Dermatology

DIAGNOSIS

Senile gluteal dermatosis (SGD). SGD is a friction- related skin injury, also known as recliner butt, chronic tissue injury, or grandfather’s disease.^1-4 The hallmarks include blanchable erythematous plaques and/or purplish discoloration of the fleshy part of the buttocks or posterior thighs, with little to no change over months to years. Additional findings may include skin erosions, lichenification, and ridging. SGD is most commonly seen in older adults with impaired mobility who spend prolonged periods in a reclined position, particularly those who slide down in a chair, “scoot,” or drag the buttocks during transfers or repositioning.

The pathogenesis of SGD is thought to involve microischemia associated with prolonged sitting.⁴ Histopathologic findings are nonspecific and may include hyperkeratosis, psoriasiform epidermal hyperplasia, vascular dilatation or proliferation in the superficial dermis, and reactive lymphohistiocytic perivascular infiltrate.⁴ The condition is poorly recognized and is likely underreported. Treatment involves reducing frictional injury by avoiding the reclined position, minimizing sliding during transfers, and frequent repositioning. Petroleum-based ointments may be applied to reduce friction and protect the skin barrier. Heat-dissipating chair cushions can be used to offload pressure and improve the local microclimate. Friction-related skin injuries need to be differentiated from pressure injuries, in which pressure and shear are the driving forces, and lesions are located over bony prominences.

Unlike SGD, chronic lichen sclerosus typically occurs in the anogenital area, including the scrotum and vulva, and is typically intensely pruritic, with white, atrophic plaques.

A stage 2 pressure injury is characterized by an area of partial-thickness skin loss with exposed dermis, usually overlying a bony prominence. Although friction-related skin injuries may contain erosions, they are often maroon or purple and are not located over a bony prominence.

Deep tissue injury (DTI) is characterized by nonblanchable dark red or purple skin discoloration, with intact or nonintact skin. While friction injuries may mimic DTIs, they lack the characteristic anatomic location over a bony prominence and the predictable evolution pattern seen in DTIs.

Incontinence-associated dermatitis (IAD) results from prolonged exposure to urine and/or feces and presents with erythema, inflammation, and epidermal erosion. Although IAD can look similar or coincide with SGD, the affected area is typically red, not purple. Skin ridging and lichenification are also not seen in IAD cases.

Sedentary behavior is prevalent among older adults, with nearly 60% spending > 4 hours per day sitting.⁵ Prolonged sitting puts them at risk for friction-related skin injuries. Even though friction-related skin injuries are typically nonprogressive, these patients are also at risk for pressure injuries that are typically acquired in a sitting position (eg, ischial and sacrococcygeal). Therefore, it is imperative that clinicians not only address SGD but also implement a pressure injury prevention plan.

DIAGNOSIS

Senile gluteal dermatosis (SGD). SGD is a friction- related skin injury, also known as recliner butt, chronic tissue injury, or grandfather’s disease.^1-4 The hallmarks include blanchable erythematous plaques and/or purplish discoloration of the fleshy part of the buttocks or posterior thighs, with little to no change over months to years. Additional findings may include skin erosions, lichenification, and ridging. SGD is most commonly seen in older adults with impaired mobility who spend prolonged periods in a reclined position, particularly those who slide down in a chair, “scoot,” or drag the buttocks during transfers or repositioning.

The pathogenesis of SGD is thought to involve microischemia associated with prolonged sitting.⁴ Histopathologic findings are nonspecific and may include hyperkeratosis, psoriasiform epidermal hyperplasia, vascular dilatation or proliferation in the superficial dermis, and reactive lymphohistiocytic perivascular infiltrate.⁴ The condition is poorly recognized and is likely underreported. Treatment involves reducing frictional injury by avoiding the reclined position, minimizing sliding during transfers, and frequent repositioning. Petroleum-based ointments may be applied to reduce friction and protect the skin barrier. Heat-dissipating chair cushions can be used to offload pressure and improve the local microclimate. Friction-related skin injuries need to be differentiated from pressure injuries, in which pressure and shear are the driving forces, and lesions are located over bony prominences.

Unlike SGD, chronic lichen sclerosus typically occurs in the anogenital area, including the scrotum and vulva, and is typically intensely pruritic, with white, atrophic plaques.

A stage 2 pressure injury is characterized by an area of partial-thickness skin loss with exposed dermis, usually overlying a bony prominence. Although friction-related skin injuries may contain erosions, they are often maroon or purple and are not located over a bony prominence.

Deep tissue injury (DTI) is characterized by nonblanchable dark red or purple skin discoloration, with intact or nonintact skin. While friction injuries may mimic DTIs, they lack the characteristic anatomic location over a bony prominence and the predictable evolution pattern seen in DTIs.

Incontinence-associated dermatitis (IAD) results from prolonged exposure to urine and/or feces and presents with erythema, inflammation, and epidermal erosion. Although IAD can look similar or coincide with SGD, the affected area is typically red, not purple. Skin ridging and lichenification are also not seen in IAD cases.

Sedentary behavior is prevalent among older adults, with nearly 60% spending > 4 hours per day sitting.⁵ Prolonged sitting puts them at risk for friction-related skin injuries. Even though friction-related skin injuries are typically nonprogressive, these patients are also at risk for pressure injuries that are typically acquired in a sitting position (eg, ischial and sacrococcygeal). Therefore, it is imperative that clinicians not only address SGD but also implement a pressure injury prevention plan.

DIAGNOSIS

Senile gluteal dermatosis (SGD). SGD is a friction- related skin injury, also known as recliner butt, chronic tissue injury, or grandfather’s disease.^1-4 The hallmarks include blanchable erythematous plaques and/or purplish discoloration of the fleshy part of the buttocks or posterior thighs, with little to no change over months to years. Additional findings may include skin erosions, lichenification, and ridging. SGD is most commonly seen in older adults with impaired mobility who spend prolonged periods in a reclined position, particularly those who slide down in a chair, “scoot,” or drag the buttocks during transfers or repositioning.

The pathogenesis of SGD is thought to involve microischemia associated with prolonged sitting.⁴ Histopathologic findings are nonspecific and may include hyperkeratosis, psoriasiform epidermal hyperplasia, vascular dilatation or proliferation in the superficial dermis, and reactive lymphohistiocytic perivascular infiltrate.⁴ The condition is poorly recognized and is likely underreported. Treatment involves reducing frictional injury by avoiding the reclined position, minimizing sliding during transfers, and frequent repositioning. Petroleum-based ointments may be applied to reduce friction and protect the skin barrier. Heat-dissipating chair cushions can be used to offload pressure and improve the local microclimate. Friction-related skin injuries need to be differentiated from pressure injuries, in which pressure and shear are the driving forces, and lesions are located over bony prominences.

Unlike SGD, chronic lichen sclerosus typically occurs in the anogenital area, including the scrotum and vulva, and is typically intensely pruritic, with white, atrophic plaques.

A stage 2 pressure injury is characterized by an area of partial-thickness skin loss with exposed dermis, usually overlying a bony prominence. Although friction-related skin injuries may contain erosions, they are often maroon or purple and are not located over a bony prominence.

Deep tissue injury (DTI) is characterized by nonblanchable dark red or purple skin discoloration, with intact or nonintact skin. While friction injuries may mimic DTIs, they lack the characteristic anatomic location over a bony prominence and the predictable evolution pattern seen in DTIs.

Incontinence-associated dermatitis (IAD) results from prolonged exposure to urine and/or feces and presents with erythema, inflammation, and epidermal erosion. Although IAD can look similar or coincide with SGD, the affected area is typically red, not purple. Skin ridging and lichenification are also not seen in IAD cases.

Sedentary behavior is prevalent among older adults, with nearly 60% spending > 4 hours per day sitting.⁵ Prolonged sitting puts them at risk for friction-related skin injuries. Even though friction-related skin injuries are typically nonprogressive, these patients are also at risk for pressure injuries that are typically acquired in a sitting position (eg, ischial and sacrococcygeal). Therefore, it is imperative that clinicians not only address SGD but also implement a pressure injury prevention plan.

TOPLINE:

In a review of physician-related malpractice cases from 1930 to 2025, melanoma was the most frequently litigated skin cancer, and failure or delay in diagnosis was the most common allegation, with documented death in nearly one third of cases.

METHODOLOGY:

Researchers conducted a review of physician-related medicolegal cases involving skin cancer using the LexisNexis legal database and identified 188 unique cases from 1930 through May 2025.

Cases were included if physicians were named as defendants and the litigation centered on diagnosis or management of a cutaneous malignancy.

Study outcomes examined case characteristics including cancer type, practice setting, defendant specialty, primary allegations, clinical outcomes, and case verdicts across the US.

TAKEAWAY:

Melanoma accounted for 49.5% of litigated cases, followed by squamous cell carcinoma (21.6%), basal cell carcinoma (14.2%), unspecified skin cancer (11.6%), and other rare tumors (3.1%). Death was reported in 29.8% of cases and metastatic disease in 39.9%.

Failure or delay in diagnosis was the leading allegation (38.1%), followed by treatment or management errors (24.2%), misdiagnosis (11.4%), “deliberate indifference” (8.3%), inadequate informed consent (7.5%), and pathology-related errors (7.2%).

Family physicians were the most common defendants (27.5%), followed by dermatologists, including Mohs surgeons (20.1%), and pathologists or dermatopathologists (14.4%), followed by general or plastic surgeons (7.9%), and internists (4.4%). Most cases originated in private practices (59.7%), and New York (16.0%) and California (13.3%) were the states with the most cases.

Among 109 closed cases, 5.5% resulted in plaintiff verdicts, whereas defense verdicts predominated in 55.0%. Plaintiff awards ranged from $10,000 to $4.25 million.

IN PRACTICE:

“This comprehensive review demonstrates that melanoma is the most frequently litigated skin cancer, particularly in cases involving metastatic disease or death, and that family physicians are the most commonly named defendants overall,” the authors wrote. “By examining both allegations and outcomes,” they added, “this analysis provides a pragmatic assessment of real-world litigation exposure and the clinical scenarios that expose physicians to legal proceedings, financial cost, reputational harm, and psychological burden, regardless of case disposition.”

SOURCE:

The study was led by Ghassan Barnawi, MD, Division of Dermatology, McGill University in Montreal, Quebec, Canada, and was published online on February 20, 2026, in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The study relied on published court decisions, which likely underestimated malpractice burden by excluding settlements and unreported claims.

DISCLOSURES:

The study did not receive any funding. The authors reported having no relevant conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

The study had no commercial funding. The authors had no relevant disclosures.

A version of this article first appeared on Medscape.com

TOPLINE:

In a review of physician-related malpractice cases from 1930 to 2025, melanoma was the most frequently litigated skin cancer, and failure or delay in diagnosis was the most common allegation, with documented death in nearly one third of cases.

METHODOLOGY:

Researchers conducted a review of physician-related medicolegal cases involving skin cancer using the LexisNexis legal database and identified 188 unique cases from 1930 through May 2025.

Cases were included if physicians were named as defendants and the litigation centered on diagnosis or management of a cutaneous malignancy.

Study outcomes examined case characteristics including cancer type, practice setting, defendant specialty, primary allegations, clinical outcomes, and case verdicts across the US.

TAKEAWAY:

Melanoma accounted for 49.5% of litigated cases, followed by squamous cell carcinoma (21.6%), basal cell carcinoma (14.2%), unspecified skin cancer (11.6%), and other rare tumors (3.1%). Death was reported in 29.8% of cases and metastatic disease in 39.9%.

Failure or delay in diagnosis was the leading allegation (38.1%), followed by treatment or management errors (24.2%), misdiagnosis (11.4%), “deliberate indifference” (8.3%), inadequate informed consent (7.5%), and pathology-related errors (7.2%).

Family physicians were the most common defendants (27.5%), followed by dermatologists, including Mohs surgeons (20.1%), and pathologists or dermatopathologists (14.4%), followed by general or plastic surgeons (7.9%), and internists (4.4%). Most cases originated in private practices (59.7%), and New York (16.0%) and California (13.3%) were the states with the most cases.

Among 109 closed cases, 5.5% resulted in plaintiff verdicts, whereas defense verdicts predominated in 55.0%. Plaintiff awards ranged from $10,000 to $4.25 million.

IN PRACTICE:

“This comprehensive review demonstrates that melanoma is the most frequently litigated skin cancer, particularly in cases involving metastatic disease or death, and that family physicians are the most commonly named defendants overall,” the authors wrote. “By examining both allegations and outcomes,” they added, “this analysis provides a pragmatic assessment of real-world litigation exposure and the clinical scenarios that expose physicians to legal proceedings, financial cost, reputational harm, and psychological burden, regardless of case disposition.”

SOURCE:

The study was led by Ghassan Barnawi, MD, Division of Dermatology, McGill University in Montreal, Quebec, Canada, and was published online on February 20, 2026, in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The study relied on published court decisions, which likely underestimated malpractice burden by excluding settlements and unreported claims.

DISCLOSURES:

The study did not receive any funding. The authors reported having no relevant conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

The study had no commercial funding. The authors had no relevant disclosures.

A version of this article first appeared on Medscape.com

TOPLINE:

In a review of physician-related malpractice cases from 1930 to 2025, melanoma was the most frequently litigated skin cancer, and failure or delay in diagnosis was the most common allegation, with documented death in nearly one third of cases.

METHODOLOGY:

Researchers conducted a review of physician-related medicolegal cases involving skin cancer using the LexisNexis legal database and identified 188 unique cases from 1930 through May 2025.

Cases were included if physicians were named as defendants and the litigation centered on diagnosis or management of a cutaneous malignancy.

Study outcomes examined case characteristics including cancer type, practice setting, defendant specialty, primary allegations, clinical outcomes, and case verdicts across the US.

TAKEAWAY:

Melanoma accounted for 49.5% of litigated cases, followed by squamous cell carcinoma (21.6%), basal cell carcinoma (14.2%), unspecified skin cancer (11.6%), and other rare tumors (3.1%). Death was reported in 29.8% of cases and metastatic disease in 39.9%.

Failure or delay in diagnosis was the leading allegation (38.1%), followed by treatment or management errors (24.2%), misdiagnosis (11.4%), “deliberate indifference” (8.3%), inadequate informed consent (7.5%), and pathology-related errors (7.2%).

Family physicians were the most common defendants (27.5%), followed by dermatologists, including Mohs surgeons (20.1%), and pathologists or dermatopathologists (14.4%), followed by general or plastic surgeons (7.9%), and internists (4.4%). Most cases originated in private practices (59.7%), and New York (16.0%) and California (13.3%) were the states with the most cases.

Among 109 closed cases, 5.5% resulted in plaintiff verdicts, whereas defense verdicts predominated in 55.0%. Plaintiff awards ranged from $10,000 to $4.25 million.

IN PRACTICE:

“This comprehensive review demonstrates that melanoma is the most frequently litigated skin cancer, particularly in cases involving metastatic disease or death, and that family physicians are the most commonly named defendants overall,” the authors wrote. “By examining both allegations and outcomes,” they added, “this analysis provides a pragmatic assessment of real-world litigation exposure and the clinical scenarios that expose physicians to legal proceedings, financial cost, reputational harm, and psychological burden, regardless of case disposition.”

SOURCE:

The study was led by Ghassan Barnawi, MD, Division of Dermatology, McGill University in Montreal, Quebec, Canada, and was published online on February 20, 2026, in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The study relied on published court decisions, which likely underestimated malpractice burden by excluding settlements and unreported claims.

DISCLOSURES:

The study did not receive any funding. The authors reported having no relevant conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

The study had no commercial funding. The authors had no relevant disclosures.

A version of this article first appeared on Medscape.com

Infantile hemangioma (IH) is the most common vascular tumor of infancy, appearing within the first few weeks of life and typically reaching peak size by age 3 to 5 months.¹ It classically manifests as a raised or flat bright-red lesion in the upper dermis of the skin and/or subcutaneous tissue and can vary in number, size, shape, and location.² It is characterized by a rapid proliferative phase, especially between 5 and 8 weeks of age, followed by gradual spontaneous regression over 1 to 10 years.^1-3

Infantile hemangiomas are categorized based on depth (superficial, deep, or mixed) and distribution pattern (focal, multifocal, segmental, or indeterminate).⁴ In most cases, complete regression occurs by age 4 years, but there can be residual telangiectasia, fibrofatty tissue, and/or scarring.^1,4 About 10% to 15% of IHs result in complications that require medical intervention (eg, visual, airway, or auditory compromise; ulceration; disfigurement); ideally, these patients should be referred to a specialist by 5 weeks of age.⁴ Prompt assessment of IH severity is essential to prevent or mitigate potential complications and ultimately improve outcomes.³ Social drivers of health contribute to delayed diagnosis and management of hemangiomas, leading to increased complications in some patient populations.^5-7

Epidemiology

Infantile hemangiomas are estimated to manifest in 4.5% of infants in the United States.¹ The most common type is superficial IH, typically found on the head or neck.⁵ Risk factors in infants include female sex, White race, premature birth, and low birth weight (< 1000 g).^1,3 Maternal risk factors include advanced gestational age (ie, > 35 years), multiple gestations, family history of IH, tobacco use, use of progesterone therapy during pregnancy, and pre-eclampsia.^1,3

Focal IH typically manifests as a single localized lesion that can occur anywhere on the body.^2,3 In contrast, segmental IH manifests in a linear pattern and/or is distributed on a large anatomic area, most commonly on the face and less frequently the extremities and trunk.^2,3 Segmental IHs are more common in Hispanic patients and carry a higher risk for morbidity, often complicated by ulceration that can lead to functional and cosmetic challenges.⁸

Key Clinical Features

Superficial IH in patients with darker skin tones may appear as a dark-red or violaceous papule or plaque compared to bright red in lighter skin tones.⁵ Deep IH may appear as a soft, round, flesh-colored or blue-hued subcutaneous mass, the color of which may be harder to appreciate in those with darker skin tones.⁵

Worth Noting

Complications from IH may require imaging, close follow-up, systemic therapy, multidisciplinary care, and advanced health literacy and patient/family navigation. Multifocal IHs (≥ 5 lesions) are more likely to be associated with infantile hepatic hemangiomas.^2,3 Large (> 5 cm) segmental IHs on the face and lumbosacral area require further evaluation for PHACES (posterior fossa malformation, hemangiomas, arterial anomalies, cardiac defects, eye anomalies, and sternal raphe/cleft defects) and LUMBAR (lower-body segmental IH; urogenital anomalies and ulceration; ­myelopathy; bony deformities; anorectal malformations and arterial anomalies; and renal anomalies) syndromes, which are more common in patients of Hispanic ethnicity.^2,3

The Infantile Hemangioma Referral Score is a recently validated tool that can assist primary care physicians in timely referral of IHs requiring early specialist intervention.^4,9 It takes into account the location, number, and size of the lesions and the age of the patient; these factors help to determine which IHs may be managed conservatively vs those that may require treatment to prevent ­life-threatening complications.^1-3 

Systemic corticosteroids historically have been the primary treatment for IH; however, in the past decade, propranolol oral solution (4.28 mg/mL) has become the first-line therapy for most infants requiring systemic management.¹⁰ It is the only medication approved by the US Food and Drug Administration for proliferating IH, with treatment initiation as young as 5 weeks corrected age.¹¹ As a nonselective beta-blocker, propranolol is believed to reduce IHs through vasoconstriction or by inhibition of angiogenesis.^1,4,10 

For small superficial IHs, treatment options include timolol maleate ophthalmic solution 0.5% (one drop applied twice daily to the IH) or pulsed dye laser therapy.^4,10 Surgical excision typically is avoided during infancy due to concerns about anesthetic risks and potential blood loss.^4,10 Surgery is reserved for cases involving residual fibrofatty tissue, postinvolution scarring, obstruction of vital structures, or lesions in aesthetically sensitive areas as well as when propranolol is contraindicated.^4,10

Health Disparity Highlight

Infants with skin of color and those of lower socioeconomic status (SES) face a heightened risk for delayed diagnosis and more advanced disease at the initial evaluation for IH.^5,7 Access barriers such as geographic limitations to specialty services, lack of insurance, underinsurance, and language differences impact timely diagnosis and treatment.^5,6 Implementation of telemedicine services in areas with limited access to specialists can facilitate early evaluation and risk stratification for IH.¹²

A retrospective cohort study of 804 children seen at a large academic hospital found that those of lower SES were more likely to seek care after 3 months of age than their higher-SES counterparts.⁶ Those who presented after 6 months of age also had higher IH severity scores compared to their counterparts with higher SES.⁶ Delayed access to care may cause children to miss the critical treatment window during the rapid proliferative growth phase.^6,12 However, children insured through Medicaid or the Children’s Health Insurance Program who participated in institutional care management programs (which assist in scheduling specialty care appointments within the institution) sought treatment earlier regardless of their SES, suggesting that such programs may help reduce disparities in timely access for children of lower SES.⁶ 

An epidemiologic study analyzing the demographics of children hospitalized across the United States demonstrated that Black infants with IH were more likely to belong to the lowest income quartile compared with White infants or those of other races. They also were 2 times older on average at initial presentation (1.8 vs 1.0 years), experienced longer hospitalizations (16.4 vs 13.8 days), and underwent more IH-related procedures than White infants and infants of other races (2.4, 1.9, and 2.1, respectively).⁷

These and other factors may contribute to missed windows of opportunity for timely treatment of high-risk IHs in patients with darker skin tones and/or those facing challenges stemming from social drivers of health.

Infantile hemangioma (IH) is the most common vascular tumor of infancy, appearing within the first few weeks of life and typically reaching peak size by age 3 to 5 months.¹ It classically manifests as a raised or flat bright-red lesion in the upper dermis of the skin and/or subcutaneous tissue and can vary in number, size, shape, and location.² It is characterized by a rapid proliferative phase, especially between 5 and 8 weeks of age, followed by gradual spontaneous regression over 1 to 10 years.^1-3

Infantile hemangiomas are categorized based on depth (superficial, deep, or mixed) and distribution pattern (focal, multifocal, segmental, or indeterminate).⁴ In most cases, complete regression occurs by age 4 years, but there can be residual telangiectasia, fibrofatty tissue, and/or scarring.^1,4 About 10% to 15% of IHs result in complications that require medical intervention (eg, visual, airway, or auditory compromise; ulceration; disfigurement); ideally, these patients should be referred to a specialist by 5 weeks of age.⁴ Prompt assessment of IH severity is essential to prevent or mitigate potential complications and ultimately improve outcomes.³ Social drivers of health contribute to delayed diagnosis and management of hemangiomas, leading to increased complications in some patient populations.^5-7

Epidemiology

Infantile hemangiomas are estimated to manifest in 4.5% of infants in the United States.¹ The most common type is superficial IH, typically found on the head or neck.⁵ Risk factors in infants include female sex, White race, premature birth, and low birth weight (< 1000 g).^1,3 Maternal risk factors include advanced gestational age (ie, > 35 years), multiple gestations, family history of IH, tobacco use, use of progesterone therapy during pregnancy, and pre-eclampsia.^1,3

Focal IH typically manifests as a single localized lesion that can occur anywhere on the body.^2,3 In contrast, segmental IH manifests in a linear pattern and/or is distributed on a large anatomic area, most commonly on the face and less frequently the extremities and trunk.^2,3 Segmental IHs are more common in Hispanic patients and carry a higher risk for morbidity, often complicated by ulceration that can lead to functional and cosmetic challenges.⁸

Key Clinical Features

Superficial IH in patients with darker skin tones may appear as a dark-red or violaceous papule or plaque compared to bright red in lighter skin tones.⁵ Deep IH may appear as a soft, round, flesh-colored or blue-hued subcutaneous mass, the color of which may be harder to appreciate in those with darker skin tones.⁵

Worth Noting

Complications from IH may require imaging, close follow-up, systemic therapy, multidisciplinary care, and advanced health literacy and patient/family navigation. Multifocal IHs (≥ 5 lesions) are more likely to be associated with infantile hepatic hemangiomas.^2,3 Large (> 5 cm) segmental IHs on the face and lumbosacral area require further evaluation for PHACES (posterior fossa malformation, hemangiomas, arterial anomalies, cardiac defects, eye anomalies, and sternal raphe/cleft defects) and LUMBAR (lower-body segmental IH; urogenital anomalies and ulceration; ­myelopathy; bony deformities; anorectal malformations and arterial anomalies; and renal anomalies) syndromes, which are more common in patients of Hispanic ethnicity.^2,3

The Infantile Hemangioma Referral Score is a recently validated tool that can assist primary care physicians in timely referral of IHs requiring early specialist intervention.^4,9 It takes into account the location, number, and size of the lesions and the age of the patient; these factors help to determine which IHs may be managed conservatively vs those that may require treatment to prevent ­life-threatening complications.^1-3 

Systemic corticosteroids historically have been the primary treatment for IH; however, in the past decade, propranolol oral solution (4.28 mg/mL) has become the first-line therapy for most infants requiring systemic management.¹⁰ It is the only medication approved by the US Food and Drug Administration for proliferating IH, with treatment initiation as young as 5 weeks corrected age.¹¹ As a nonselective beta-blocker, propranolol is believed to reduce IHs through vasoconstriction or by inhibition of angiogenesis.^1,4,10 

For small superficial IHs, treatment options include timolol maleate ophthalmic solution 0.5% (one drop applied twice daily to the IH) or pulsed dye laser therapy.^4,10 Surgical excision typically is avoided during infancy due to concerns about anesthetic risks and potential blood loss.^4,10 Surgery is reserved for cases involving residual fibrofatty tissue, postinvolution scarring, obstruction of vital structures, or lesions in aesthetically sensitive areas as well as when propranolol is contraindicated.^4,10

Health Disparity Highlight

Infants with skin of color and those of lower socioeconomic status (SES) face a heightened risk for delayed diagnosis and more advanced disease at the initial evaluation for IH.^5,7 Access barriers such as geographic limitations to specialty services, lack of insurance, underinsurance, and language differences impact timely diagnosis and treatment.^5,6 Implementation of telemedicine services in areas with limited access to specialists can facilitate early evaluation and risk stratification for IH.¹²

A retrospective cohort study of 804 children seen at a large academic hospital found that those of lower SES were more likely to seek care after 3 months of age than their higher-SES counterparts.⁶ Those who presented after 6 months of age also had higher IH severity scores compared to their counterparts with higher SES.⁶ Delayed access to care may cause children to miss the critical treatment window during the rapid proliferative growth phase.^6,12 However, children insured through Medicaid or the Children’s Health Insurance Program who participated in institutional care management programs (which assist in scheduling specialty care appointments within the institution) sought treatment earlier regardless of their SES, suggesting that such programs may help reduce disparities in timely access for children of lower SES.⁶ 

An epidemiologic study analyzing the demographics of children hospitalized across the United States demonstrated that Black infants with IH were more likely to belong to the lowest income quartile compared with White infants or those of other races. They also were 2 times older on average at initial presentation (1.8 vs 1.0 years), experienced longer hospitalizations (16.4 vs 13.8 days), and underwent more IH-related procedures than White infants and infants of other races (2.4, 1.9, and 2.1, respectively).⁷

These and other factors may contribute to missed windows of opportunity for timely treatment of high-risk IHs in patients with darker skin tones and/or those facing challenges stemming from social drivers of health.

Infantile hemangioma (IH) is the most common vascular tumor of infancy, appearing within the first few weeks of life and typically reaching peak size by age 3 to 5 months.¹ It classically manifests as a raised or flat bright-red lesion in the upper dermis of the skin and/or subcutaneous tissue and can vary in number, size, shape, and location.² It is characterized by a rapid proliferative phase, especially between 5 and 8 weeks of age, followed by gradual spontaneous regression over 1 to 10 years.^1-3

Infantile hemangiomas are categorized based on depth (superficial, deep, or mixed) and distribution pattern (focal, multifocal, segmental, or indeterminate).⁴ In most cases, complete regression occurs by age 4 years, but there can be residual telangiectasia, fibrofatty tissue, and/or scarring.^1,4 About 10% to 15% of IHs result in complications that require medical intervention (eg, visual, airway, or auditory compromise; ulceration; disfigurement); ideally, these patients should be referred to a specialist by 5 weeks of age.⁴ Prompt assessment of IH severity is essential to prevent or mitigate potential complications and ultimately improve outcomes.³ Social drivers of health contribute to delayed diagnosis and management of hemangiomas, leading to increased complications in some patient populations.^5-7

Epidemiology

Infantile hemangiomas are estimated to manifest in 4.5% of infants in the United States.¹ The most common type is superficial IH, typically found on the head or neck.⁵ Risk factors in infants include female sex, White race, premature birth, and low birth weight (< 1000 g).^1,3 Maternal risk factors include advanced gestational age (ie, > 35 years), multiple gestations, family history of IH, tobacco use, use of progesterone therapy during pregnancy, and pre-eclampsia.^1,3

Focal IH typically manifests as a single localized lesion that can occur anywhere on the body.^2,3 In contrast, segmental IH manifests in a linear pattern and/or is distributed on a large anatomic area, most commonly on the face and less frequently the extremities and trunk.^2,3 Segmental IHs are more common in Hispanic patients and carry a higher risk for morbidity, often complicated by ulceration that can lead to functional and cosmetic challenges.⁸

Key Clinical Features

Superficial IH in patients with darker skin tones may appear as a dark-red or violaceous papule or plaque compared to bright red in lighter skin tones.⁵ Deep IH may appear as a soft, round, flesh-colored or blue-hued subcutaneous mass, the color of which may be harder to appreciate in those with darker skin tones.⁵

Worth Noting

Complications from IH may require imaging, close follow-up, systemic therapy, multidisciplinary care, and advanced health literacy and patient/family navigation. Multifocal IHs (≥ 5 lesions) are more likely to be associated with infantile hepatic hemangiomas.^2,3 Large (> 5 cm) segmental IHs on the face and lumbosacral area require further evaluation for PHACES (posterior fossa malformation, hemangiomas, arterial anomalies, cardiac defects, eye anomalies, and sternal raphe/cleft defects) and LUMBAR (lower-body segmental IH; urogenital anomalies and ulceration; ­myelopathy; bony deformities; anorectal malformations and arterial anomalies; and renal anomalies) syndromes, which are more common in patients of Hispanic ethnicity.^2,3

The Infantile Hemangioma Referral Score is a recently validated tool that can assist primary care physicians in timely referral of IHs requiring early specialist intervention.^4,9 It takes into account the location, number, and size of the lesions and the age of the patient; these factors help to determine which IHs may be managed conservatively vs those that may require treatment to prevent ­life-threatening complications.^1-3 

Systemic corticosteroids historically have been the primary treatment for IH; however, in the past decade, propranolol oral solution (4.28 mg/mL) has become the first-line therapy for most infants requiring systemic management.¹⁰ It is the only medication approved by the US Food and Drug Administration for proliferating IH, with treatment initiation as young as 5 weeks corrected age.¹¹ As a nonselective beta-blocker, propranolol is believed to reduce IHs through vasoconstriction or by inhibition of angiogenesis.^1,4,10 

For small superficial IHs, treatment options include timolol maleate ophthalmic solution 0.5% (one drop applied twice daily to the IH) or pulsed dye laser therapy.^4,10 Surgical excision typically is avoided during infancy due to concerns about anesthetic risks and potential blood loss.^4,10 Surgery is reserved for cases involving residual fibrofatty tissue, postinvolution scarring, obstruction of vital structures, or lesions in aesthetically sensitive areas as well as when propranolol is contraindicated.^4,10

Health Disparity Highlight

Infants with skin of color and those of lower socioeconomic status (SES) face a heightened risk for delayed diagnosis and more advanced disease at the initial evaluation for IH.^5,7 Access barriers such as geographic limitations to specialty services, lack of insurance, underinsurance, and language differences impact timely diagnosis and treatment.^5,6 Implementation of telemedicine services in areas with limited access to specialists can facilitate early evaluation and risk stratification for IH.¹²

A retrospective cohort study of 804 children seen at a large academic hospital found that those of lower SES were more likely to seek care after 3 months of age than their higher-SES counterparts.⁶ Those who presented after 6 months of age also had higher IH severity scores compared to their counterparts with higher SES.⁶ Delayed access to care may cause children to miss the critical treatment window during the rapid proliferative growth phase.^6,12 However, children insured through Medicaid or the Children’s Health Insurance Program who participated in institutional care management programs (which assist in scheduling specialty care appointments within the institution) sought treatment earlier regardless of their SES, suggesting that such programs may help reduce disparities in timely access for children of lower SES.⁶ 

An epidemiologic study analyzing the demographics of children hospitalized across the United States demonstrated that Black infants with IH were more likely to belong to the lowest income quartile compared with White infants or those of other races. They also were 2 times older on average at initial presentation (1.8 vs 1.0 years), experienced longer hospitalizations (16.4 vs 13.8 days), and underwent more IH-related procedures than White infants and infants of other races (2.4, 1.9, and 2.1, respectively).⁷

These and other factors may contribute to missed windows of opportunity for timely treatment of high-risk IHs in patients with darker skin tones and/or those facing challenges stemming from social drivers of health.

Discussion

A diagnosis of lichen sclerosus (LS) was made based on clinical and dermoscopic features, followed by confirmation with histology. The patient’s presentation included typical signs and symptoms of LS: itching, burning, intermittent bleeding, perianal hemorrhage, fusion of the clitoral head, and fissures. Other presentations can include dyspareunia, erosions, and excoriations; however, these symptoms and signs were not reported or seen in this patient.

LS typically affects the anogenital region and has 2 peak incidences: in preadolescent teens and during the fifth to sixth decade of life.¹ This patient presented with a case of extragenital LS, which is less common than the classic presentation of LS that affects the genitals. This variant’s epidemiology differs, as it is less common in children and more common in postmenopausal women.² Extragenital LS presents as white, atrophic plaques with a predilection for sites including the trunk, breasts, upper arms, and sites of physical trauma, with symptoms of dryness and pruritus. Over time, the papules can coalesce and form ivory, scar-like papules or plaques with a wrinkled surface. In advanced stages, telangiectasia or follicular plugging can be present, along with flattening of the dermal-epidermal junction. This flat interface is fragile and can result in bullae that may become hemorrhagic.

Cutaneous squamous cell carcinoma (SCC) may infrequently arise from LS, similar to other chronic inflammatory dermatoses.³ Lichen planus is typically not associated with an increased risk of SCC, except in the oral and hypertrophic variants. However, LS may be considered a premalignant process, and many vulvar SCC cases are noted to have adjacent LS lesions.³

Autoimmune and genetic factors contribute to the pathogenesis of LS. Extracellular matrix protein 1 (ECM1) binds molecules of the basement membrane zone and dermis, contributing to the structure and integrity of skin. Autoantibodies against ECM1 and other antigens of the basement membrane zone, including BP180 and BP320, were found in LS.² HLA-DQ7 major histocompatibility complex class II antigens have been associated with LS.¹

On histologic examination, the epidermis of LS is atrophic with hyperkeratosis. The dermis shows homogenization and sclerosis of superficial collagen with a band-like lymphocytic infiltrate below the sclerosis. The basal layer is thickened, showing basal cell vacuolization and hydropic degeneration.⁴

First-line treatment for genital and extragenital variants of LS is high-potency topical steroids for 3 months or until the skin texture and color resolve (ie, clobetasol 0.05% cream or ointment). The second-line treatment is a topical calcineurin inhibitor. These treatments are used for management. They are not cures for LS, as relapse is possible after the initial treatment course is completed. Adverse effects of high potency topical steroids are skin burning, skin atrophy, and fragility, telangiectasia. The adverse effects of topical calcineurin inhibitors are stinging and burning on application.

Other Diagnostic Considerations

Inverse psoriasis (IP) is a variant of psoriasis that presents as erythematous, well-demarcated plaques with minimal scale in intertriginous areas and flexural surfaces. Localized dermatophyte, candidal, or bacterial infections can trigger IP.⁵ It occurs in about 3% to 7% of patients with plaque psoriasis and is thought to form due to koebnerization via mechanical friction of flexural zones.⁶ The patient described in this case did not have IP because IP would be more likely to present as a well-demarcated erythematous plaque rather than a patch.

Histologically, IP shows regular psoriasiform acanthosis and hypogranulosis of the epidermis, Munro microabscess, spongiform pustules of Kogoj, dilated tortuous dermal vessels, and thinning of the suprapapillary plates.⁵

Lichen planus pigmentosus-inversus (LPPI) is also known as lichen planus pigmentosus—intertriginous variant. This variant of lichen planus pigmentosus presents as multiple gray to dark brown macules and patches with poorly defined borders in a linear distribution limited to intertriginous areas, flexural surfaces, or following the lines of Blaschko.⁷ About 20% of cases present with frontal fibrosing alopecia. It is most common in individuals with intermediate and darker skin pigmentation, has a higher prevalence in females, and typically occurs within the third and fifth decades of life. Friction is a common trigger of LPPI.⁷ A diagnosis of LPPI is incorrect because the lesions would present as gray to dark brown macules, as opposed to the shiny white atrophic thin papules with surrounding pink and purple patches seen in this case.

Histologically, while both LS and LPPI share band-like lymphocytic infiltrate and basal cell vacuolization, findings in the dermis differ. LPPI shows melanophages and prominent melanin incontinence, while LS shows homogenization and sclerosis of superficial collagen.^1,8 LPPI also shows absence of compensatory keratinocyte proliferation.

Morphea is an inflammatory disease that affects the dermis and subcutaneous fat, resulting in sclerosis that appears scarlike. Its prevalence increases with age and has a 4:1 prevalence in females, with the plaque type being the most common variant. ⁹ The typical presentation of plaque-type morphea is an insidious onset of asymptomatic, slightly elevated, erythematous or violaceous, slightly edematous plaques with centrifugal expansion. The center of the plaque may become sclerotic and indurated, acquiring a shiny white color with a peripheral “lilac” ring. Trunk and upper extremity involvement is common. Morphea is associated with increased antisingle-stranded DNA, antitopoisomerase IIa, antiphospholipid, antifibrillin-1, and antihistone antibodies. Triggers of morphea are believed to be localized insults to the skin, including mechanical trauma, injections, vaccinations, and irradiation.⁹ This answer is incorrect because the patient’s lesions were pruritic and had genital involvement, which are not typical of morphea. Morphea can be differentiated with based on symptoms (lack of pruritus, pain, burning), morphology of lesions (induration versus atrophy), dermoscopy (fibrotic beams with less scale and hemorrhage vs keratotic follicular plugs), and histopathology (depth of inflammation in superficial and deep dermis).

Histology of morphea can differ based on the stage, whether the lesion is sampled in the inflammatory margin or central sclerosis, and the depth of affected skin. At the inflammatory margin, vascular changes, including endothelial swelling and edema, are present, as well as CD4+ T cells, eosinophils, plasma cells, and mast cells surrounding smaller blood vessels. In late stages, the inflammatory infiltrate is no longer present, the epidermis appears regular, and there is a flattened dermal-epidermal junction. Distinct features include homogenous collagen bundles that replace many dermal structures, with atrophic eccrine glands that appear “trapped” in the thickened dermis, and homogenized and hyalinized subcutis.⁹

Mycosis fungoides (MF) is the most common type of cutaneous T-cell lymphoma and presents as annular, erythematous or hypopigmented patches and plaques with fine scale and tumors on the buttocks and sun-protected areas of the limbs and trunk. Lesions can appear with prominent poikiloderma or atrophic or lichenified skin.¹⁰ It is most common in males of African descent aged 50 to 55 years. The etiology is largely unknown but believed to be multifactorial. This answer is incorrect because the lesions in this patient appeared more atrophic, were less well demarcated, and lacked the scale that would be present in MF.

On histology, both LS and MF show band-like lymphocytic infiltrate, however MF lacks the homogenization and sclerosis of superficial collagen that is present in the dermis of LS. Also, MF demonstrates epidermotropism of atypical lymphocytes forming Pautrier microabscess.¹⁰

Primary Care Role

Primary care physicians can diagnose and treat LS. Referral to dermatology is not mandatory. Note that topical steroids can be used daily for up to 12 weeks. In LS, early treatment is associated with improved outcomes and minimizes the risk of irreversible skin changes.¹¹ Follow-up during the treatment period is recommended to monitor subjective and objective response to treatment. Follow-up after the initial treatment is recommended since LS is typically chronic, can relapse, and SCC can infrequently arise from LS lesions.¹¹

Discussion

A diagnosis of lichen sclerosus (LS) was made based on clinical and dermoscopic features, followed by confirmation with histology. The patient’s presentation included typical signs and symptoms of LS: itching, burning, intermittent bleeding, perianal hemorrhage, fusion of the clitoral head, and fissures. Other presentations can include dyspareunia, erosions, and excoriations; however, these symptoms and signs were not reported or seen in this patient.

LS typically affects the anogenital region and has 2 peak incidences: in preadolescent teens and during the fifth to sixth decade of life.¹ This patient presented with a case of extragenital LS, which is less common than the classic presentation of LS that affects the genitals. This variant’s epidemiology differs, as it is less common in children and more common in postmenopausal women.² Extragenital LS presents as white, atrophic plaques with a predilection for sites including the trunk, breasts, upper arms, and sites of physical trauma, with symptoms of dryness and pruritus. Over time, the papules can coalesce and form ivory, scar-like papules or plaques with a wrinkled surface. In advanced stages, telangiectasia or follicular plugging can be present, along with flattening of the dermal-epidermal junction. This flat interface is fragile and can result in bullae that may become hemorrhagic.

Cutaneous squamous cell carcinoma (SCC) may infrequently arise from LS, similar to other chronic inflammatory dermatoses.³ Lichen planus is typically not associated with an increased risk of SCC, except in the oral and hypertrophic variants. However, LS may be considered a premalignant process, and many vulvar SCC cases are noted to have adjacent LS lesions.³

Autoimmune and genetic factors contribute to the pathogenesis of LS. Extracellular matrix protein 1 (ECM1) binds molecules of the basement membrane zone and dermis, contributing to the structure and integrity of skin. Autoantibodies against ECM1 and other antigens of the basement membrane zone, including BP180 and BP320, were found in LS.² HLA-DQ7 major histocompatibility complex class II antigens have been associated with LS.¹

On histologic examination, the epidermis of LS is atrophic with hyperkeratosis. The dermis shows homogenization and sclerosis of superficial collagen with a band-like lymphocytic infiltrate below the sclerosis. The basal layer is thickened, showing basal cell vacuolization and hydropic degeneration.⁴

First-line treatment for genital and extragenital variants of LS is high-potency topical steroids for 3 months or until the skin texture and color resolve (ie, clobetasol 0.05% cream or ointment). The second-line treatment is a topical calcineurin inhibitor. These treatments are used for management. They are not cures for LS, as relapse is possible after the initial treatment course is completed. Adverse effects of high potency topical steroids are skin burning, skin atrophy, and fragility, telangiectasia. The adverse effects of topical calcineurin inhibitors are stinging and burning on application.

Other Diagnostic Considerations

Inverse psoriasis (IP) is a variant of psoriasis that presents as erythematous, well-demarcated plaques with minimal scale in intertriginous areas and flexural surfaces. Localized dermatophyte, candidal, or bacterial infections can trigger IP.⁵ It occurs in about 3% to 7% of patients with plaque psoriasis and is thought to form due to koebnerization via mechanical friction of flexural zones.⁶ The patient described in this case did not have IP because IP would be more likely to present as a well-demarcated erythematous plaque rather than a patch.

Histologically, IP shows regular psoriasiform acanthosis and hypogranulosis of the epidermis, Munro microabscess, spongiform pustules of Kogoj, dilated tortuous dermal vessels, and thinning of the suprapapillary plates.⁵

Lichen planus pigmentosus-inversus (LPPI) is also known as lichen planus pigmentosus—intertriginous variant. This variant of lichen planus pigmentosus presents as multiple gray to dark brown macules and patches with poorly defined borders in a linear distribution limited to intertriginous areas, flexural surfaces, or following the lines of Blaschko.⁷ About 20% of cases present with frontal fibrosing alopecia. It is most common in individuals with intermediate and darker skin pigmentation, has a higher prevalence in females, and typically occurs within the third and fifth decades of life. Friction is a common trigger of LPPI.⁷ A diagnosis of LPPI is incorrect because the lesions would present as gray to dark brown macules, as opposed to the shiny white atrophic thin papules with surrounding pink and purple patches seen in this case.

Histologically, while both LS and LPPI share band-like lymphocytic infiltrate and basal cell vacuolization, findings in the dermis differ. LPPI shows melanophages and prominent melanin incontinence, while LS shows homogenization and sclerosis of superficial collagen.^1,8 LPPI also shows absence of compensatory keratinocyte proliferation.

Morphea is an inflammatory disease that affects the dermis and subcutaneous fat, resulting in sclerosis that appears scarlike. Its prevalence increases with age and has a 4:1 prevalence in females, with the plaque type being the most common variant. ⁹ The typical presentation of plaque-type morphea is an insidious onset of asymptomatic, slightly elevated, erythematous or violaceous, slightly edematous plaques with centrifugal expansion. The center of the plaque may become sclerotic and indurated, acquiring a shiny white color with a peripheral “lilac” ring. Trunk and upper extremity involvement is common. Morphea is associated with increased antisingle-stranded DNA, antitopoisomerase IIa, antiphospholipid, antifibrillin-1, and antihistone antibodies. Triggers of morphea are believed to be localized insults to the skin, including mechanical trauma, injections, vaccinations, and irradiation.⁹ This answer is incorrect because the patient’s lesions were pruritic and had genital involvement, which are not typical of morphea. Morphea can be differentiated with based on symptoms (lack of pruritus, pain, burning), morphology of lesions (induration versus atrophy), dermoscopy (fibrotic beams with less scale and hemorrhage vs keratotic follicular plugs), and histopathology (depth of inflammation in superficial and deep dermis).

Histology of morphea can differ based on the stage, whether the lesion is sampled in the inflammatory margin or central sclerosis, and the depth of affected skin. At the inflammatory margin, vascular changes, including endothelial swelling and edema, are present, as well as CD4+ T cells, eosinophils, plasma cells, and mast cells surrounding smaller blood vessels. In late stages, the inflammatory infiltrate is no longer present, the epidermis appears regular, and there is a flattened dermal-epidermal junction. Distinct features include homogenous collagen bundles that replace many dermal structures, with atrophic eccrine glands that appear “trapped” in the thickened dermis, and homogenized and hyalinized subcutis.⁹

Mycosis fungoides (MF) is the most common type of cutaneous T-cell lymphoma and presents as annular, erythematous or hypopigmented patches and plaques with fine scale and tumors on the buttocks and sun-protected areas of the limbs and trunk. Lesions can appear with prominent poikiloderma or atrophic or lichenified skin.¹⁰ It is most common in males of African descent aged 50 to 55 years. The etiology is largely unknown but believed to be multifactorial. This answer is incorrect because the lesions in this patient appeared more atrophic, were less well demarcated, and lacked the scale that would be present in MF.

On histology, both LS and MF show band-like lymphocytic infiltrate, however MF lacks the homogenization and sclerosis of superficial collagen that is present in the dermis of LS. Also, MF demonstrates epidermotropism of atypical lymphocytes forming Pautrier microabscess.¹⁰

Primary Care Role

Primary care physicians can diagnose and treat LS. Referral to dermatology is not mandatory. Note that topical steroids can be used daily for up to 12 weeks. In LS, early treatment is associated with improved outcomes and minimizes the risk of irreversible skin changes.¹¹ Follow-up during the treatment period is recommended to monitor subjective and objective response to treatment. Follow-up after the initial treatment is recommended since LS is typically chronic, can relapse, and SCC can infrequently arise from LS lesions.¹¹

Discussion

A diagnosis of lichen sclerosus (LS) was made based on clinical and dermoscopic features, followed by confirmation with histology. The patient’s presentation included typical signs and symptoms of LS: itching, burning, intermittent bleeding, perianal hemorrhage, fusion of the clitoral head, and fissures. Other presentations can include dyspareunia, erosions, and excoriations; however, these symptoms and signs were not reported or seen in this patient.

LS typically affects the anogenital region and has 2 peak incidences: in preadolescent teens and during the fifth to sixth decade of life.¹ This patient presented with a case of extragenital LS, which is less common than the classic presentation of LS that affects the genitals. This variant’s epidemiology differs, as it is less common in children and more common in postmenopausal women.² Extragenital LS presents as white, atrophic plaques with a predilection for sites including the trunk, breasts, upper arms, and sites of physical trauma, with symptoms of dryness and pruritus. Over time, the papules can coalesce and form ivory, scar-like papules or plaques with a wrinkled surface. In advanced stages, telangiectasia or follicular plugging can be present, along with flattening of the dermal-epidermal junction. This flat interface is fragile and can result in bullae that may become hemorrhagic.

Cutaneous squamous cell carcinoma (SCC) may infrequently arise from LS, similar to other chronic inflammatory dermatoses.³ Lichen planus is typically not associated with an increased risk of SCC, except in the oral and hypertrophic variants. However, LS may be considered a premalignant process, and many vulvar SCC cases are noted to have adjacent LS lesions.³

Autoimmune and genetic factors contribute to the pathogenesis of LS. Extracellular matrix protein 1 (ECM1) binds molecules of the basement membrane zone and dermis, contributing to the structure and integrity of skin. Autoantibodies against ECM1 and other antigens of the basement membrane zone, including BP180 and BP320, were found in LS.² HLA-DQ7 major histocompatibility complex class II antigens have been associated with LS.¹

On histologic examination, the epidermis of LS is atrophic with hyperkeratosis. The dermis shows homogenization and sclerosis of superficial collagen with a band-like lymphocytic infiltrate below the sclerosis. The basal layer is thickened, showing basal cell vacuolization and hydropic degeneration.⁴

First-line treatment for genital and extragenital variants of LS is high-potency topical steroids for 3 months or until the skin texture and color resolve (ie, clobetasol 0.05% cream or ointment). The second-line treatment is a topical calcineurin inhibitor. These treatments are used for management. They are not cures for LS, as relapse is possible after the initial treatment course is completed. Adverse effects of high potency topical steroids are skin burning, skin atrophy, and fragility, telangiectasia. The adverse effects of topical calcineurin inhibitors are stinging and burning on application.

Other Diagnostic Considerations

Inverse psoriasis (IP) is a variant of psoriasis that presents as erythematous, well-demarcated plaques with minimal scale in intertriginous areas and flexural surfaces. Localized dermatophyte, candidal, or bacterial infections can trigger IP.⁵ It occurs in about 3% to 7% of patients with plaque psoriasis and is thought to form due to koebnerization via mechanical friction of flexural zones.⁶ The patient described in this case did not have IP because IP would be more likely to present as a well-demarcated erythematous plaque rather than a patch.

Histologically, IP shows regular psoriasiform acanthosis and hypogranulosis of the epidermis, Munro microabscess, spongiform pustules of Kogoj, dilated tortuous dermal vessels, and thinning of the suprapapillary plates.⁵

Lichen planus pigmentosus-inversus (LPPI) is also known as lichen planus pigmentosus—intertriginous variant. This variant of lichen planus pigmentosus presents as multiple gray to dark brown macules and patches with poorly defined borders in a linear distribution limited to intertriginous areas, flexural surfaces, or following the lines of Blaschko.⁷ About 20% of cases present with frontal fibrosing alopecia. It is most common in individuals with intermediate and darker skin pigmentation, has a higher prevalence in females, and typically occurs within the third and fifth decades of life. Friction is a common trigger of LPPI.⁷ A diagnosis of LPPI is incorrect because the lesions would present as gray to dark brown macules, as opposed to the shiny white atrophic thin papules with surrounding pink and purple patches seen in this case.

Histologically, while both LS and LPPI share band-like lymphocytic infiltrate and basal cell vacuolization, findings in the dermis differ. LPPI shows melanophages and prominent melanin incontinence, while LS shows homogenization and sclerosis of superficial collagen.^1,8 LPPI also shows absence of compensatory keratinocyte proliferation.

Morphea is an inflammatory disease that affects the dermis and subcutaneous fat, resulting in sclerosis that appears scarlike. Its prevalence increases with age and has a 4:1 prevalence in females, with the plaque type being the most common variant. ⁹ The typical presentation of plaque-type morphea is an insidious onset of asymptomatic, slightly elevated, erythematous or violaceous, slightly edematous plaques with centrifugal expansion. The center of the plaque may become sclerotic and indurated, acquiring a shiny white color with a peripheral “lilac” ring. Trunk and upper extremity involvement is common. Morphea is associated with increased antisingle-stranded DNA, antitopoisomerase IIa, antiphospholipid, antifibrillin-1, and antihistone antibodies. Triggers of morphea are believed to be localized insults to the skin, including mechanical trauma, injections, vaccinations, and irradiation.⁹ This answer is incorrect because the patient’s lesions were pruritic and had genital involvement, which are not typical of morphea. Morphea can be differentiated with based on symptoms (lack of pruritus, pain, burning), morphology of lesions (induration versus atrophy), dermoscopy (fibrotic beams with less scale and hemorrhage vs keratotic follicular plugs), and histopathology (depth of inflammation in superficial and deep dermis).

Histology of morphea can differ based on the stage, whether the lesion is sampled in the inflammatory margin or central sclerosis, and the depth of affected skin. At the inflammatory margin, vascular changes, including endothelial swelling and edema, are present, as well as CD4+ T cells, eosinophils, plasma cells, and mast cells surrounding smaller blood vessels. In late stages, the inflammatory infiltrate is no longer present, the epidermis appears regular, and there is a flattened dermal-epidermal junction. Distinct features include homogenous collagen bundles that replace many dermal structures, with atrophic eccrine glands that appear “trapped” in the thickened dermis, and homogenized and hyalinized subcutis.⁹

Mycosis fungoides (MF) is the most common type of cutaneous T-cell lymphoma and presents as annular, erythematous or hypopigmented patches and plaques with fine scale and tumors on the buttocks and sun-protected areas of the limbs and trunk. Lesions can appear with prominent poikiloderma or atrophic or lichenified skin.¹⁰ It is most common in males of African descent aged 50 to 55 years. The etiology is largely unknown but believed to be multifactorial. This answer is incorrect because the lesions in this patient appeared more atrophic, were less well demarcated, and lacked the scale that would be present in MF.

On histology, both LS and MF show band-like lymphocytic infiltrate, however MF lacks the homogenization and sclerosis of superficial collagen that is present in the dermis of LS. Also, MF demonstrates epidermotropism of atypical lymphocytes forming Pautrier microabscess.¹⁰

Primary Care Role

Primary care physicians can diagnose and treat LS. Referral to dermatology is not mandatory. Note that topical steroids can be used daily for up to 12 weeks. In LS, early treatment is associated with improved outcomes and minimizes the risk of irreversible skin changes.¹¹ Follow-up during the treatment period is recommended to monitor subjective and objective response to treatment. Follow-up after the initial treatment is recommended since LS is typically chronic, can relapse, and SCC can infrequently arise from LS lesions.¹¹

TOPLINE:

The incidence of skin cancer in England varied by ethnicity: White individuals had higher rates of melanoma, cutaneous squamous cell carcinoma, and basal cell carcinoma than Asian or Black individuals. In contrast, acral lentiginous melanoma was most common among Black individuals, whereas cutaneous T-cell lymphoma and Kaposi sarcoma were highest among those in the "Other" ethnic group.

METHODOLOGY:

• Researchers analysed all cases of cutaneous melanoma (melanoma and acral lentiginous melanoma), basal cell carcinoma, cutaneous squamous cell carcinoma, cutaneous T-cell lymphoma, and Kaposi sarcoma using data from the NHS National Disease Registration Service cancer registry between 2013 and 2020.
• Data collection incorporated ethnicity information from multiple health care datasets, including Clinical Outcomes and Services Dataset, Patient Administration System, Radiotherapy Dataset, Diagnostic Imaging Dataset, and Hospital Episode Statistics.
• A population analysis categorised patients into 7 standardised ethnic groups (on the basis of Office for National Statistics classifications): White, Asian, Chinese, Black, mixed, other, and unknown groups, with ethnicity data being self-reported by patients.
• Outcomes included European age-standardised rates calculated using the 2013 European Standard Population and reported per 100,000 person-years (PYs).

TAKEAWAY:

• White Individuals had 13-fold higher rates of cutaneous squamous cell carcinoma (61.75 per 100,000 PYs), 26-fold and 27-fold higher rates of basal cell carcinoma (153.69 per 100,000 PYs), and 33-fold and 16-fold higher rates of cutaneous melanoma (27.29 per 100,000 PYs) than Asian and Black individuals, respectively.
• Black individuals had the highest incidence of acral lentiginous melanoma (0.85 per 100,000 PYs), and those in the other ethnic group had the highest incidence of cutaneous T-cell lymphoma (1.74 per 100,000 PYs) and Kaposi sarcoma (1.57 per 100,000 PYs).
• The presentation of early-stage melanoma was low among Asian (53.5%), Black (62.4%), mixed (62.5%), and other (76.4%) ethnic groups compared to that among White ethnicities (79.8%).
• Acral lentiginous melanomas were less likely to get urgent suspected cancer pathway referrals than overall melanoma (40.1% vs 44.6%; P < .001) and more likely to be diagnosed late than overall melanoma (stage I/II at diagnosis; 72% vs 80%; P < .0001).

IN PRACTICE:

"The findings emphasise the need for better, targeted ethnicity data collection strategies to address incidence, outcomes and health care equity for not just skin cancer but all health conditions in underserved populations," the authors wrote. "While projects like the Global Burden of Disease have improved global health care reporting, continuous audit and improvement of collected data are essential to provide better care across people of all ethnicities."

SOURCE:

This study was led by Shehnaz Ahmed, British Association of Dermatologists, London, England. It was published online on September 10, 2025, in the British Journal of Dermatology.

LIMITATIONS:

Census data collection after every 10 years could have contributed to inaccurate population estimates and incidence rates. Small sample sizes in certain ethnic groups could have led to potential confounders, requiring a cautious interpretation of relative incidence. The NHS data included only self-reported ethnicity data with no available details of skin phototypes, skin tones, or racial ancestry. This study lacked granular ethnicity census data and stage data for basal cell carcinoma, cutaneous small cell carcinoma, and Kaposi sarcoma.

DISCLOSURES:

This research was supported through a partnership between the British Association of Dermatologists and NHS England's National Disease Registration Service. Two authors reported being employees of the British Association of Dermatologists.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article first appeared on Medscape.com.

TOPLINE:

The incidence of skin cancer in England varied by ethnicity: White individuals had higher rates of melanoma, cutaneous squamous cell carcinoma, and basal cell carcinoma than Asian or Black individuals. In contrast, acral lentiginous melanoma was most common among Black individuals, whereas cutaneous T-cell lymphoma and Kaposi sarcoma were highest among those in the "Other" ethnic group.

METHODOLOGY:

• Researchers analysed all cases of cutaneous melanoma (melanoma and acral lentiginous melanoma), basal cell carcinoma, cutaneous squamous cell carcinoma, cutaneous T-cell lymphoma, and Kaposi sarcoma using data from the NHS National Disease Registration Service cancer registry between 2013 and 2020.
• Data collection incorporated ethnicity information from multiple health care datasets, including Clinical Outcomes and Services Dataset, Patient Administration System, Radiotherapy Dataset, Diagnostic Imaging Dataset, and Hospital Episode Statistics.
• A population analysis categorised patients into 7 standardised ethnic groups (on the basis of Office for National Statistics classifications): White, Asian, Chinese, Black, mixed, other, and unknown groups, with ethnicity data being self-reported by patients.
• Outcomes included European age-standardised rates calculated using the 2013 European Standard Population and reported per 100,000 person-years (PYs).

TAKEAWAY:

• White Individuals had 13-fold higher rates of cutaneous squamous cell carcinoma (61.75 per 100,000 PYs), 26-fold and 27-fold higher rates of basal cell carcinoma (153.69 per 100,000 PYs), and 33-fold and 16-fold higher rates of cutaneous melanoma (27.29 per 100,000 PYs) than Asian and Black individuals, respectively.
• Black individuals had the highest incidence of acral lentiginous melanoma (0.85 per 100,000 PYs), and those in the other ethnic group had the highest incidence of cutaneous T-cell lymphoma (1.74 per 100,000 PYs) and Kaposi sarcoma (1.57 per 100,000 PYs).
• The presentation of early-stage melanoma was low among Asian (53.5%), Black (62.4%), mixed (62.5%), and other (76.4%) ethnic groups compared to that among White ethnicities (79.8%).
• Acral lentiginous melanomas were less likely to get urgent suspected cancer pathway referrals than overall melanoma (40.1% vs 44.6%; P < .001) and more likely to be diagnosed late than overall melanoma (stage I/II at diagnosis; 72% vs 80%; P < .0001).

IN PRACTICE:

"The findings emphasise the need for better, targeted ethnicity data collection strategies to address incidence, outcomes and health care equity for not just skin cancer but all health conditions in underserved populations," the authors wrote. "While projects like the Global Burden of Disease have improved global health care reporting, continuous audit and improvement of collected data are essential to provide better care across people of all ethnicities."

SOURCE:

This study was led by Shehnaz Ahmed, British Association of Dermatologists, London, England. It was published online on September 10, 2025, in the British Journal of Dermatology.

LIMITATIONS:

Census data collection after every 10 years could have contributed to inaccurate population estimates and incidence rates. Small sample sizes in certain ethnic groups could have led to potential confounders, requiring a cautious interpretation of relative incidence. The NHS data included only self-reported ethnicity data with no available details of skin phototypes, skin tones, or racial ancestry. This study lacked granular ethnicity census data and stage data for basal cell carcinoma, cutaneous small cell carcinoma, and Kaposi sarcoma.

DISCLOSURES:

This research was supported through a partnership between the British Association of Dermatologists and NHS England's National Disease Registration Service. Two authors reported being employees of the British Association of Dermatologists.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article first appeared on Medscape.com.

TOPLINE:

The incidence of skin cancer in England varied by ethnicity: White individuals had higher rates of melanoma, cutaneous squamous cell carcinoma, and basal cell carcinoma than Asian or Black individuals. In contrast, acral lentiginous melanoma was most common among Black individuals, whereas cutaneous T-cell lymphoma and Kaposi sarcoma were highest among those in the "Other" ethnic group.

METHODOLOGY:

• Researchers analysed all cases of cutaneous melanoma (melanoma and acral lentiginous melanoma), basal cell carcinoma, cutaneous squamous cell carcinoma, cutaneous T-cell lymphoma, and Kaposi sarcoma using data from the NHS National Disease Registration Service cancer registry between 2013 and 2020.
• Data collection incorporated ethnicity information from multiple health care datasets, including Clinical Outcomes and Services Dataset, Patient Administration System, Radiotherapy Dataset, Diagnostic Imaging Dataset, and Hospital Episode Statistics.
• A population analysis categorised patients into 7 standardised ethnic groups (on the basis of Office for National Statistics classifications): White, Asian, Chinese, Black, mixed, other, and unknown groups, with ethnicity data being self-reported by patients.
• Outcomes included European age-standardised rates calculated using the 2013 European Standard Population and reported per 100,000 person-years (PYs).

TAKEAWAY:

• White Individuals had 13-fold higher rates of cutaneous squamous cell carcinoma (61.75 per 100,000 PYs), 26-fold and 27-fold higher rates of basal cell carcinoma (153.69 per 100,000 PYs), and 33-fold and 16-fold higher rates of cutaneous melanoma (27.29 per 100,000 PYs) than Asian and Black individuals, respectively.
• Black individuals had the highest incidence of acral lentiginous melanoma (0.85 per 100,000 PYs), and those in the other ethnic group had the highest incidence of cutaneous T-cell lymphoma (1.74 per 100,000 PYs) and Kaposi sarcoma (1.57 per 100,000 PYs).
• The presentation of early-stage melanoma was low among Asian (53.5%), Black (62.4%), mixed (62.5%), and other (76.4%) ethnic groups compared to that among White ethnicities (79.8%).
• Acral lentiginous melanomas were less likely to get urgent suspected cancer pathway referrals than overall melanoma (40.1% vs 44.6%; P < .001) and more likely to be diagnosed late than overall melanoma (stage I/II at diagnosis; 72% vs 80%; P < .0001).

IN PRACTICE:

"The findings emphasise the need for better, targeted ethnicity data collection strategies to address incidence, outcomes and health care equity for not just skin cancer but all health conditions in underserved populations," the authors wrote. "While projects like the Global Burden of Disease have improved global health care reporting, continuous audit and improvement of collected data are essential to provide better care across people of all ethnicities."

SOURCE:

This study was led by Shehnaz Ahmed, British Association of Dermatologists, London, England. It was published online on September 10, 2025, in the British Journal of Dermatology.

LIMITATIONS:

Census data collection after every 10 years could have contributed to inaccurate population estimates and incidence rates. Small sample sizes in certain ethnic groups could have led to potential confounders, requiring a cautious interpretation of relative incidence. The NHS data included only self-reported ethnicity data with no available details of skin phototypes, skin tones, or racial ancestry. This study lacked granular ethnicity census data and stage data for basal cell carcinoma, cutaneous small cell carcinoma, and Kaposi sarcoma.

DISCLOSURES:

This research was supported through a partnership between the British Association of Dermatologists and NHS England's National Disease Registration Service. Two authors reported being employees of the British Association of Dermatologists.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A version of this article first appeared on Medscape.com.

The Comparison

A. Alopecia areata in a young girl with a lighter skin tone. The fine white vellus hairs are signs of regrowth. 

B. Alopecia areata in a 49-year-old man with tightly coiled hair and darker skin tone. Coiled white hairs are noted in the alopecia patches.

Alopecia areata (AA) is a common autoimmune condition characterized by hair loss resulting from a T cell–mediated attack on the hair follicles. It manifests as nonscarring patches of hair loss on the scalp, eyebrows, eyelashes, and beard area as well as more extensive complete loss of scalp and body hair. While AA may affect individuals of any age, most patients develop their first patch(es) of hair loss during childhood.¹ The treatment landscape for AA has evolved considerably in recent years, but barriers to access to newer treatments persist. 

Epidemiology 

AA is most prevalent among pediatric and adult individuals of African, Asian, or Hispanic/Latino descent.^2-4 In some studies, Black individuals had higher odds and Asian individuals had lower odds of developing AA, while other studies have reported the highest standardized prevalence among Asian individuals.⁵ In the United States, AA affects about 1.47% of adults and as many as 0.11% of children.^6-8 In Black patients, AA often manifests early with a female predominance.⁵ 

AA frequently is associated with autoimmune comorbidities, the most common being thyroid disease.^3,5 In Black patients, AA is associated with more atopic comorbidities, including asthma, atopic dermatitis, and allergic rhinitis.⁵ 

Key Clinical Features 

AA clinically manifests similarly across different skin tones; however, in patients with more tightly coiled or curly hair, the extent of scalp hair loss may be underestimated without a full examination. Culturally sensitive approaches to hair and scalp evaluation are essential, especially for Black women, whose hair care practices and scalp conditions may be overlooked or misunderstood during visits to evaluate hair loss. A thoughtful history and gentle examination of the hair and scalp that considers hair texture, cultural practices such as head coverings (eg, headwraps, turbans, hijabs), use of hair adornments (eg, clips, beads, bows), traditional braiding, and use of natural oils or herbal treatments, as well as styling methods including tight hairstyles, use of heat styling tools (eg, flat irons, curling irons), chemical application (eg, straighteners, hair color), and washing or styling frequency can improve diagnostic accuracy and help build trust in the patient-provider relationship. 

Classic signs of AA visualized with dermoscopy include yellow and/or black dots on the scalp and exclamation point hairs. The appearance of fine white vellus hairs within the alopecic patches also may indicate early regrowth. On scalp trichoscopy, black dots are more prominent, and yellow dots are less prominent, in individuals with darker skin tones vs lighter skin tones.⁹ 

Worth Noting 

In addition to a full examination of the scalp, documenting the extent of hair loss using validated severity scales, including the severity of alopecia tool (SALT), AA severity index (AASI), clinician-reported outcome assessment, and patient-reported outcome measures, can standardize disease severity assessment, facilitate timely insurance or medication approvals, and support objective tracking of treatment response, which may ultimately enhance access to care.¹⁰ 

Prompt treatment of AA is essential. Not surprisingly, patients given a diagnosis of AA may experience considerable emotional and psychological distress—regardless of the extent of the loss.¹¹ Treatment options include mid- to high-potency topical or intralesional corticosteroids and newer and more targeted systemic options, including 3 Janus kinase (JAK) inhibitors—baricitinib, ritlecitinib, and deuruxolitinib—for more extensive disease.¹² Treatment with intralesional corticosteroids may cause transient hypopigmentation, which may be more noticeable in patients with darker skin tones. Delays in treatment with JAK inhibitors can lead to a less-than-optimal response. Of the 3 JAK inhibitors that are approved by the US Food and Drug Administration for AA, only ritlecitinib is approved for children 12 years and older, leaving a therapeutic gap for younger patients that often leads to uncomfortable scalp injections, delayed or no treatment, off-label use of JAK inhibitors as well as the pairing of off-label dupilumab with oral minoxidil.¹² 

Based on adult data, patients with severe disease and a shorter duration of hair loss (ie, < 4 years) tend to respond better to JAK inhibitors than those experiencing hair loss for longer periods. Also, those with more severe AA tend to have poorer outcomes than those with less severe disease.¹³ If treatment proves less than optimal, wigs and hair pieces may need to be considered. It is worth noting that some insurance companies will cover the cost of wigs for patients when prescribed as cranial prostheses. 

Health Disparity Highlight 

Health disparities in AA can be influenced by socioeconomic status and access to care. Patients from lower-income backgrounds often face barriers to accessing dermatologic care and treatments such as JAK inhibitors, which may remain inaccessible due to high costs and insurance limitations.¹⁴ These barriers can intersect with other factors such as age, sex, and race, potentially exacerbating disparities. Women with skin of color in underserved communities may experience delayed diagnosis, limited treatment options, and greater psychosocial distress from hair loss.¹⁴ Addressing these inequities requires advocacy, education for both patients and clinicians, and improved access to treatment to ensure comprehensive care for all patients. 

The Comparison

A. Alopecia areata in a young girl with a lighter skin tone. The fine white vellus hairs are signs of regrowth. 

B. Alopecia areata in a 49-year-old man with tightly coiled hair and darker skin tone. Coiled white hairs are noted in the alopecia patches.

Alopecia areata (AA) is a common autoimmune condition characterized by hair loss resulting from a T cell–mediated attack on the hair follicles. It manifests as nonscarring patches of hair loss on the scalp, eyebrows, eyelashes, and beard area as well as more extensive complete loss of scalp and body hair. While AA may affect individuals of any age, most patients develop their first patch(es) of hair loss during childhood.¹ The treatment landscape for AA has evolved considerably in recent years, but barriers to access to newer treatments persist. 

Epidemiology 

AA is most prevalent among pediatric and adult individuals of African, Asian, or Hispanic/Latino descent.^2-4 In some studies, Black individuals had higher odds and Asian individuals had lower odds of developing AA, while other studies have reported the highest standardized prevalence among Asian individuals.⁵ In the United States, AA affects about 1.47% of adults and as many as 0.11% of children.^6-8 In Black patients, AA often manifests early with a female predominance.⁵ 

AA frequently is associated with autoimmune comorbidities, the most common being thyroid disease.^3,5 In Black patients, AA is associated with more atopic comorbidities, including asthma, atopic dermatitis, and allergic rhinitis.⁵ 

Key Clinical Features 

AA clinically manifests similarly across different skin tones; however, in patients with more tightly coiled or curly hair, the extent of scalp hair loss may be underestimated without a full examination. Culturally sensitive approaches to hair and scalp evaluation are essential, especially for Black women, whose hair care practices and scalp conditions may be overlooked or misunderstood during visits to evaluate hair loss. A thoughtful history and gentle examination of the hair and scalp that considers hair texture, cultural practices such as head coverings (eg, headwraps, turbans, hijabs), use of hair adornments (eg, clips, beads, bows), traditional braiding, and use of natural oils or herbal treatments, as well as styling methods including tight hairstyles, use of heat styling tools (eg, flat irons, curling irons), chemical application (eg, straighteners, hair color), and washing or styling frequency can improve diagnostic accuracy and help build trust in the patient-provider relationship. 

Classic signs of AA visualized with dermoscopy include yellow and/or black dots on the scalp and exclamation point hairs. The appearance of fine white vellus hairs within the alopecic patches also may indicate early regrowth. On scalp trichoscopy, black dots are more prominent, and yellow dots are less prominent, in individuals with darker skin tones vs lighter skin tones.⁹ 

Worth Noting 

In addition to a full examination of the scalp, documenting the extent of hair loss using validated severity scales, including the severity of alopecia tool (SALT), AA severity index (AASI), clinician-reported outcome assessment, and patient-reported outcome measures, can standardize disease severity assessment, facilitate timely insurance or medication approvals, and support objective tracking of treatment response, which may ultimately enhance access to care.¹⁰ 

Prompt treatment of AA is essential. Not surprisingly, patients given a diagnosis of AA may experience considerable emotional and psychological distress—regardless of the extent of the loss.¹¹ Treatment options include mid- to high-potency topical or intralesional corticosteroids and newer and more targeted systemic options, including 3 Janus kinase (JAK) inhibitors—baricitinib, ritlecitinib, and deuruxolitinib—for more extensive disease.¹² Treatment with intralesional corticosteroids may cause transient hypopigmentation, which may be more noticeable in patients with darker skin tones. Delays in treatment with JAK inhibitors can lead to a less-than-optimal response. Of the 3 JAK inhibitors that are approved by the US Food and Drug Administration for AA, only ritlecitinib is approved for children 12 years and older, leaving a therapeutic gap for younger patients that often leads to uncomfortable scalp injections, delayed or no treatment, off-label use of JAK inhibitors as well as the pairing of off-label dupilumab with oral minoxidil.¹² 

Based on adult data, patients with severe disease and a shorter duration of hair loss (ie, < 4 years) tend to respond better to JAK inhibitors than those experiencing hair loss for longer periods. Also, those with more severe AA tend to have poorer outcomes than those with less severe disease.¹³ If treatment proves less than optimal, wigs and hair pieces may need to be considered. It is worth noting that some insurance companies will cover the cost of wigs for patients when prescribed as cranial prostheses. 

Health Disparity Highlight 

Health disparities in AA can be influenced by socioeconomic status and access to care. Patients from lower-income backgrounds often face barriers to accessing dermatologic care and treatments such as JAK inhibitors, which may remain inaccessible due to high costs and insurance limitations.¹⁴ These barriers can intersect with other factors such as age, sex, and race, potentially exacerbating disparities. Women with skin of color in underserved communities may experience delayed diagnosis, limited treatment options, and greater psychosocial distress from hair loss.¹⁴ Addressing these inequities requires advocacy, education for both patients and clinicians, and improved access to treatment to ensure comprehensive care for all patients. 

The Comparison

A. Alopecia areata in a young girl with a lighter skin tone. The fine white vellus hairs are signs of regrowth. 

B. Alopecia areata in a 49-year-old man with tightly coiled hair and darker skin tone. Coiled white hairs are noted in the alopecia patches.

Alopecia areata (AA) is a common autoimmune condition characterized by hair loss resulting from a T cell–mediated attack on the hair follicles. It manifests as nonscarring patches of hair loss on the scalp, eyebrows, eyelashes, and beard area as well as more extensive complete loss of scalp and body hair. While AA may affect individuals of any age, most patients develop their first patch(es) of hair loss during childhood.¹ The treatment landscape for AA has evolved considerably in recent years, but barriers to access to newer treatments persist. 

Epidemiology 

AA is most prevalent among pediatric and adult individuals of African, Asian, or Hispanic/Latino descent.^2-4 In some studies, Black individuals had higher odds and Asian individuals had lower odds of developing AA, while other studies have reported the highest standardized prevalence among Asian individuals.⁵ In the United States, AA affects about 1.47% of adults and as many as 0.11% of children.^6-8 In Black patients, AA often manifests early with a female predominance.⁵ 

AA frequently is associated with autoimmune comorbidities, the most common being thyroid disease.^3,5 In Black patients, AA is associated with more atopic comorbidities, including asthma, atopic dermatitis, and allergic rhinitis.⁵ 

Key Clinical Features 

AA clinically manifests similarly across different skin tones; however, in patients with more tightly coiled or curly hair, the extent of scalp hair loss may be underestimated without a full examination. Culturally sensitive approaches to hair and scalp evaluation are essential, especially for Black women, whose hair care practices and scalp conditions may be overlooked or misunderstood during visits to evaluate hair loss. A thoughtful history and gentle examination of the hair and scalp that considers hair texture, cultural practices such as head coverings (eg, headwraps, turbans, hijabs), use of hair adornments (eg, clips, beads, bows), traditional braiding, and use of natural oils or herbal treatments, as well as styling methods including tight hairstyles, use of heat styling tools (eg, flat irons, curling irons), chemical application (eg, straighteners, hair color), and washing or styling frequency can improve diagnostic accuracy and help build trust in the patient-provider relationship. 

Classic signs of AA visualized with dermoscopy include yellow and/or black dots on the scalp and exclamation point hairs. The appearance of fine white vellus hairs within the alopecic patches also may indicate early regrowth. On scalp trichoscopy, black dots are more prominent, and yellow dots are less prominent, in individuals with darker skin tones vs lighter skin tones.⁹ 

Worth Noting 

In addition to a full examination of the scalp, documenting the extent of hair loss using validated severity scales, including the severity of alopecia tool (SALT), AA severity index (AASI), clinician-reported outcome assessment, and patient-reported outcome measures, can standardize disease severity assessment, facilitate timely insurance or medication approvals, and support objective tracking of treatment response, which may ultimately enhance access to care.¹⁰ 

Prompt treatment of AA is essential. Not surprisingly, patients given a diagnosis of AA may experience considerable emotional and psychological distress—regardless of the extent of the loss.¹¹ Treatment options include mid- to high-potency topical or intralesional corticosteroids and newer and more targeted systemic options, including 3 Janus kinase (JAK) inhibitors—baricitinib, ritlecitinib, and deuruxolitinib—for more extensive disease.¹² Treatment with intralesional corticosteroids may cause transient hypopigmentation, which may be more noticeable in patients with darker skin tones. Delays in treatment with JAK inhibitors can lead to a less-than-optimal response. Of the 3 JAK inhibitors that are approved by the US Food and Drug Administration for AA, only ritlecitinib is approved for children 12 years and older, leaving a therapeutic gap for younger patients that often leads to uncomfortable scalp injections, delayed or no treatment, off-label use of JAK inhibitors as well as the pairing of off-label dupilumab with oral minoxidil.¹² 

Based on adult data, patients with severe disease and a shorter duration of hair loss (ie, < 4 years) tend to respond better to JAK inhibitors than those experiencing hair loss for longer periods. Also, those with more severe AA tend to have poorer outcomes than those with less severe disease.¹³ If treatment proves less than optimal, wigs and hair pieces may need to be considered. It is worth noting that some insurance companies will cover the cost of wigs for patients when prescribed as cranial prostheses. 

Health Disparity Highlight 

Health disparities in AA can be influenced by socioeconomic status and access to care. Patients from lower-income backgrounds often face barriers to accessing dermatologic care and treatments such as JAK inhibitors, which may remain inaccessible due to high costs and insurance limitations.¹⁴ These barriers can intersect with other factors such as age, sex, and race, potentially exacerbating disparities. Women with skin of color in underserved communities may experience delayed diagnosis, limited treatment options, and greater psychosocial distress from hair loss.¹⁴ Addressing these inequities requires advocacy, education for both patients and clinicians, and improved access to treatment to ensure comprehensive care for all patients. 

Click here to view more from Federal Health Care Data Trends 2025.

Click here to view more from Federal Health Care Data Trends 2025.

Click here to view more from Federal Health Care Data Trends 2025.

Pseudofolliculitis barbae (PFB), also known as razor bumps, is a common inflammatory condition characterized by papules and pustules that typically appear in the beard and cheek regions. It occurs when shaved hair regrows and penetrates the skin, leading to irritation and inflammation. While anyone who shaves can develop PFB, it is more prevalent and severe in individuals with naturally tightly coiled, coarse-textured hair.^1,2 PFB is common in individuals who shave frequently due to personal choice or profession, such as members of the US military^3,4 and firefighters, who are required to remain clean shaven for safety (eg, ensuring proper fit of a respirator mask).⁵ Early diagnosis and treatment of PFB are essential to prevent long-term complications such as scarring or hyperpigmentation, which may be more severe in those with darker skin tones.

Epidemiology

PFB is most common in Black men, affecting 45% to 83% of men of African ancestry.^1,2 This condition also can affect individuals of various ethnicities with coarse or curly hair. The spiral shape of the hair increases the likelihood that it will regrow into the skin after shaving.⁶ Women with hirsutism who shave also can develop PFB.

Key Clinical Features

The papules and pustules seen in PFB may be flesh colored, erythematous, hyperpigmented, brown, or violaceous. Erythema may be less pronounced in darker vs lighter skin tones. Persistent and severe postinflammatory hyperpigmentation may occur, and hypertrophic or keloidal scars may develop in affected areas. Dermoscopy may reveal extrafollicular hair penetration as well as follicular or perifollicular pustules accompanied by hyperkeratosis.

Worth Noting

The most effective management for PFB is to discontinue shaving.¹ If shaving is desired or necessary, it is recommended that patients apply lukewarm water to the affected area followed by a generous amount of shaving foam or gel to create a protective antifriction layer that allows the razor to glide more smoothly over the skin and reduces subsequent irritation.² Using the right razor technology also may help alleviate symptoms. Research has shown that multiblade razors used in conjunction with preshave hair hydration and postshave moisturization do not worsen PFB.² A recent study found that multiblade razor technology paired with use of a shave foam or gel actually improved skin appearance in patients with PFB.⁷

It is important to direct patients to shave in the direction of hair growth; however, this may not be possible for individuals with curly or coarse hair, as the hair may grow in many directions.^8,9 Patients also should avoid pulling the skin taut while shaving, as doing so allows the hair to be clipped below the surface, where it can repenetrate the skin and cause further irritation. As an alternative to shaving with a razor, patients can use hair clippers to trim beard hair, which leaves behind stubble and interrupts the cycle of retracted hairs under the skin. Nd:YAG laser therapy has demonstrated efficacy in reduction of PFB papules and pustules.^9-12 Greater mean improvement in inflammatory papules and reduction in hair density was noted in participants who received Nd:YAG laser plus eflornithine compared with those who received the laser or eflornithine alone.¹¹ Patients should not pluck or dig into the skin to remove any ingrown hairs. If a tweezer is used, the patient should gently lift the tip of the ingrown hair with the tweezer to dislodge it from the skin and prevent plucking out the hair completely.

To help manage inflammation after shaving, topical treatments such as benzoyl peroxide 5%/clindamycin 1% gel can be used.^3,13 A low-potency steroid such as topical hydrocortisone 2.5% applied once or twice daily for up to 2 to 3 days may be helpful.^1,14 Adjunctive treatments including keratolytics (eg, topical retinoids, hydroxy acids) reduce perifollicular hyperkeratosis.^14,15 Agents containing alpha hydroxy acids (eg, glycolic acid) also can decrease the curvature of the hair itself by reducing the sulfhydryl bonds.⁶ If secondary bacterial infections occur, oral antibiotics (eg, doxycycline) may be necessary.

Health Disparity Highlight

Individuals with darker skin tones are at higher risk for PFB and associated complications. Limited access to dermatology services may further exacerbate these challenges. Individuals with PFB may not seek medical treatment until the condition becomes severe. Clinicians also may underestimate the severity of PFB—particularly in those with darker skin tones—based on erythema alone because it may be less pronounced in darker vs lighter skin tones.¹⁶

While permanent hair reduction with laser therapy is a treatment option for PFB, it may be inaccessible to some patients because it can be expensive and is coded as a cosmetic procedure. Additionally, patients may not have access to specialists who are experienced in performing the procedure in those with darker skin tones.⁹ Some patients also may not want to permanently reduce the amount of hair that grows in the beard area for personal or religious reasons.¹⁷

Pseudofolliculitis barbae also has been linked to professional disparities. One study found that members of the US Air Force who had medical shaving waivers experienced longer times to promotion than those with no waiver.¹⁸ Delays in promotion may be linked to perceptions of unprofessionalism, exclusion from high-profile duties, and concerns about career progression. While this delay was similar for individuals of all races, the majority of those in the waiver group were Black/African American. In 2021, 4 Black firefighters with PFB were unsuccessful in their bid to get a medical accommodation regarding a New York City Fire Department policy requiring them to be clean shaven where the oxygen mask seals against the skin.⁵ More research is needed on mask safety and efficiency relative to the length of facial hair. Accommodations or tailored masks for facial hair conditions also are necessary so individuals with PFB can meet job requirements while managing their condition.

Pseudofolliculitis barbae (PFB), also known as razor bumps, is a common inflammatory condition characterized by papules and pustules that typically appear in the beard and cheek regions. It occurs when shaved hair regrows and penetrates the skin, leading to irritation and inflammation. While anyone who shaves can develop PFB, it is more prevalent and severe in individuals with naturally tightly coiled, coarse-textured hair.^1,2 PFB is common in individuals who shave frequently due to personal choice or profession, such as members of the US military^3,4 and firefighters, who are required to remain clean shaven for safety (eg, ensuring proper fit of a respirator mask).⁵ Early diagnosis and treatment of PFB are essential to prevent long-term complications such as scarring or hyperpigmentation, which may be more severe in those with darker skin tones.

Epidemiology

PFB is most common in Black men, affecting 45% to 83% of men of African ancestry.^1,2 This condition also can affect individuals of various ethnicities with coarse or curly hair. The spiral shape of the hair increases the likelihood that it will regrow into the skin after shaving.⁶ Women with hirsutism who shave also can develop PFB.

Key Clinical Features

The papules and pustules seen in PFB may be flesh colored, erythematous, hyperpigmented, brown, or violaceous. Erythema may be less pronounced in darker vs lighter skin tones. Persistent and severe postinflammatory hyperpigmentation may occur, and hypertrophic or keloidal scars may develop in affected areas. Dermoscopy may reveal extrafollicular hair penetration as well as follicular or perifollicular pustules accompanied by hyperkeratosis.

Worth Noting

The most effective management for PFB is to discontinue shaving.¹ If shaving is desired or necessary, it is recommended that patients apply lukewarm water to the affected area followed by a generous amount of shaving foam or gel to create a protective antifriction layer that allows the razor to glide more smoothly over the skin and reduces subsequent irritation.² Using the right razor technology also may help alleviate symptoms. Research has shown that multiblade razors used in conjunction with preshave hair hydration and postshave moisturization do not worsen PFB.² A recent study found that multiblade razor technology paired with use of a shave foam or gel actually improved skin appearance in patients with PFB.⁷

It is important to direct patients to shave in the direction of hair growth; however, this may not be possible for individuals with curly or coarse hair, as the hair may grow in many directions.^8,9 Patients also should avoid pulling the skin taut while shaving, as doing so allows the hair to be clipped below the surface, where it can repenetrate the skin and cause further irritation. As an alternative to shaving with a razor, patients can use hair clippers to trim beard hair, which leaves behind stubble and interrupts the cycle of retracted hairs under the skin. Nd:YAG laser therapy has demonstrated efficacy in reduction of PFB papules and pustules.^9-12 Greater mean improvement in inflammatory papules and reduction in hair density was noted in participants who received Nd:YAG laser plus eflornithine compared with those who received the laser or eflornithine alone.¹¹ Patients should not pluck or dig into the skin to remove any ingrown hairs. If a tweezer is used, the patient should gently lift the tip of the ingrown hair with the tweezer to dislodge it from the skin and prevent plucking out the hair completely.

To help manage inflammation after shaving, topical treatments such as benzoyl peroxide 5%/clindamycin 1% gel can be used.^3,13 A low-potency steroid such as topical hydrocortisone 2.5% applied once or twice daily for up to 2 to 3 days may be helpful.^1,14 Adjunctive treatments including keratolytics (eg, topical retinoids, hydroxy acids) reduce perifollicular hyperkeratosis.^14,15 Agents containing alpha hydroxy acids (eg, glycolic acid) also can decrease the curvature of the hair itself by reducing the sulfhydryl bonds.⁶ If secondary bacterial infections occur, oral antibiotics (eg, doxycycline) may be necessary.

Health Disparity Highlight

Individuals with darker skin tones are at higher risk for PFB and associated complications. Limited access to dermatology services may further exacerbate these challenges. Individuals with PFB may not seek medical treatment until the condition becomes severe. Clinicians also may underestimate the severity of PFB—particularly in those with darker skin tones—based on erythema alone because it may be less pronounced in darker vs lighter skin tones.¹⁶

While permanent hair reduction with laser therapy is a treatment option for PFB, it may be inaccessible to some patients because it can be expensive and is coded as a cosmetic procedure. Additionally, patients may not have access to specialists who are experienced in performing the procedure in those with darker skin tones.⁹ Some patients also may not want to permanently reduce the amount of hair that grows in the beard area for personal or religious reasons.¹⁷

Pseudofolliculitis barbae also has been linked to professional disparities. One study found that members of the US Air Force who had medical shaving waivers experienced longer times to promotion than those with no waiver.¹⁸ Delays in promotion may be linked to perceptions of unprofessionalism, exclusion from high-profile duties, and concerns about career progression. While this delay was similar for individuals of all races, the majority of those in the waiver group were Black/African American. In 2021, 4 Black firefighters with PFB were unsuccessful in their bid to get a medical accommodation regarding a New York City Fire Department policy requiring them to be clean shaven where the oxygen mask seals against the skin.⁵ More research is needed on mask safety and efficiency relative to the length of facial hair. Accommodations or tailored masks for facial hair conditions also are necessary so individuals with PFB can meet job requirements while managing their condition.

Pseudofolliculitis barbae (PFB), also known as razor bumps, is a common inflammatory condition characterized by papules and pustules that typically appear in the beard and cheek regions. It occurs when shaved hair regrows and penetrates the skin, leading to irritation and inflammation. While anyone who shaves can develop PFB, it is more prevalent and severe in individuals with naturally tightly coiled, coarse-textured hair.^1,2 PFB is common in individuals who shave frequently due to personal choice or profession, such as members of the US military^3,4 and firefighters, who are required to remain clean shaven for safety (eg, ensuring proper fit of a respirator mask).⁵ Early diagnosis and treatment of PFB are essential to prevent long-term complications such as scarring or hyperpigmentation, which may be more severe in those with darker skin tones.

Epidemiology

PFB is most common in Black men, affecting 45% to 83% of men of African ancestry.^1,2 This condition also can affect individuals of various ethnicities with coarse or curly hair. The spiral shape of the hair increases the likelihood that it will regrow into the skin after shaving.⁶ Women with hirsutism who shave also can develop PFB.

Key Clinical Features

The papules and pustules seen in PFB may be flesh colored, erythematous, hyperpigmented, brown, or violaceous. Erythema may be less pronounced in darker vs lighter skin tones. Persistent and severe postinflammatory hyperpigmentation may occur, and hypertrophic or keloidal scars may develop in affected areas. Dermoscopy may reveal extrafollicular hair penetration as well as follicular or perifollicular pustules accompanied by hyperkeratosis.

Worth Noting

The most effective management for PFB is to discontinue shaving.¹ If shaving is desired or necessary, it is recommended that patients apply lukewarm water to the affected area followed by a generous amount of shaving foam or gel to create a protective antifriction layer that allows the razor to glide more smoothly over the skin and reduces subsequent irritation.² Using the right razor technology also may help alleviate symptoms. Research has shown that multiblade razors used in conjunction with preshave hair hydration and postshave moisturization do not worsen PFB.² A recent study found that multiblade razor technology paired with use of a shave foam or gel actually improved skin appearance in patients with PFB.⁷

It is important to direct patients to shave in the direction of hair growth; however, this may not be possible for individuals with curly or coarse hair, as the hair may grow in many directions.^8,9 Patients also should avoid pulling the skin taut while shaving, as doing so allows the hair to be clipped below the surface, where it can repenetrate the skin and cause further irritation. As an alternative to shaving with a razor, patients can use hair clippers to trim beard hair, which leaves behind stubble and interrupts the cycle of retracted hairs under the skin. Nd:YAG laser therapy has demonstrated efficacy in reduction of PFB papules and pustules.^9-12 Greater mean improvement in inflammatory papules and reduction in hair density was noted in participants who received Nd:YAG laser plus eflornithine compared with those who received the laser or eflornithine alone.¹¹ Patients should not pluck or dig into the skin to remove any ingrown hairs. If a tweezer is used, the patient should gently lift the tip of the ingrown hair with the tweezer to dislodge it from the skin and prevent plucking out the hair completely.

To help manage inflammation after shaving, topical treatments such as benzoyl peroxide 5%/clindamycin 1% gel can be used.^3,13 A low-potency steroid such as topical hydrocortisone 2.5% applied once or twice daily for up to 2 to 3 days may be helpful.^1,14 Adjunctive treatments including keratolytics (eg, topical retinoids, hydroxy acids) reduce perifollicular hyperkeratosis.^14,15 Agents containing alpha hydroxy acids (eg, glycolic acid) also can decrease the curvature of the hair itself by reducing the sulfhydryl bonds.⁶ If secondary bacterial infections occur, oral antibiotics (eg, doxycycline) may be necessary.

Health Disparity Highlight

Individuals with darker skin tones are at higher risk for PFB and associated complications. Limited access to dermatology services may further exacerbate these challenges. Individuals with PFB may not seek medical treatment until the condition becomes severe. Clinicians also may underestimate the severity of PFB—particularly in those with darker skin tones—based on erythema alone because it may be less pronounced in darker vs lighter skin tones.¹⁶

While permanent hair reduction with laser therapy is a treatment option for PFB, it may be inaccessible to some patients because it can be expensive and is coded as a cosmetic procedure. Additionally, patients may not have access to specialists who are experienced in performing the procedure in those with darker skin tones.⁹ Some patients also may not want to permanently reduce the amount of hair that grows in the beard area for personal or religious reasons.¹⁷

Pseudofolliculitis barbae also has been linked to professional disparities. One study found that members of the US Air Force who had medical shaving waivers experienced longer times to promotion than those with no waiver.¹⁸ Delays in promotion may be linked to perceptions of unprofessionalism, exclusion from high-profile duties, and concerns about career progression. While this delay was similar for individuals of all races, the majority of those in the waiver group were Black/African American. In 2021, 4 Black firefighters with PFB were unsuccessful in their bid to get a medical accommodation regarding a New York City Fire Department policy requiring them to be clean shaven where the oxygen mask seals against the skin.⁵ More research is needed on mask safety and efficiency relative to the length of facial hair. Accommodations or tailored masks for facial hair conditions also are necessary so individuals with PFB can meet job requirements while managing their condition.