.

In the combined patient and provider cases, there were 434 instances in which provider diagnoses and patient interpretations were incorrect, 320 (73.7%) of which involved infectious disorders. By contrast, of the 413 instances of provider and patient missed diagnoses 289 (70.0%) were inflammatory dermatoses. The pattern was similar for patients’ incorrect interpretations compared to the incorrect diagnoses of the medical providers. Patients incorrectly interpreted their dermatoses as infectious in 79.5% (101/127) of cases. Similarly, providers incorrectly diagnosed their patients’ dermatoses as infectious in 75.4% (211/280) of cases (Table 3). For patients’ missed diagnoses, 70.7% (82/116) involved inflammatory dermatoses. For providers’ missed diagnoses, 63.9% (179/280) involved inflammatory dermatoses (Table 4).

Treatment errors in the context of correct diagnoses were uncommon. Fifteen (3.4%) such cases were noted in the 446 error-containing patient visits. In 4 (26.7%) of the 15 cases, potent topical corticosteroids were used long term on inappropriate cutaneous sites (eg, genital, facial, or intertriginous areas). Another 4 (26.7%) cases involved fungal infections: nystatin used for tinea versicolor in 1 case and for dermatophytosis in another, widespread dermatophytosis treated topically, and use of a nonindicated topical antifungal for onychomycosis. Other examples involved inadequate dosing of systemic corticosteroids for extensive acute contact dermatitis, psoriasis treated with systemic corticosteroids, inadequate dosing of medication for seborrheic dermatitis, and treatment with valacyclovir based solely on serologic testing.

Comment

The results of our study indicate that errors in management of cutaneous disorders are overwhelmingly diagnostic in nature, while treatment errors appear to be unusual when the correct diagnosis is made. Both the current study and the 1987 study indicated a notable tendency of providers to incorrectly diagnose infectious disorders and to miss the diagnosis of inflammatory dermatoses.⁷ The current study extends this finding to include patients’ interpretive errors. 

It is notable that many of the incorrect and missed diagnoses can be confirmed or ruled out by rapid bedside techniques, namely potassium hydroxide (KOH) preparation for dermatophytes, candidiasis, and tinea versicolor; wet preparation for scabies and pediculosis; Tzanck preparation for herpes simplex and herpes zoster; and crush preparation for molluscum contagiosum. Notably, 57.8% (281/486) of cases in which error was noted involved disorders for which the use of one of these bedside diagnostic tests could have correctly established a diagnosis or ruled out an incorrect one; thus in an ideal world in which these tests were performed perfectly in all appropriate cases, more than half of the errors detected in this study could have been avoided. Dermatophytosis was involved in 35.8% (174/486) of the error-containing patient encounters in this study; therefore, if only the KOH preparation is considered, more than one-third of all errors documented in this study could have been avoided. Unfortunately, surveys have suggested that among dermatologists in the United States and some other countries, KOH preparations are used infrequently.^10-12

Certain limitations were inherent to this study. The data were derived from a single dermatology practice by one physician in one geographic region over a short period of time. These factors may limit the generalizability of the results. Although the goal was to identify all errors made for the patients seen, some errors likely were missed due to incomplete patient history or inaccurate medication listings. There is no absolute way to determine if the diagnoses or the treatments deemed correct by the dermatologist were, in fact, correct. For cases in which a patient’s interpretation or a provider’s diagnosis was imputed from the indication(s) associated with the medication(s) being used, one cannot exclude the possibility that a medication was used appropriately for a nonlabeled or nonstandard indication. The designation of treatment errors may be subject to different interpretations by different clinicians. Despite these limitations, it is likely that the results of this study can be extrapolated to reasonably similar dermatology practices. The apparently persistent and consistent tendency of clinicians to incorrectly diagnose infectious dermatoses and to miss inflammatory conditions has implications for teaching of medical dermatology in the academic and clinical settings. In particular, given that dermatophytosis is the diagnosis involved in the highest number of errors, special emphasis should be placed on this infection in clinician education.

Acknowledgement—The authors would like to acknowledge the essential contributions to this study by Urvi Jain (Virginia Beach, Virginia), particularly for analysis and interpretation of data and for suggestions to improve the manuscript.

Humans are inherently prone to errors. The extent and consequences of medical errors were documented in the 2000 publication of To Err is Human: Building a Safer Health System.¹ Published research on medical errors in dermatology has emphasized the heuristic issues involved in diagnosis,^2-6 essentially approaching the “why?” and “how?” of such errors. By contrast, the current study aimed to elucidate the “what?”—what are the dermatologic conditions most prone to diagnostic and/or management errors? One study published in 1987 approached this question by analyzing patterns of errors for dermatologic conditions in patients referred for specialty care by primary care physicians.⁷ The current study aimed to update and expand on the findings of this 1987 report by comparing more recent data on the errors made by providers and patients regarding skin conditions.

Methods

Data were collected prospectively from March 18, 2021, through July 25, 2023. Prospective data were obtained by recording the nature of errors noted for all patients seen by a board-certified dermatologist (R.J.P.) during routine outpatient practice in Norfolk, Virginia. This practice is limited to medical dermatology and accepts patients of any age from any referral source, with or without medical insurance. Retrospective data were obtained by review of electronic medical records for all patients seen by the same board-certified dermatologist from June 5, 2020, through March 12, 2021, who previously had been seen by an outside provider or were self-referred. In this study, the term diagnosis is used to describe providers’ explicit or imputed conclusions as to the nature of a dermatosis, and the term interpretation is used to describe patients' conclusions about their own condition. For this study, the patients’ self-made interpretations of their dermatoses were deemed to be correct when they agreed with those made by the dermatologist using standard clinicopathologic criteria supplemented by rapid bedside diagnostic techniques, as detailed in the 1987 study.⁷

Cases in which diagnostic or therapeutic errors were noted were entered into a spreadsheet that excluded patients’ names or other identifiers. For each noted case of diagnostic or therapeutic error, the following data were entered: patient’s age and sex; the name of the incorrect diagnosis, interpretation, or treatment; and the name of the correct (missed) diagnosis, along with the source of the error (provider or patient). Provider diagnoses were determined from medical records or patient statements or were imputed from the generally accepted indications for prescribed treatments. A provider was deemed to be any practitioner with prescriptive authority. Patients’ interpretations of their conditions were determined by patient statements or were imputed based on the indications for treatments being used. A treatment error was recorded when a diagnosis or interpretation was deemed to be correct, but treatment was deemed to be inappropriate. The same dermatologist (R.J.P) made all determinations as to the nature of the errors and their source.

Diagnostic errors were determined in several situations: (1) if the interpretation made by the patient of their dermatosis differed from the correct diagnosis in the absence of any additional diagnostic documentation, the correct diagnosis was scored as a missed diagnosis and the incorrect interpretation was scored as such; (2) if the provider’s diagnosis in the patient’s medical record differed from the correct diagnosis, both the correct (missed) and incorrect diagnoses were recorded; and (3) if the indication(s) of the medication(s) prescribed by the provider or used by the patient for their condition differed from the correct diagnosis, an imputed diagnosis based on this indication was scored as the incorrect diagnosis and the correct (missed) diagnosis was recorded; for example, an error would be entered into the spreadsheet for a patient using terbinafine cream for what was actually psoriasis. For a medication with multiple active agents, an error would be entered into the spreadsheet only if none of its indications matched the correct diagnosis; for example, if the patient had been prescribed a betamethasone/clotrimazole product, no error would be scored if the correct diagnosis was a steroid-responsive dermatosis, dermatophytosis, candidiasis, or tinea versicolor. For a single medication with multiple indications, no error would be recorded if the correct diagnosis was any of these indications; for example, in a patient who had been prescribed topical ketoconazole, no error would be scored if the correct diagnosis was dermatophytosis, candidiasis, tinea versicolor, or seborrheic dermatitis. Additionally, no error would be recorded if the correct diagnosis was uncertain at the time of initial patient evaluation or during chart review.

Standard spreadsheet functions and the pandas package⁸ from the Python programming language⁹ were used to extract relevant data from the spreadsheet (Tables 1-4).

Results

A total of 446 patient visits (182 males, 264 females) were included in the study, in which a total of 486 errors were found in the combined prospective and retrospective portions of the study. These errors involved 1.4% of all patient visits for the study period—specifically, all in routine practice as well as all patient records retrospectively reviewed. The age of the patients ranged from 4 to 95 years; the mean age was 51.5 years for males and 50.8 years for females.

The study results are outlined in Tables 1 through 4. To minimize the amount of data provided with no appreciable effect on the results, cases in which an incorrect or missed diagnosis/interpretation occurred only once (ie, unique case errors) were excluded from the tables. Tables 1 and 2 indicate the numbers and types of incorrect and missed diagnoses.

In the combined patient and provider cases, there were 434 instances in which provider diagnoses and patient interpretations were incorrect, 320 (73.7%) of which involved infectious disorders. By contrast, of the 413 instances of provider and patient missed diagnoses 289 (70.0%) were inflammatory dermatoses. The pattern was similar for patients’ incorrect interpretations compared to the incorrect diagnoses of the medical providers. Patients incorrectly interpreted their dermatoses as infectious in 79.5% (101/127) of cases. Similarly, providers incorrectly diagnosed their patients’ dermatoses as infectious in 75.4% (211/280) of cases (Table 3). For patients’ missed diagnoses, 70.7% (82/116) involved inflammatory dermatoses. For providers’ missed diagnoses, 63.9% (179/280) involved inflammatory dermatoses (Table 4).

Treatment errors in the context of correct diagnoses were uncommon. Fifteen (3.4%) such cases were noted in the 446 error-containing patient visits. In 4 (26.7%) of the 15 cases, potent topical corticosteroids were used long term on inappropriate cutaneous sites (eg, genital, facial, or intertriginous areas). Another 4 (26.7%) cases involved fungal infections: nystatin used for tinea versicolor in 1 case and for dermatophytosis in another, widespread dermatophytosis treated topically, and use of a nonindicated topical antifungal for onychomycosis. Other examples involved inadequate dosing of systemic corticosteroids for extensive acute contact dermatitis, psoriasis treated with systemic corticosteroids, inadequate dosing of medication for seborrheic dermatitis, and treatment with valacyclovir based solely on serologic testing.

Comment

The results of our study indicate that errors in management of cutaneous disorders are overwhelmingly diagnostic in nature, while treatment errors appear to be unusual when the correct diagnosis is made. Both the current study and the 1987 study indicated a notable tendency of providers to incorrectly diagnose infectious disorders and to miss the diagnosis of inflammatory dermatoses.⁷ The current study extends this finding to include patients’ interpretive errors. 

It is notable that many of the incorrect and missed diagnoses can be confirmed or ruled out by rapid bedside techniques, namely potassium hydroxide (KOH) preparation for dermatophytes, candidiasis, and tinea versicolor; wet preparation for scabies and pediculosis; Tzanck preparation for herpes simplex and herpes zoster; and crush preparation for molluscum contagiosum. Notably, 57.8% (281/486) of cases in which error was noted involved disorders for which the use of one of these bedside diagnostic tests could have correctly established a diagnosis or ruled out an incorrect one; thus in an ideal world in which these tests were performed perfectly in all appropriate cases, more than half of the errors detected in this study could have been avoided. Dermatophytosis was involved in 35.8% (174/486) of the error-containing patient encounters in this study; therefore, if only the KOH preparation is considered, more than one-third of all errors documented in this study could have been avoided. Unfortunately, surveys have suggested that among dermatologists in the United States and some other countries, KOH preparations are used infrequently.^10-12

Certain limitations were inherent to this study. The data were derived from a single dermatology practice by one physician in one geographic region over a short period of time. These factors may limit the generalizability of the results. Although the goal was to identify all errors made for the patients seen, some errors likely were missed due to incomplete patient history or inaccurate medication listings. There is no absolute way to determine if the diagnoses or the treatments deemed correct by the dermatologist were, in fact, correct. For cases in which a patient’s interpretation or a provider’s diagnosis was imputed from the indication(s) associated with the medication(s) being used, one cannot exclude the possibility that a medication was used appropriately for a nonlabeled or nonstandard indication. The designation of treatment errors may be subject to different interpretations by different clinicians. Despite these limitations, it is likely that the results of this study can be extrapolated to reasonably similar dermatology practices. The apparently persistent and consistent tendency of clinicians to incorrectly diagnose infectious dermatoses and to miss inflammatory conditions has implications for teaching of medical dermatology in the academic and clinical settings. In particular, given that dermatophytosis is the diagnosis involved in the highest number of errors, special emphasis should be placed on this infection in clinician education.

Acknowledgement—The authors would like to acknowledge the essential contributions to this study by Urvi Jain (Virginia Beach, Virginia), particularly for analysis and interpretation of data and for suggestions to improve the manuscript.

THE DIAGNOSIS: Lichen Sclerosus

Given the clinical appearance of white atrophic plaques with characteristic wrinkling of the skin, a diagnosis of lichen sclerosus was strongly suspected. At the initial office visit, the patient was prescribed clobetasol 0.05% ointment twice daily for 6 weeks. Histopathology revealed hyperkeratosis, follicular plugging, papillary dermal pallor, and adjacent lymphocytic inflammation, confirming the clinical diagnosis of lichen sclerosus (Figure). The patient then was lost to follow-up.

Lichen sclerosus is a chronic benign dermatologic condition of unknown etiology that is characterized by epidermal atrophy and inflammation and is common in postmenopausal women. It features pale, ivory-colored lesions with partially atrophic skin and a wrinkled cigarette paper appearance.¹ The differential for lichen sclerosus is broad, and definitive diagnosis is made via biopsy to rule out potential malignancy and other inflammatory skin diseases.¹ Lichen sclerosus is an immune-mediated disorder driven by type 1 T helper cells and regulated by miR-155. There has been an association with extracellular matrix protein 1, a glycoprotein that is found in the dermal-epidermal basement membrane zone, which provides structural integrity to the skin. Autoantibodies against extracellular matrix protein 1 and other antigens in the basement membrane generally are found in anogenital lichen sclerosus; however, their precise roles in the pathogenesis of lichen sclerosus remains unclear.¹

The differential diagnoses for lichen sclerosus include psoriasis, tinea corporis, lichen simplex chronicus, and atopic dermatitis. Psoriasis typically manifests as pink plaques with silver scales on the elbows, knees, and scalp in adult patients.² Our patient’s white plaques may have suggested psoriasis, but the partially atrophic skin with a wrinkled cigarette paper appearance was not compatible with that diagnosis.

Tinea corporis, a superficial fungal infection of the skin, manifests as circular or ovoid lesions with raised erythematous scaly borders, often with central clearing resembling a ring, that can occur anywhere on the body other than the feet, groin, face, scalp, or beard area.³ The fact that our patient previously had tried topical antifungal medications with no relief and that the skin lesions were atrophic rather than ring shaped made the diagnosis of tinea corporis unlikely.

Lichen simplex chronicus is a chronic condition caused by friction or scratching that is characterized by dry, patchy, scaly, and thickened areas of the skin. Typically affecting the head, arms, neck, scalp, and genital region, lichen simplex chronicus manifests with violaceous or hyperpigmented lesions.⁴ The nonpruritic atrophic plaques on the inner thighs and the presence of white patches on the vaginal area were not indicative of lichen simplex chronicus in our patient.

Atopic dermatitis manifests as pruritic erythematous scaly papules and plaques with secondary excoriation and possible lichenification. In adults, atopic dermatitis commonly appears on flexural surfaces.² Atopic dermatitis does not manifest with atrophy and skin wrinkling as seen in our patient.

In the management of lichen sclerosus, the standard treatment is potent topical corticosteroids. Alternatively, topical calcineurin inhibitors can be employed; however, due to the unknown nature of the condition’s underlying cause, targeted treatment is challenging. Our case underscores how lichen sclerosus can be misdiagnosed, highlighting the need for more frequent reporting in the literature to enhance early recognition and reduce delays in patient treatment.

THE DIAGNOSIS: Lichen Sclerosus

Given the clinical appearance of white atrophic plaques with characteristic wrinkling of the skin, a diagnosis of lichen sclerosus was strongly suspected. At the initial office visit, the patient was prescribed clobetasol 0.05% ointment twice daily for 6 weeks. Histopathology revealed hyperkeratosis, follicular plugging, papillary dermal pallor, and adjacent lymphocytic inflammation, confirming the clinical diagnosis of lichen sclerosus (Figure). The patient then was lost to follow-up.

Lichen sclerosus is a chronic benign dermatologic condition of unknown etiology that is characterized by epidermal atrophy and inflammation and is common in postmenopausal women. It features pale, ivory-colored lesions with partially atrophic skin and a wrinkled cigarette paper appearance.¹ The differential for lichen sclerosus is broad, and definitive diagnosis is made via biopsy to rule out potential malignancy and other inflammatory skin diseases.¹ Lichen sclerosus is an immune-mediated disorder driven by type 1 T helper cells and regulated by miR-155. There has been an association with extracellular matrix protein 1, a glycoprotein that is found in the dermal-epidermal basement membrane zone, which provides structural integrity to the skin. Autoantibodies against extracellular matrix protein 1 and other antigens in the basement membrane generally are found in anogenital lichen sclerosus; however, their precise roles in the pathogenesis of lichen sclerosus remains unclear.¹

The differential diagnoses for lichen sclerosus include psoriasis, tinea corporis, lichen simplex chronicus, and atopic dermatitis. Psoriasis typically manifests as pink plaques with silver scales on the elbows, knees, and scalp in adult patients.² Our patient’s white plaques may have suggested psoriasis, but the partially atrophic skin with a wrinkled cigarette paper appearance was not compatible with that diagnosis.

Tinea corporis, a superficial fungal infection of the skin, manifests as circular or ovoid lesions with raised erythematous scaly borders, often with central clearing resembling a ring, that can occur anywhere on the body other than the feet, groin, face, scalp, or beard area.³ The fact that our patient previously had tried topical antifungal medications with no relief and that the skin lesions were atrophic rather than ring shaped made the diagnosis of tinea corporis unlikely.

Lichen simplex chronicus is a chronic condition caused by friction or scratching that is characterized by dry, patchy, scaly, and thickened areas of the skin. Typically affecting the head, arms, neck, scalp, and genital region, lichen simplex chronicus manifests with violaceous or hyperpigmented lesions.⁴ The nonpruritic atrophic plaques on the inner thighs and the presence of white patches on the vaginal area were not indicative of lichen simplex chronicus in our patient.

Atopic dermatitis manifests as pruritic erythematous scaly papules and plaques with secondary excoriation and possible lichenification. In adults, atopic dermatitis commonly appears on flexural surfaces.² Atopic dermatitis does not manifest with atrophy and skin wrinkling as seen in our patient.

In the management of lichen sclerosus, the standard treatment is potent topical corticosteroids. Alternatively, topical calcineurin inhibitors can be employed; however, due to the unknown nature of the condition’s underlying cause, targeted treatment is challenging. Our case underscores how lichen sclerosus can be misdiagnosed, highlighting the need for more frequent reporting in the literature to enhance early recognition and reduce delays in patient treatment.

THE DIAGNOSIS: Lichen Sclerosus

Given the clinical appearance of white atrophic plaques with characteristic wrinkling of the skin, a diagnosis of lichen sclerosus was strongly suspected. At the initial office visit, the patient was prescribed clobetasol 0.05% ointment twice daily for 6 weeks. Histopathology revealed hyperkeratosis, follicular plugging, papillary dermal pallor, and adjacent lymphocytic inflammation, confirming the clinical diagnosis of lichen sclerosus (Figure). The patient then was lost to follow-up.

Lichen sclerosus is a chronic benign dermatologic condition of unknown etiology that is characterized by epidermal atrophy and inflammation and is common in postmenopausal women. It features pale, ivory-colored lesions with partially atrophic skin and a wrinkled cigarette paper appearance.¹ The differential for lichen sclerosus is broad, and definitive diagnosis is made via biopsy to rule out potential malignancy and other inflammatory skin diseases.¹ Lichen sclerosus is an immune-mediated disorder driven by type 1 T helper cells and regulated by miR-155. There has been an association with extracellular matrix protein 1, a glycoprotein that is found in the dermal-epidermal basement membrane zone, which provides structural integrity to the skin. Autoantibodies against extracellular matrix protein 1 and other antigens in the basement membrane generally are found in anogenital lichen sclerosus; however, their precise roles in the pathogenesis of lichen sclerosus remains unclear.¹

The differential diagnoses for lichen sclerosus include psoriasis, tinea corporis, lichen simplex chronicus, and atopic dermatitis. Psoriasis typically manifests as pink plaques with silver scales on the elbows, knees, and scalp in adult patients.² Our patient’s white plaques may have suggested psoriasis, but the partially atrophic skin with a wrinkled cigarette paper appearance was not compatible with that diagnosis.

Tinea corporis, a superficial fungal infection of the skin, manifests as circular or ovoid lesions with raised erythematous scaly borders, often with central clearing resembling a ring, that can occur anywhere on the body other than the feet, groin, face, scalp, or beard area.³ The fact that our patient previously had tried topical antifungal medications with no relief and that the skin lesions were atrophic rather than ring shaped made the diagnosis of tinea corporis unlikely.

Lichen simplex chronicus is a chronic condition caused by friction or scratching that is characterized by dry, patchy, scaly, and thickened areas of the skin. Typically affecting the head, arms, neck, scalp, and genital region, lichen simplex chronicus manifests with violaceous or hyperpigmented lesions.⁴ The nonpruritic atrophic plaques on the inner thighs and the presence of white patches on the vaginal area were not indicative of lichen simplex chronicus in our patient.

Atopic dermatitis manifests as pruritic erythematous scaly papules and plaques with secondary excoriation and possible lichenification. In adults, atopic dermatitis commonly appears on flexural surfaces.² Atopic dermatitis does not manifest with atrophy and skin wrinkling as seen in our patient.

In the management of lichen sclerosus, the standard treatment is potent topical corticosteroids. Alternatively, topical calcineurin inhibitors can be employed; however, due to the unknown nature of the condition’s underlying cause, targeted treatment is challenging. Our case underscores how lichen sclerosus can be misdiagnosed, highlighting the need for more frequent reporting in the literature to enhance early recognition and reduce delays in patient treatment.

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