Candrice R. Heath, MD

Acne keloidalis nuchae (AKN) is a chronic inflammatory condition commonly affecting the occipital scalp and posterior neck. It causes discrete or extensive fibrosing papules that may coalesce to form pronounced ­tumorlike masses^1,2 with scarring alopecia (Figure, A–C).³ Pustules, hair tufts, secondary bacterial infections, abscesses, and sinus tracts also may occur.¹ The pathogenesis of AKN has been characterized as varying stages of follicular inflammation at the infundibular and isthmus levels followed by fibrotic occlusion of the ­follicular lumen.⁴ Pruritus, pain, bleeding, oozing, and a feeling of scalp tightness may occur.^1,5

Umar et al⁶ performed a retrospective review of 108 men with AKN—58% of African descent, 37% Hispanic, 3% Asian, and 2% Middle Eastern—and proposed a 3-tier classification system for AKN. Tier 1 focused on the distribution and sagittal spread of AKN lesions between the clinical demarcation lines of the occipital notch and posterior hairline. Tier 2 focused on the type of lesions present—discrete papules or nodules, coalescing/abutting lesions, plaques (raised, atrophic, or indurated), or dome-shaped tumoral masses. Tier 3 focused on the presence or absence of co-existing dissecting cellulitis or folliculitis decalvans.⁶

Epidemiology

Acne keloidalis nuchae primarily manifests in adolescent and adult men of African or Afro-Caribbean descent.⁷ Among African American men, the prevalence of AKN ranges from 0.5% to 13.6%.⁸ Similar ranges have been reported among Nigerian, South African, and West African men.¹ Acne keloidalis nuchae also affects Asian and Hispanic men but rarely is seen in non-Hispanic White men or in women of any ethnicity.^9,10 The male to female ratio is 20:1.^1,11 Hair texture, hairstyling practices such as closely shaved or faded haircuts, and genetics likely contribute to development of AKN. Sports and occupations that require the use of headgear or a tight collar may increase the risk for AKN.¹²

Key clinical features in people with darker skin tones

• The lesions of AKN range in color from pink to dark brown or black. Postinflammatory hyperpigmentation or hyperchromia may be present around AKN lesions.
• Chronicity of AKN may lead to extended use of high-potency topical or intralesional corticosteroids, which causes transient or long-lasting hypopigmentation, especially in those with darker skin tones.

Worth noting

• Acne keloidalis nuchae can be disfiguring, which negatively impacts quality of life and self-esteem.¹²
• Some occupations (eg, military, police) have hair policies that may not be favorable to those with or at risk for AKN.
• Patients with AKN are 2 to 3 times more likely to present with metabolic syndrome, hypertension, type 2 diabetes mellitus, or obesity.¹³

Treatment

There are no treatments approved by the US Food and Drug Administration specifically for AKN. Treatment approaches are based on the pathophysiology, secondary impacts on the skin, and disease severity. Growing out the hair may prevent worsening and/or decrease the risk for new lesions.⁶

• Options include but are not limited to topical and systemic therapies (eg, topical corticosteroids, oral or topical antibiotics, isotretinoin, topical retinoids, imiquimod, pimecrolimus), light devices (eg, phototherapy, laser), ablative therapies (eg, laser, cryotherapy, radiotherapy), and surgery (eg, excision, follicular unit excision), often in combination.^6,14,15
• Intralesional triamcinolone injections are considered standard of care. Adotama et al found that injecting ­triamcinolone into the deep dermis in the area of flat or papular AKN yielded better control of inflammation and decreased appearance of lesions compared with injecting individual lesions.¹⁶
• For extensive AKN lesions that do not respond to ­less-invasive therapies, consider surgical techniques,^6,17 such as follicular unit excision¹⁸ and more extensive surgical excisions building on approaches from pioneers Drs. John Kenney and Harold Pierce.¹⁹ An innovative surgical approach for removal of large AKNs is the bat excision technique—wound shape resembles a bat in a spread-eagled position—with secondary intention healing with or without debridement and/or tension sutures. The resulting linear scar acts as a new posterior hair line.²⁰

Health disparity highlights

Access to a dermatologic or plastic surgeon with expertise in the surgical treatment of large AKNs may be challenging but is needed to reduce risk for recurrence and adverse events.

Close-cropped haircuts on the occipital scalp, which are particularly popular among men of African descent, increase the risk for AKN.⁵ Although this grooming style may be a personal preference, other hairstyles commonly worn by those with tightly coiled hair may be deemed “unprofessional” in society or the workplace, which leads to hairstyling practices that may increase the risk for AKN.²¹

Acne keloidalis nuchae remains an understudied entity that adversely affects patients with skin of color.

Acne keloidalis nuchae (AKN) is a chronic inflammatory condition commonly affecting the occipital scalp and posterior neck. It causes discrete or extensive fibrosing papules that may coalesce to form pronounced ­tumorlike masses^1,2 with scarring alopecia (Figure, A–C).³ Pustules, hair tufts, secondary bacterial infections, abscesses, and sinus tracts also may occur.¹ The pathogenesis of AKN has been characterized as varying stages of follicular inflammation at the infundibular and isthmus levels followed by fibrotic occlusion of the ­follicular lumen.⁴ Pruritus, pain, bleeding, oozing, and a feeling of scalp tightness may occur.^1,5

Umar et al⁶ performed a retrospective review of 108 men with AKN—58% of African descent, 37% Hispanic, 3% Asian, and 2% Middle Eastern—and proposed a 3-tier classification system for AKN. Tier 1 focused on the distribution and sagittal spread of AKN lesions between the clinical demarcation lines of the occipital notch and posterior hairline. Tier 2 focused on the type of lesions present—discrete papules or nodules, coalescing/abutting lesions, plaques (raised, atrophic, or indurated), or dome-shaped tumoral masses. Tier 3 focused on the presence or absence of co-existing dissecting cellulitis or folliculitis decalvans.⁶

Epidemiology

Acne keloidalis nuchae primarily manifests in adolescent and adult men of African or Afro-Caribbean descent.⁷ Among African American men, the prevalence of AKN ranges from 0.5% to 13.6%.⁸ Similar ranges have been reported among Nigerian, South African, and West African men.¹ Acne keloidalis nuchae also affects Asian and Hispanic men but rarely is seen in non-Hispanic White men or in women of any ethnicity.^9,10 The male to female ratio is 20:1.^1,11 Hair texture, hairstyling practices such as closely shaved or faded haircuts, and genetics likely contribute to development of AKN. Sports and occupations that require the use of headgear or a tight collar may increase the risk for AKN.¹²

Key clinical features in people with darker skin tones

• The lesions of AKN range in color from pink to dark brown or black. Postinflammatory hyperpigmentation or hyperchromia may be present around AKN lesions.
• Chronicity of AKN may lead to extended use of high-potency topical or intralesional corticosteroids, which causes transient or long-lasting hypopigmentation, especially in those with darker skin tones.

Worth noting

• Acne keloidalis nuchae can be disfiguring, which negatively impacts quality of life and self-esteem.¹²
• Some occupations (eg, military, police) have hair policies that may not be favorable to those with or at risk for AKN.
• Patients with AKN are 2 to 3 times more likely to present with metabolic syndrome, hypertension, type 2 diabetes mellitus, or obesity.¹³

Treatment

There are no treatments approved by the US Food and Drug Administration specifically for AKN. Treatment approaches are based on the pathophysiology, secondary impacts on the skin, and disease severity. Growing out the hair may prevent worsening and/or decrease the risk for new lesions.⁶

• Options include but are not limited to topical and systemic therapies (eg, topical corticosteroids, oral or topical antibiotics, isotretinoin, topical retinoids, imiquimod, pimecrolimus), light devices (eg, phototherapy, laser), ablative therapies (eg, laser, cryotherapy, radiotherapy), and surgery (eg, excision, follicular unit excision), often in combination.^6,14,15
• Intralesional triamcinolone injections are considered standard of care. Adotama et al found that injecting ­triamcinolone into the deep dermis in the area of flat or papular AKN yielded better control of inflammation and decreased appearance of lesions compared with injecting individual lesions.¹⁶
• For extensive AKN lesions that do not respond to ­less-invasive therapies, consider surgical techniques,^6,17 such as follicular unit excision¹⁸ and more extensive surgical excisions building on approaches from pioneers Drs. John Kenney and Harold Pierce.¹⁹ An innovative surgical approach for removal of large AKNs is the bat excision technique—wound shape resembles a bat in a spread-eagled position—with secondary intention healing with or without debridement and/or tension sutures. The resulting linear scar acts as a new posterior hair line.²⁰

Health disparity highlights

Access to a dermatologic or plastic surgeon with expertise in the surgical treatment of large AKNs may be challenging but is needed to reduce risk for recurrence and adverse events.

Close-cropped haircuts on the occipital scalp, which are particularly popular among men of African descent, increase the risk for AKN.⁵ Although this grooming style may be a personal preference, other hairstyles commonly worn by those with tightly coiled hair may be deemed “unprofessional” in society or the workplace, which leads to hairstyling practices that may increase the risk for AKN.²¹

Acne keloidalis nuchae remains an understudied entity that adversely affects patients with skin of color.

Acne keloidalis nuchae (AKN) is a chronic inflammatory condition commonly affecting the occipital scalp and posterior neck. It causes discrete or extensive fibrosing papules that may coalesce to form pronounced ­tumorlike masses^1,2 with scarring alopecia (Figure, A–C).³ Pustules, hair tufts, secondary bacterial infections, abscesses, and sinus tracts also may occur.¹ The pathogenesis of AKN has been characterized as varying stages of follicular inflammation at the infundibular and isthmus levels followed by fibrotic occlusion of the ­follicular lumen.⁴ Pruritus, pain, bleeding, oozing, and a feeling of scalp tightness may occur.^1,5

Umar et al⁶ performed a retrospective review of 108 men with AKN—58% of African descent, 37% Hispanic, 3% Asian, and 2% Middle Eastern—and proposed a 3-tier classification system for AKN. Tier 1 focused on the distribution and sagittal spread of AKN lesions between the clinical demarcation lines of the occipital notch and posterior hairline. Tier 2 focused on the type of lesions present—discrete papules or nodules, coalescing/abutting lesions, plaques (raised, atrophic, or indurated), or dome-shaped tumoral masses. Tier 3 focused on the presence or absence of co-existing dissecting cellulitis or folliculitis decalvans.⁶

Epidemiology

Acne keloidalis nuchae primarily manifests in adolescent and adult men of African or Afro-Caribbean descent.⁷ Among African American men, the prevalence of AKN ranges from 0.5% to 13.6%.⁸ Similar ranges have been reported among Nigerian, South African, and West African men.¹ Acne keloidalis nuchae also affects Asian and Hispanic men but rarely is seen in non-Hispanic White men or in women of any ethnicity.^9,10 The male to female ratio is 20:1.^1,11 Hair texture, hairstyling practices such as closely shaved or faded haircuts, and genetics likely contribute to development of AKN. Sports and occupations that require the use of headgear or a tight collar may increase the risk for AKN.¹²

Key clinical features in people with darker skin tones

• The lesions of AKN range in color from pink to dark brown or black. Postinflammatory hyperpigmentation or hyperchromia may be present around AKN lesions.
• Chronicity of AKN may lead to extended use of high-potency topical or intralesional corticosteroids, which causes transient or long-lasting hypopigmentation, especially in those with darker skin tones.

Worth noting

• Acne keloidalis nuchae can be disfiguring, which negatively impacts quality of life and self-esteem.¹²
• Some occupations (eg, military, police) have hair policies that may not be favorable to those with or at risk for AKN.
• Patients with AKN are 2 to 3 times more likely to present with metabolic syndrome, hypertension, type 2 diabetes mellitus, or obesity.¹³

Treatment

There are no treatments approved by the US Food and Drug Administration specifically for AKN. Treatment approaches are based on the pathophysiology, secondary impacts on the skin, and disease severity. Growing out the hair may prevent worsening and/or decrease the risk for new lesions.⁶

• Options include but are not limited to topical and systemic therapies (eg, topical corticosteroids, oral or topical antibiotics, isotretinoin, topical retinoids, imiquimod, pimecrolimus), light devices (eg, phototherapy, laser), ablative therapies (eg, laser, cryotherapy, radiotherapy), and surgery (eg, excision, follicular unit excision), often in combination.^6,14,15
• Intralesional triamcinolone injections are considered standard of care. Adotama et al found that injecting ­triamcinolone into the deep dermis in the area of flat or papular AKN yielded better control of inflammation and decreased appearance of lesions compared with injecting individual lesions.¹⁶
• For extensive AKN lesions that do not respond to ­less-invasive therapies, consider surgical techniques,^6,17 such as follicular unit excision¹⁸ and more extensive surgical excisions building on approaches from pioneers Drs. John Kenney and Harold Pierce.¹⁹ An innovative surgical approach for removal of large AKNs is the bat excision technique—wound shape resembles a bat in a spread-eagled position—with secondary intention healing with or without debridement and/or tension sutures. The resulting linear scar acts as a new posterior hair line.²⁰

Health disparity highlights

Access to a dermatologic or plastic surgeon with expertise in the surgical treatment of large AKNs may be challenging but is needed to reduce risk for recurrence and adverse events.

Close-cropped haircuts on the occipital scalp, which are particularly popular among men of African descent, increase the risk for AKN.⁵ Although this grooming style may be a personal preference, other hairstyles commonly worn by those with tightly coiled hair may be deemed “unprofessional” in society or the workplace, which leads to hairstyling practices that may increase the risk for AKN.²¹

Acne keloidalis nuchae remains an understudied entity that adversely affects patients with skin of color.

The Comparison

A A 25-year-old man of Hispanic ethnicity with pink papules, pustules, and large keloidal tumors on the occipital scalp characteristic of acne keloidalis nuchae (AKN). There is hair loss and some tufting of remaining hairs.

B A 17-year-old adolescent boy of African descent with small papules on the occipital scalp and some hair loss from AKN.

C A 19-year-old man of African descent with extensive papules and keloidal tumors on the occipital scalp as well as scarring hair loss and tufting of hairs from AKN.

Acne keloidalis nuchae (AKN) is a chronic inflammatory condition commonly affecting the occipital scalp and posterior neck. It causes discrete or extensive fibrosing papules that may coalesce to form pronounced ­tumorlike masses^1,2 with scarring alopecia (Figure, A–C).³ Pustules, hair tufts, secondary bacterial infections, abscesses, and sinus tracts also may occur.¹ The pathogenesis of AKN has been characterized as varying stages of follicular inflammation at the infundibular and isthmus levels followed by fibrotic occlusion of the ­follicular lumen.⁴ Pruritus, pain, bleeding, oozing, and a feeling of scalp tightness may occur.^1,5

Umar et al⁶ performed a retrospective review of 108 men with AKN—58% of African descent, 37% Hispanic, 3% Asian, and 2% Middle Eastern—and proposed a 3-tier classification system for AKN. Tier 1 focused on the distribution and sagittal spread of AKN lesions between the clinical demarcation lines of the occipital notch and posterior hairline. Tier 2 focused on the type of lesions present—discrete papules or nodules, coalescing/abutting lesions, plaques (raised, atrophic, or indurated), or dome-shaped tumoral masses. Tier 3 focused on the presence or absence of co-existing dissecting cellulitis or folliculitis decalvans.⁶

Epidemiology

Acne keloidalis nuchae primarily manifests in adolescent and adult men of African or Afro-Caribbean descent.⁷ Among African American men, the prevalence of AKN ranges from 0.5% to 13.6%.⁸ Similar ranges have been reported among Nigerian, South African, and West African men.¹ Acne keloidalis nuchae also affects Asian and Hispanic men but rarely is seen in non-Hispanic White men or in women of any ethnicity.^9,10 The male to female ratio is 20:1.^1,11 Hair texture, hairstyling practices such as closely shaved or faded haircuts, and genetics likely contribute to development of AKN. Sports and occupations that require the use of headgear or a tight collar may increase the risk for AKN.¹²

Key clinical features in people with darker skin tones

• The lesions of AKN range in color from pink to dark brown or black. Postinflammatory hyperpigmentation or hyperchromia may be present around AKN lesions.
• Chronicity of AKN may lead to extended use of high-potency topical or intralesional corticosteroids, which causes transient or long-lasting hypopigmentation, especially in those with darker skin tones.

Worth noting

• Acne keloidalis nuchae can be disfiguring, which negatively impacts quality of life and self-esteem.¹²
• Some occupations (eg, military, police) have hair policies that may not be favorable to those with or at risk for AKN.
• Patients with AKN are 2 to 3 times more likely to present with metabolic syndrome, hypertension, type 2 diabetes mellitus, or obesity.¹³

Treatment

There are no treatments approved by the US Food and Drug Administration specifically for AKN. Treatment approaches are based on the pathophysiology, secondary impacts on the skin, and disease severity. Growing out the hair may prevent worsening and/or decrease the risk for new lesions.⁶

• Options include but are not limited to topical and systemic therapies (eg, topical corticosteroids, oral or topical antibiotics, isotretinoin, topical retinoids, imiquimod, pimecrolimus), light devices (eg, phototherapy, laser), ablative therapies (eg, laser, cryotherapy, radiotherapy), and surgery (eg, excision, follicular unit excision), often in combination.^6,14,15
• Intralesional triamcinolone injections are considered standard of care. Adotama et al¹⁶ found that injecting ­triamcinolone into the deep dermis in the area of flat or papular AKN yielded better control of inflammation and decreased appearance of lesions compared with injecting individual lesions.
• For extensive AKN lesions that do not respond to ­less-invasive therapies, consider surgical techniques,^6,17 such as follicular unit excision¹⁸ and more extensive surgical excisions building on approaches from pioneers Drs. John Kenney and Harold Pierce.¹⁹ An innovative surgical approach for removal of large AKNs is the bat excision technique—wound shape resembles a bat in a spread-eagled position—with secondary intention healing with or without debridement and/or tension sutures. The resulting linear scar acts as a new posterior hair line.²⁰

Health disparity highlights

Access to a dermatologic or plastic surgeon with expertise in the surgical treatment of large AKNs may be challenging but is needed to reduce risk for recurrence and adverse events.

Close-cropped haircuts on the occipital scalp, which are particularly popular among men of African descent, increase the risk for AKN.⁵ Although this grooming style may be a personal preference, other hairstyles commonly worn by those with tightly coiled hair may be deemed “unprofessional” in society or the workplace,²¹ which leads to hairstyling practices that may increase the risk for AKN.

Acne keloidalis nuchae remains an understudied entity that adversely affects patients with skin of color.

The Comparison

A A 25-year-old man of Hispanic ethnicity with pink papules, pustules, and large keloidal tumors on the occipital scalp characteristic of acne keloidalis nuchae (AKN). There is hair loss and some tufting of remaining hairs.

B A 17-year-old adolescent boy of African descent with small papules on the occipital scalp and some hair loss from AKN.

C A 19-year-old man of African descent with extensive papules and keloidal tumors on the occipital scalp as well as scarring hair loss and tufting of hairs from AKN.

Acne keloidalis nuchae (AKN) is a chronic inflammatory condition commonly affecting the occipital scalp and posterior neck. It causes discrete or extensive fibrosing papules that may coalesce to form pronounced ­tumorlike masses^1,2 with scarring alopecia (Figure, A–C).³ Pustules, hair tufts, secondary bacterial infections, abscesses, and sinus tracts also may occur.¹ The pathogenesis of AKN has been characterized as varying stages of follicular inflammation at the infundibular and isthmus levels followed by fibrotic occlusion of the ­follicular lumen.⁴ Pruritus, pain, bleeding, oozing, and a feeling of scalp tightness may occur.^1,5

Umar et al⁶ performed a retrospective review of 108 men with AKN—58% of African descent, 37% Hispanic, 3% Asian, and 2% Middle Eastern—and proposed a 3-tier classification system for AKN. Tier 1 focused on the distribution and sagittal spread of AKN lesions between the clinical demarcation lines of the occipital notch and posterior hairline. Tier 2 focused on the type of lesions present—discrete papules or nodules, coalescing/abutting lesions, plaques (raised, atrophic, or indurated), or dome-shaped tumoral masses. Tier 3 focused on the presence or absence of co-existing dissecting cellulitis or folliculitis decalvans.⁶

Epidemiology

Acne keloidalis nuchae primarily manifests in adolescent and adult men of African or Afro-Caribbean descent.⁷ Among African American men, the prevalence of AKN ranges from 0.5% to 13.6%.⁸ Similar ranges have been reported among Nigerian, South African, and West African men.¹ Acne keloidalis nuchae also affects Asian and Hispanic men but rarely is seen in non-Hispanic White men or in women of any ethnicity.^9,10 The male to female ratio is 20:1.^1,11 Hair texture, hairstyling practices such as closely shaved or faded haircuts, and genetics likely contribute to development of AKN. Sports and occupations that require the use of headgear or a tight collar may increase the risk for AKN.¹²

Key clinical features in people with darker skin tones

• The lesions of AKN range in color from pink to dark brown or black. Postinflammatory hyperpigmentation or hyperchromia may be present around AKN lesions.
• Chronicity of AKN may lead to extended use of high-potency topical or intralesional corticosteroids, which causes transient or long-lasting hypopigmentation, especially in those with darker skin tones.

Worth noting

• Acne keloidalis nuchae can be disfiguring, which negatively impacts quality of life and self-esteem.¹²
• Some occupations (eg, military, police) have hair policies that may not be favorable to those with or at risk for AKN.
• Patients with AKN are 2 to 3 times more likely to present with metabolic syndrome, hypertension, type 2 diabetes mellitus, or obesity.¹³

Treatment

There are no treatments approved by the US Food and Drug Administration specifically for AKN. Treatment approaches are based on the pathophysiology, secondary impacts on the skin, and disease severity. Growing out the hair may prevent worsening and/or decrease the risk for new lesions.⁶

• Options include but are not limited to topical and systemic therapies (eg, topical corticosteroids, oral or topical antibiotics, isotretinoin, topical retinoids, imiquimod, pimecrolimus), light devices (eg, phototherapy, laser), ablative therapies (eg, laser, cryotherapy, radiotherapy), and surgery (eg, excision, follicular unit excision), often in combination.^6,14,15
• Intralesional triamcinolone injections are considered standard of care. Adotama et al¹⁶ found that injecting ­triamcinolone into the deep dermis in the area of flat or papular AKN yielded better control of inflammation and decreased appearance of lesions compared with injecting individual lesions.
• For extensive AKN lesions that do not respond to ­less-invasive therapies, consider surgical techniques,^6,17 such as follicular unit excision¹⁸ and more extensive surgical excisions building on approaches from pioneers Drs. John Kenney and Harold Pierce.¹⁹ An innovative surgical approach for removal of large AKNs is the bat excision technique—wound shape resembles a bat in a spread-eagled position—with secondary intention healing with or without debridement and/or tension sutures. The resulting linear scar acts as a new posterior hair line.²⁰

Health disparity highlights

Access to a dermatologic or plastic surgeon with expertise in the surgical treatment of large AKNs may be challenging but is needed to reduce risk for recurrence and adverse events.

Close-cropped haircuts on the occipital scalp, which are particularly popular among men of African descent, increase the risk for AKN.⁵ Although this grooming style may be a personal preference, other hairstyles commonly worn by those with tightly coiled hair may be deemed “unprofessional” in society or the workplace,²¹ which leads to hairstyling practices that may increase the risk for AKN.

Acne keloidalis nuchae remains an understudied entity that adversely affects patients with skin of color.

The Comparison

A A 25-year-old man of Hispanic ethnicity with pink papules, pustules, and large keloidal tumors on the occipital scalp characteristic of acne keloidalis nuchae (AKN). There is hair loss and some tufting of remaining hairs.

B A 17-year-old adolescent boy of African descent with small papules on the occipital scalp and some hair loss from AKN.

C A 19-year-old man of African descent with extensive papules and keloidal tumors on the occipital scalp as well as scarring hair loss and tufting of hairs from AKN.

Acne keloidalis nuchae (AKN) is a chronic inflammatory condition commonly affecting the occipital scalp and posterior neck. It causes discrete or extensive fibrosing papules that may coalesce to form pronounced ­tumorlike masses^1,2 with scarring alopecia (Figure, A–C).³ Pustules, hair tufts, secondary bacterial infections, abscesses, and sinus tracts also may occur.¹ The pathogenesis of AKN has been characterized as varying stages of follicular inflammation at the infundibular and isthmus levels followed by fibrotic occlusion of the ­follicular lumen.⁴ Pruritus, pain, bleeding, oozing, and a feeling of scalp tightness may occur.^1,5

Umar et al⁶ performed a retrospective review of 108 men with AKN—58% of African descent, 37% Hispanic, 3% Asian, and 2% Middle Eastern—and proposed a 3-tier classification system for AKN. Tier 1 focused on the distribution and sagittal spread of AKN lesions between the clinical demarcation lines of the occipital notch and posterior hairline. Tier 2 focused on the type of lesions present—discrete papules or nodules, coalescing/abutting lesions, plaques (raised, atrophic, or indurated), or dome-shaped tumoral masses. Tier 3 focused on the presence or absence of co-existing dissecting cellulitis or folliculitis decalvans.⁶

Epidemiology

Acne keloidalis nuchae primarily manifests in adolescent and adult men of African or Afro-Caribbean descent.⁷ Among African American men, the prevalence of AKN ranges from 0.5% to 13.6%.⁸ Similar ranges have been reported among Nigerian, South African, and West African men.¹ Acne keloidalis nuchae also affects Asian and Hispanic men but rarely is seen in non-Hispanic White men or in women of any ethnicity.^9,10 The male to female ratio is 20:1.^1,11 Hair texture, hairstyling practices such as closely shaved or faded haircuts, and genetics likely contribute to development of AKN. Sports and occupations that require the use of headgear or a tight collar may increase the risk for AKN.¹²

Key clinical features in people with darker skin tones

• The lesions of AKN range in color from pink to dark brown or black. Postinflammatory hyperpigmentation or hyperchromia may be present around AKN lesions.
• Chronicity of AKN may lead to extended use of high-potency topical or intralesional corticosteroids, which causes transient or long-lasting hypopigmentation, especially in those with darker skin tones.

Worth noting

• Acne keloidalis nuchae can be disfiguring, which negatively impacts quality of life and self-esteem.¹²
• Some occupations (eg, military, police) have hair policies that may not be favorable to those with or at risk for AKN.
• Patients with AKN are 2 to 3 times more likely to present with metabolic syndrome, hypertension, type 2 diabetes mellitus, or obesity.¹³

Treatment

There are no treatments approved by the US Food and Drug Administration specifically for AKN. Treatment approaches are based on the pathophysiology, secondary impacts on the skin, and disease severity. Growing out the hair may prevent worsening and/or decrease the risk for new lesions.⁶

• Options include but are not limited to topical and systemic therapies (eg, topical corticosteroids, oral or topical antibiotics, isotretinoin, topical retinoids, imiquimod, pimecrolimus), light devices (eg, phototherapy, laser), ablative therapies (eg, laser, cryotherapy, radiotherapy), and surgery (eg, excision, follicular unit excision), often in combination.^6,14,15
• Intralesional triamcinolone injections are considered standard of care. Adotama et al¹⁶ found that injecting ­triamcinolone into the deep dermis in the area of flat or papular AKN yielded better control of inflammation and decreased appearance of lesions compared with injecting individual lesions.
• For extensive AKN lesions that do not respond to ­less-invasive therapies, consider surgical techniques,^6,17 such as follicular unit excision¹⁸ and more extensive surgical excisions building on approaches from pioneers Drs. John Kenney and Harold Pierce.¹⁹ An innovative surgical approach for removal of large AKNs is the bat excision technique—wound shape resembles a bat in a spread-eagled position—with secondary intention healing with or without debridement and/or tension sutures. The resulting linear scar acts as a new posterior hair line.²⁰

Health disparity highlights

Access to a dermatologic or plastic surgeon with expertise in the surgical treatment of large AKNs may be challenging but is needed to reduce risk for recurrence and adverse events.

Close-cropped haircuts on the occipital scalp, which are particularly popular among men of African descent, increase the risk for AKN.⁵ Although this grooming style may be a personal preference, other hairstyles commonly worn by those with tightly coiled hair may be deemed “unprofessional” in society or the workplace,²¹ which leads to hairstyling practices that may increase the risk for AKN.

Acne keloidalis nuchae remains an understudied entity that adversely affects patients with skin of color.

Traction alopecia (TA) is a common type of alopecia that ultimately can result in permanent hair loss. It often is caused or worsened by repetitive and prolonged hairstyling practices such as tight ponytails, braids, or locs, or use of wigs or weaves.¹ Use of headwear, as in certain religious or ethnic groups, also can be contributory.² Individuals participating in or training for occupations involving military service or ballet are at risk for TA due to hairstyling-specific policies. Early stages of TA are reversible with proper treatment and avoidance of exacerbating factors, emphasizing the importance of prompt recognition.³

Epidemiology

Data on the true prevalence of TA are lacking. It can occur in individuals of any race or any hair type. However, it is most common in women of African descent, affecting approximately one-third of this population.⁴ Other commonly affected groups include ballerinas and active-duty service members due to tight ponytails and buns, as well as the Sikh population due to the use of turbans as a part of their religious practice.^2,5,6

Traction alopecia also impacts children, particularly those of African descent. A 2007 study of schoolchildren in South Africa determined that more than 17% of young African girls had evidence of TA—even some as young as 6 years of age.⁷

Traction alopecia can be caused or exacerbated by the use of hair clips and bobby pins that aid holding styles in place.⁸ Hair shaft morphology may contribute to the risk for TA, with more tightly coiled hair types being more susceptible.⁸ Variables such as use of chemical relaxers also increase the risk for disease, especially when combined with high-tension styling methods such as braids.⁹

Key clinical features

Patients with TA clinically present with hair loss and breakage in areas with tension, most commonly the marginal areas of the scalp as well as the frontal hairline and temporal scalp. Hair loss can result in a “fringe sign,” in which a patient may have preservation of a thin line of hairs at the frontal aspect of the hairline with a band of hair loss behind.¹⁰ This presentation may be used to differentiate TA from other forms of alopecia, including frontal fibrosing alopecia and female pattern hair loss. When the hair loss is not marginal, it may mimic other forms of patchy hair loss including alopecia areata and trichotillomania. Other clinical findings in TA may include broken hairs, pustules, and follicular papules.¹⁰ Patients also may describe symptoms such as scalp tenderness with specific hairstyles or headaches,¹¹ or they may be completely asymptomatic.

Trichoscopy can be helpful in guiding diagnosis and treatment. Patients with TA often have perifollicular erythema and hair casts (cylindrical structures that encircle the proximal hair shafts) in the earlier stages of the disease, with eventual loss of follicular ostia in the later stages.^10,12 Hair casts also may indicate ongoing traction.¹² The flambeau sign—white tracks seen on trichoscopy in the direction the hair is pulled—resembles a lit torch.¹³

Early-stage TA can be reversed by avoiding hair tension. However, patients may not be amenable to this due to personal hairstyling preferences, job duties, or religious practices. Treatment with topical or intralesional steroids or even oral antibiotics such as doxycycline for its anti-inflammatory ability may result in regrowth of lost hair if the follicles are not permanently lost and exacerbating factors are avoided.^3,14 Both topical and oral minoxidil have been used with success, with minoxidil thought to increase hair density by extending the anagen (growth) phase of hair follicles.^3,15 Culturally sensitive patient counseling on the condition and potential exacerbating factors is critical.¹⁶

At later stages of the disease—after loss of follicular ostia has occurred—surgical interventions should be considered,¹⁷ such as hair transplantation, which can be successful but remains a technical challenge due to variability in hair shaft curvature.¹⁸ Additionally, the cost of the procedure can limit use, and some patients may not be optimal candidates due to the extent of their hair loss. Traction alopecia may not be the only hair loss condition present. Examining the scalp is important even if the chief area of concern is the marginal scalp.

Health disparity highlight

Prevention, early identification, and treatment initiated in a timely fashion are crucial to prevent permanent hair loss. There are added societal and cultural pressures that impact hairstyle and hair care practices, especially for those with tightly coiled hair.¹⁹ Historically, tightly coiled hair has been unfairly viewed as “unprofessional,” “unkempt,” and a challenge to “manage” by some. Thus, heat, chemical relaxers, and tight hairstyles holding hair in one position have been used to straighten the hair permanently or temporarily or to keep it maintained in a style that did not necessitate excessive manipulation—often contributing to further tension on the hair.

Military service branches have evaluated and changed some hair-related policies to reflect the diverse hair types of military personnel.²⁰ The CROWN Act (www.thecrownact.com/about)—“Creating a Respectful and Open World for Natural Hair”—is a model law passed by 26 states that prohibits race-based hair discrimination, which is the denial of employment and educational opportunities because of hair texture. Although the law has not been passed in every state, it may help individuals with tightly coiled hair to embrace natural hairstyles. However, even hairstyles with one’s own natural curl pattern can contribute to tension and thus potential development of TA.

Traction alopecia (TA) is a common type of alopecia that ultimately can result in permanent hair loss. It often is caused or worsened by repetitive and prolonged hairstyling practices such as tight ponytails, braids, or locs, or use of wigs or weaves.¹ Use of headwear, as in certain religious or ethnic groups, also can be contributory.² Individuals participating in or training for occupations involving military service or ballet are at risk for TA due to hairstyling-specific policies. Early stages of TA are reversible with proper treatment and avoidance of exacerbating factors, emphasizing the importance of prompt recognition.³

Epidemiology

Data on the true prevalence of TA are lacking. It can occur in individuals of any race or any hair type. However, it is most common in women of African descent, affecting approximately one-third of this population.⁴ Other commonly affected groups include ballerinas and active-duty service members due to tight ponytails and buns, as well as the Sikh population due to the use of turbans as a part of their religious practice.^2,5,6

Traction alopecia also impacts children, particularly those of African descent. A 2007 study of schoolchildren in South Africa determined that more than 17% of young African girls had evidence of TA—even some as young as 6 years of age.⁷

Traction alopecia can be caused or exacerbated by the use of hair clips and bobby pins that aid holding styles in place.⁸ Hair shaft morphology may contribute to the risk for TA, with more tightly coiled hair types being more susceptible.⁸ Variables such as use of chemical relaxers also increase the risk for disease, especially when combined with high-tension styling methods such as braids.⁹

Key clinical features

Patients with TA clinically present with hair loss and breakage in areas with tension, most commonly the marginal areas of the scalp as well as the frontal hairline and temporal scalp. Hair loss can result in a “fringe sign,” in which a patient may have preservation of a thin line of hairs at the frontal aspect of the hairline with a band of hair loss behind.¹⁰ This presentation may be used to differentiate TA from other forms of alopecia, including frontal fibrosing alopecia and female pattern hair loss. When the hair loss is not marginal, it may mimic other forms of patchy hair loss including alopecia areata and trichotillomania. Other clinical findings in TA may include broken hairs, pustules, and follicular papules.¹⁰ Patients also may describe symptoms such as scalp tenderness with specific hairstyles or headaches,¹¹ or they may be completely asymptomatic.

Trichoscopy can be helpful in guiding diagnosis and treatment. Patients with TA often have perifollicular erythema and hair casts (cylindrical structures that encircle the proximal hair shafts) in the earlier stages of the disease, with eventual loss of follicular ostia in the later stages.^10,12 Hair casts also may indicate ongoing traction.¹² The flambeau sign—white tracks seen on trichoscopy in the direction the hair is pulled—resembles a lit torch.¹³

Early-stage TA can be reversed by avoiding hair tension. However, patients may not be amenable to this due to personal hairstyling preferences, job duties, or religious practices. Treatment with topical or intralesional steroids or even oral antibiotics such as doxycycline for its anti-inflammatory ability may result in regrowth of lost hair if the follicles are not permanently lost and exacerbating factors are avoided.^3,14 Both topical and oral minoxidil have been used with success, with minoxidil thought to increase hair density by extending the anagen (growth) phase of hair follicles.^3,15 Culturally sensitive patient counseling on the condition and potential exacerbating factors is critical.¹⁶

At later stages of the disease—after loss of follicular ostia has occurred—surgical interventions should be considered,¹⁷ such as hair transplantation, which can be successful but remains a technical challenge due to variability in hair shaft curvature.¹⁸ Additionally, the cost of the procedure can limit use, and some patients may not be optimal candidates due to the extent of their hair loss. Traction alopecia may not be the only hair loss condition present. Examining the scalp is important even if the chief area of concern is the marginal scalp.

Health disparity highlight

Prevention, early identification, and treatment initiated in a timely fashion are crucial to prevent permanent hair loss. There are added societal and cultural pressures that impact hairstyle and hair care practices, especially for those with tightly coiled hair.¹⁹ Historically, tightly coiled hair has been unfairly viewed as “unprofessional,” “unkempt,” and a challenge to “manage” by some. Thus, heat, chemical relaxers, and tight hairstyles holding hair in one position have been used to straighten the hair permanently or temporarily or to keep it maintained in a style that did not necessitate excessive manipulation—often contributing to further tension on the hair.

Military service branches have evaluated and changed some hair-related policies to reflect the diverse hair types of military personnel.²⁰ The CROWN Act (www.thecrownact.com/about)—“Creating a Respectful and Open World for Natural Hair”—is a model law passed by 26 states that prohibits race-based hair discrimination, which is the denial of employment and educational opportunities because of hair texture. Although the law has not been passed in every state, it may help individuals with tightly coiled hair to embrace natural hairstyles. However, even hairstyles with one’s own natural curl pattern can contribute to tension and thus potential development of TA.

Traction alopecia (TA) is a common type of alopecia that ultimately can result in permanent hair loss. It often is caused or worsened by repetitive and prolonged hairstyling practices such as tight ponytails, braids, or locs, or use of wigs or weaves.¹ Use of headwear, as in certain religious or ethnic groups, also can be contributory.² Individuals participating in or training for occupations involving military service or ballet are at risk for TA due to hairstyling-specific policies. Early stages of TA are reversible with proper treatment and avoidance of exacerbating factors, emphasizing the importance of prompt recognition.³

Epidemiology

Data on the true prevalence of TA are lacking. It can occur in individuals of any race or any hair type. However, it is most common in women of African descent, affecting approximately one-third of this population.⁴ Other commonly affected groups include ballerinas and active-duty service members due to tight ponytails and buns, as well as the Sikh population due to the use of turbans as a part of their religious practice.^2,5,6

Traction alopecia also impacts children, particularly those of African descent. A 2007 study of schoolchildren in South Africa determined that more than 17% of young African girls had evidence of TA—even some as young as 6 years of age.⁷

Traction alopecia can be caused or exacerbated by the use of hair clips and bobby pins that aid holding styles in place.⁸ Hair shaft morphology may contribute to the risk for TA, with more tightly coiled hair types being more susceptible.⁸ Variables such as use of chemical relaxers also increase the risk for disease, especially when combined with high-tension styling methods such as braids.⁹

Key clinical features

Patients with TA clinically present with hair loss and breakage in areas with tension, most commonly the marginal areas of the scalp as well as the frontal hairline and temporal scalp. Hair loss can result in a “fringe sign,” in which a patient may have preservation of a thin line of hairs at the frontal aspect of the hairline with a band of hair loss behind.¹⁰ This presentation may be used to differentiate TA from other forms of alopecia, including frontal fibrosing alopecia and female pattern hair loss. When the hair loss is not marginal, it may mimic other forms of patchy hair loss including alopecia areata and trichotillomania. Other clinical findings in TA may include broken hairs, pustules, and follicular papules.¹⁰ Patients also may describe symptoms such as scalp tenderness with specific hairstyles or headaches,¹¹ or they may be completely asymptomatic.

Trichoscopy can be helpful in guiding diagnosis and treatment. Patients with TA often have perifollicular erythema and hair casts (cylindrical structures that encircle the proximal hair shafts) in the earlier stages of the disease, with eventual loss of follicular ostia in the later stages.^10,12 Hair casts also may indicate ongoing traction.¹² The flambeau sign—white tracks seen on trichoscopy in the direction the hair is pulled—resembles a lit torch.¹³

Early-stage TA can be reversed by avoiding hair tension. However, patients may not be amenable to this due to personal hairstyling preferences, job duties, or religious practices. Treatment with topical or intralesional steroids or even oral antibiotics such as doxycycline for its anti-inflammatory ability may result in regrowth of lost hair if the follicles are not permanently lost and exacerbating factors are avoided.^3,14 Both topical and oral minoxidil have been used with success, with minoxidil thought to increase hair density by extending the anagen (growth) phase of hair follicles.^3,15 Culturally sensitive patient counseling on the condition and potential exacerbating factors is critical.¹⁶

At later stages of the disease—after loss of follicular ostia has occurred—surgical interventions should be considered,¹⁷ such as hair transplantation, which can be successful but remains a technical challenge due to variability in hair shaft curvature.¹⁸ Additionally, the cost of the procedure can limit use, and some patients may not be optimal candidates due to the extent of their hair loss. Traction alopecia may not be the only hair loss condition present. Examining the scalp is important even if the chief area of concern is the marginal scalp.

Health disparity highlight

Prevention, early identification, and treatment initiated in a timely fashion are crucial to prevent permanent hair loss. There are added societal and cultural pressures that impact hairstyle and hair care practices, especially for those with tightly coiled hair.¹⁹ Historically, tightly coiled hair has been unfairly viewed as “unprofessional,” “unkempt,” and a challenge to “manage” by some. Thus, heat, chemical relaxers, and tight hairstyles holding hair in one position have been used to straighten the hair permanently or temporarily or to keep it maintained in a style that did not necessitate excessive manipulation—often contributing to further tension on the hair.

Military service branches have evaluated and changed some hair-related policies to reflect the diverse hair types of military personnel.²⁰ The CROWN Act (www.thecrownact.com/about)—“Creating a Respectful and Open World for Natural Hair”—is a model law passed by 26 states that prohibits race-based hair discrimination, which is the denial of employment and educational opportunities because of hair texture. Although the law has not been passed in every state, it may help individuals with tightly coiled hair to embrace natural hairstyles. However, even hairstyles with one’s own natural curl pattern can contribute to tension and thus potential development of TA.

The Comparison

A Traction alopecia in a Hispanic woman who wears her hair in a tight bun.

B Traction alopecia in a Black adolescent girl who wears her hair in tight hairstyles.

Traction alopecia (TA) is a common type of alopecia that ultimately can result in permanent hair loss. It often is caused or worsened by repetitive and prolonged hairstyling practices such as tight ponytails, braids, or locs, or use of wigs or weaves.¹ Use of headwear, as in certain religious or ethnic groups, also can be contributory.² Individuals participating in or training for occupations involving military service or ballet are at risk for TA due to hairstyling-specific policies. Early stages of TA are reversible with proper treatment and avoidance of exacerbating factors, emphasizing the importance of prompt recognition.³

Epidemiology

Data on the true prevalence of TA are lacking. It can occur in individuals of any race or any hair type. However, it is most common in women of African descent, affecting approximately one-third of this population.⁴ Other commonly affected groups include ballerinas and active-duty service members due to tight ponytails and buns, as well as the Sikh population due to the use of turbans as a part of their religious practice.^2,5,6

Traction alopecia also impacts children, particularly those of African descent. A 2007 study of schoolchildren in South Africa determined that more than 17% of young African girls had evidence of TA—even some as young as 6 years of age.⁷

Traction alopecia can be caused or exacerbated by the use of hair clips and bobby pins that aid holding styles in place.⁸

Hair shaft morphology may contribute to the risk for TA, with more tightly coiled hair types being more susceptible.⁸ Variables such as use of chemical relaxers also increase the risk for disease, especially when combined with high-tension styling methods such as braids.⁹

Key clinical features

Patients with TA clinically present with hair loss and breakage in areas with tension, most commonly the marginal areas of the scalp as well as the frontal hairline and temporal scalp. Hair loss can result in a “fringe sign,” in which a patient may have preservation of a thin line of hairs at the frontal aspect of the hairline with a band of hair loss behind.¹⁰ This presentation may be used to differentiate TA from other forms of alopecia, including frontal fibrosing alopecia and female pattern hair loss. When the hair loss is not marginal, it may mimic other forms of patchy hair loss including alopecia areata and trichotillomania. Other clinical findings in TA may include broken hairs, pustules, and follicular papules.¹⁰ Patients also may describe symptoms such as scalp tenderness with specific hairstyles or headaches,¹¹ or they may be completely asymptomatic.

Trichoscopy can be helpful in guiding diagnosis and treatment. Patients with TA often have perifollicular erythema and hair casts (cylindrical structures that encircle the proximal hair shafts) in the earlier stages of the disease, with eventual loss of follicular ostia in the later stages.^10,12 Hair casts also may indicate ongoing traction.¹² The flambeau sign—white tracks seen on trichoscopy in the direction the hair is pulled—resembles a lit torch.¹³

Worth noting

Early-stage TA can be reversed by avoiding hair tension. However, patients may not be amenable to this due to personal hairstyling preferences, job duties, or religious practices. Treatment with topical or intralesional steroids or even oral antibiotics such as doxycycline for its anti-inflammatory ability may result in regrowth of lost hair if the follicles are not permanently lost and exacerbating factors are avoided.^3,14 Both topical and oral minoxidil have been used with success, with minoxidil thought to increase hair density by extending the anagen (growth) phase of hair follicles.^3,15 Culturally sensitive patient counseling on the condition and potential exacerbating factors is critical.¹⁶

At later stages of the disease—after loss of follicular ostia has occurred—surgical interventions should be considered,¹⁷ such as hair transplantation, which can be successful but remains a technical challenge due to variability in hair shaft curvature.¹⁸ Additionally, the cost of the procedure can limit use, and some patients may not be optimal candidates due to the extent of their hair loss. Traction alopecia may not be the only hair loss condition present. Examining the scalp is important even if the chief area of concern is the marginal scalp.

Health disparity highlight

Prevention, early identification, and treatment initiated in a timely fashion are crucial to prevent permanent hair loss. There are added societal and cultural pressures that impact hairstyle and hair care practices, especially for those with tightly coiled hair.¹⁹ Historically, tightly coiled hair has been unfairly viewed as “unprofessional,” “unkempt,” and a challenge to “manage” by some. Thus, heat, chemical relaxers, and tight hairstyles holding hair in one position have been used to straighten the hair permanently or temporarily or to keep it maintained in a style that did not necessitate excessive manipulation—often contributing to further tension on the hair.

Military service branches have evaluated and changed some hair-related policies to reflect the diverse hair types of military personnel.²⁰ The CROWN Act (www.thecrownact.com/about)—“Creating a Respectful and Open World for Natural Hair”—is a model law passed by 26 states that prohibits race-based hair discrimination, which is the denial of employment and educational opportunities because of hair texture. Although the law has not been passed in every state, it may help individuals with tightly coiled hair to embrace natural hairstyles. However, even hairstyles with one’s own natural curl pattern can contribute to tension and thus potential development of TA.

The Comparison

A Traction alopecia in a Hispanic woman who wears her hair in a tight bun.

B Traction alopecia in a Black adolescent girl who wears her hair in tight hairstyles.

Traction alopecia (TA) is a common type of alopecia that ultimately can result in permanent hair loss. It often is caused or worsened by repetitive and prolonged hairstyling practices such as tight ponytails, braids, or locs, or use of wigs or weaves.¹ Use of headwear, as in certain religious or ethnic groups, also can be contributory.² Individuals participating in or training for occupations involving military service or ballet are at risk for TA due to hairstyling-specific policies. Early stages of TA are reversible with proper treatment and avoidance of exacerbating factors, emphasizing the importance of prompt recognition.³

Epidemiology

Data on the true prevalence of TA are lacking. It can occur in individuals of any race or any hair type. However, it is most common in women of African descent, affecting approximately one-third of this population.⁴ Other commonly affected groups include ballerinas and active-duty service members due to tight ponytails and buns, as well as the Sikh population due to the use of turbans as a part of their religious practice.^2,5,6

Traction alopecia also impacts children, particularly those of African descent. A 2007 study of schoolchildren in South Africa determined that more than 17% of young African girls had evidence of TA—even some as young as 6 years of age.⁷

Traction alopecia can be caused or exacerbated by the use of hair clips and bobby pins that aid holding styles in place.⁸

Hair shaft morphology may contribute to the risk for TA, with more tightly coiled hair types being more susceptible.⁸ Variables such as use of chemical relaxers also increase the risk for disease, especially when combined with high-tension styling methods such as braids.⁹

Key clinical features

Patients with TA clinically present with hair loss and breakage in areas with tension, most commonly the marginal areas of the scalp as well as the frontal hairline and temporal scalp. Hair loss can result in a “fringe sign,” in which a patient may have preservation of a thin line of hairs at the frontal aspect of the hairline with a band of hair loss behind.¹⁰ This presentation may be used to differentiate TA from other forms of alopecia, including frontal fibrosing alopecia and female pattern hair loss. When the hair loss is not marginal, it may mimic other forms of patchy hair loss including alopecia areata and trichotillomania. Other clinical findings in TA may include broken hairs, pustules, and follicular papules.¹⁰ Patients also may describe symptoms such as scalp tenderness with specific hairstyles or headaches,¹¹ or they may be completely asymptomatic.

Trichoscopy can be helpful in guiding diagnosis and treatment. Patients with TA often have perifollicular erythema and hair casts (cylindrical structures that encircle the proximal hair shafts) in the earlier stages of the disease, with eventual loss of follicular ostia in the later stages.^10,12 Hair casts also may indicate ongoing traction.¹² The flambeau sign—white tracks seen on trichoscopy in the direction the hair is pulled—resembles a lit torch.¹³

Worth noting

Early-stage TA can be reversed by avoiding hair tension. However, patients may not be amenable to this due to personal hairstyling preferences, job duties, or religious practices. Treatment with topical or intralesional steroids or even oral antibiotics such as doxycycline for its anti-inflammatory ability may result in regrowth of lost hair if the follicles are not permanently lost and exacerbating factors are avoided.^3,14 Both topical and oral minoxidil have been used with success, with minoxidil thought to increase hair density by extending the anagen (growth) phase of hair follicles.^3,15 Culturally sensitive patient counseling on the condition and potential exacerbating factors is critical.¹⁶

At later stages of the disease—after loss of follicular ostia has occurred—surgical interventions should be considered,¹⁷ such as hair transplantation, which can be successful but remains a technical challenge due to variability in hair shaft curvature.¹⁸ Additionally, the cost of the procedure can limit use, and some patients may not be optimal candidates due to the extent of their hair loss. Traction alopecia may not be the only hair loss condition present. Examining the scalp is important even if the chief area of concern is the marginal scalp.

Health disparity highlight

Prevention, early identification, and treatment initiated in a timely fashion are crucial to prevent permanent hair loss. There are added societal and cultural pressures that impact hairstyle and hair care practices, especially for those with tightly coiled hair.¹⁹ Historically, tightly coiled hair has been unfairly viewed as “unprofessional,” “unkempt,” and a challenge to “manage” by some. Thus, heat, chemical relaxers, and tight hairstyles holding hair in one position have been used to straighten the hair permanently or temporarily or to keep it maintained in a style that did not necessitate excessive manipulation—often contributing to further tension on the hair.

Military service branches have evaluated and changed some hair-related policies to reflect the diverse hair types of military personnel.²⁰ The CROWN Act (www.thecrownact.com/about)—“Creating a Respectful and Open World for Natural Hair”—is a model law passed by 26 states that prohibits race-based hair discrimination, which is the denial of employment and educational opportunities because of hair texture. Although the law has not been passed in every state, it may help individuals with tightly coiled hair to embrace natural hairstyles. However, even hairstyles with one’s own natural curl pattern can contribute to tension and thus potential development of TA.

The Comparison

A Traction alopecia in a Hispanic woman who wears her hair in a tight bun.

B Traction alopecia in a Black adolescent girl who wears her hair in tight hairstyles.

Traction alopecia (TA) is a common type of alopecia that ultimately can result in permanent hair loss. It often is caused or worsened by repetitive and prolonged hairstyling practices such as tight ponytails, braids, or locs, or use of wigs or weaves.¹ Use of headwear, as in certain religious or ethnic groups, also can be contributory.² Individuals participating in or training for occupations involving military service or ballet are at risk for TA due to hairstyling-specific policies. Early stages of TA are reversible with proper treatment and avoidance of exacerbating factors, emphasizing the importance of prompt recognition.³

Epidemiology

Data on the true prevalence of TA are lacking. It can occur in individuals of any race or any hair type. However, it is most common in women of African descent, affecting approximately one-third of this population.⁴ Other commonly affected groups include ballerinas and active-duty service members due to tight ponytails and buns, as well as the Sikh population due to the use of turbans as a part of their religious practice.^2,5,6

Traction alopecia also impacts children, particularly those of African descent. A 2007 study of schoolchildren in South Africa determined that more than 17% of young African girls had evidence of TA—even some as young as 6 years of age.⁷

Traction alopecia can be caused or exacerbated by the use of hair clips and bobby pins that aid holding styles in place.⁸

Hair shaft morphology may contribute to the risk for TA, with more tightly coiled hair types being more susceptible.⁸ Variables such as use of chemical relaxers also increase the risk for disease, especially when combined with high-tension styling methods such as braids.⁹

Key clinical features

Patients with TA clinically present with hair loss and breakage in areas with tension, most commonly the marginal areas of the scalp as well as the frontal hairline and temporal scalp. Hair loss can result in a “fringe sign,” in which a patient may have preservation of a thin line of hairs at the frontal aspect of the hairline with a band of hair loss behind.¹⁰ This presentation may be used to differentiate TA from other forms of alopecia, including frontal fibrosing alopecia and female pattern hair loss. When the hair loss is not marginal, it may mimic other forms of patchy hair loss including alopecia areata and trichotillomania. Other clinical findings in TA may include broken hairs, pustules, and follicular papules.¹⁰ Patients also may describe symptoms such as scalp tenderness with specific hairstyles or headaches,¹¹ or they may be completely asymptomatic.

Trichoscopy can be helpful in guiding diagnosis and treatment. Patients with TA often have perifollicular erythema and hair casts (cylindrical structures that encircle the proximal hair shafts) in the earlier stages of the disease, with eventual loss of follicular ostia in the later stages.^10,12 Hair casts also may indicate ongoing traction.¹² The flambeau sign—white tracks seen on trichoscopy in the direction the hair is pulled—resembles a lit torch.¹³

Worth noting

Early-stage TA can be reversed by avoiding hair tension. However, patients may not be amenable to this due to personal hairstyling preferences, job duties, or religious practices. Treatment with topical or intralesional steroids or even oral antibiotics such as doxycycline for its anti-inflammatory ability may result in regrowth of lost hair if the follicles are not permanently lost and exacerbating factors are avoided.^3,14 Both topical and oral minoxidil have been used with success, with minoxidil thought to increase hair density by extending the anagen (growth) phase of hair follicles.^3,15 Culturally sensitive patient counseling on the condition and potential exacerbating factors is critical.¹⁶

At later stages of the disease—after loss of follicular ostia has occurred—surgical interventions should be considered,¹⁷ such as hair transplantation, which can be successful but remains a technical challenge due to variability in hair shaft curvature.¹⁸ Additionally, the cost of the procedure can limit use, and some patients may not be optimal candidates due to the extent of their hair loss. Traction alopecia may not be the only hair loss condition present. Examining the scalp is important even if the chief area of concern is the marginal scalp.

Health disparity highlight

Prevention, early identification, and treatment initiated in a timely fashion are crucial to prevent permanent hair loss. There are added societal and cultural pressures that impact hairstyle and hair care practices, especially for those with tightly coiled hair.¹⁹ Historically, tightly coiled hair has been unfairly viewed as “unprofessional,” “unkempt,” and a challenge to “manage” by some. Thus, heat, chemical relaxers, and tight hairstyles holding hair in one position have been used to straighten the hair permanently or temporarily or to keep it maintained in a style that did not necessitate excessive manipulation—often contributing to further tension on the hair.

Military service branches have evaluated and changed some hair-related policies to reflect the diverse hair types of military personnel.²⁰ The CROWN Act (www.thecrownact.com/about)—“Creating a Respectful and Open World for Natural Hair”—is a model law passed by 26 states that prohibits race-based hair discrimination, which is the denial of employment and educational opportunities because of hair texture. Although the law has not been passed in every state, it may help individuals with tightly coiled hair to embrace natural hairstyles. However, even hairstyles with one’s own natural curl pattern can contribute to tension and thus potential development of TA.

The Comparison

A Plantar hyperpigmentation (benign ethnic melanosis) on the sole of the foot in a 62-year-old man of African descent with deeply pigmented skin. Dermoscopy showed a parallel ridge pattern even though the hyperpigmentation was benign (inset).

B Melanoma in situ with multicomponent hyperpigmentation on the sole of the foot in a 65-year-old Hispanic woman. Dermoscopy revealed a parallel ridge pattern (inset).

Plantar hyperpigmentation (also known as plantar melanosis [increased melanin], volar pigmented macules, benign racial melanosis, acral pigmentation, acral ethnic melanosis, or mottled hyperpigmentation of the plantar surface) is a benign finding in many individuals and is especially prevalent in those with darker skin tones. Acral refers to manifestation on the hands and feet, volar on the palms and soles, and plantar on the soles only. Here, we focus on plantar hyperpigmentation. We use the terms ethnic and racial interchangeably.

It is critically important to differentiate benign hyperpigmentation, which is common in patients with skin of color, from melanoma. Although rare, Black patients in the United States experience high morbidity and mortality from acral melanoma, which often is diagnosed late in the disease course.¹

There are many causes of hyperpigmentation on the plantar surfaces, including benign ethnic melanosis, nevi, melanoma, infections such as syphilis and tinea nigra, conditions such as Peutz-Jeghers syndrome and Laugier-Hunziker syndrome, and postinflammatory hyperpigmentation secondary to atopic dermatitis and psoriasis. We focus on the most common causes, ethnic melanosis and nevi, as well as melanoma, which is the deadliest cause.

Epidemiology

In a 1980 study (N=251), Black Americans had a high incidence of plantar hyperpigmentation, with 52% of affected patients having dark brown skin and 31% having light brown skin.²

The epidemiology of melanoma varies by race/ethnicity. Melanoma in Black individuals is relatively rare, with an annual incidence of approximately 1 in 100,000 individuals.³ However, when individuals with skin of color develop melanoma, they are more likely than their White counterparts to have acral melanoma (acral lentiginous melanoma), one of the deadliest types.¹ In a case series of Black patients with melanoma (N=48) from 2 tertiary care centers in Texas, 30 of 40 primary cutaneous melanomas (75%) were located on acral skin.⁴ Overall, 13 patients developed stage IV disease and 12 died due to disease progression. All patients who developed distant metastases or died of melanoma had acral melanoma.⁴ Individuals of Asian descent also have a high incidence of acral melanoma, as shown in research from Japan.^5-9

Key clinical features in individuals with darker skin tones

Dermoscopy is an evidence-based clinical examination method for earlier diagnosis of cutaneous melanoma, including on acral skin.^10,11 Benign nevi on the volar skin as well as the palms and soles tend to have one of these 3 dermoscopic patterns: parallel furrow, lattice, or irregular fibrillar. The pattern that is most predictive of volar melanoma is the parallel ridge pattern (PRP) (Figures A and B [insets]), which showed a high specificity (99.0%) and very high negative predictive value (97.7%) for malignant melanoma in a Japanese population.⁷ The PRP data from this study cannot be applied reliably to Black individuals, especially because benign ethnic melanosis and other benign conditions can demonstrate PRP.¹² Reliance on the PRP as a diagnostic clue could result in unneccessary biopsies in as many as 50% of Black patients with benign plantar hyperpigmentation.² Furthermore, biopsies of the plantar surface can be painful and cause pain while walking.

It has been suggested that PRP seen on dermoscopy in benign hyperpigmentation such as ethnic melanosis and nevi may preserve the acrosyringia (eccrine gland openings on the ridge), whereas PRP in melanoma may obliterate the acrosyringia.¹³ This observation is based on case reports only and needs further study. However, if validated, it could be a useful diagnostic clue.

Worth noting

In a retrospective cohort study of skin cancer in Black individuals (n=165) at a New York City–based cancer center from 2000 to 2020, 68% of patients were diagnosed with melanomas—80% were the acral subtype and 75% displayed a PRP. However, the surrounding uninvolved background skin, which was visible in most cases, also demonstrated a PRP.¹⁴ Because of the high morbidity and mortality rates of acral melanoma, clinicians should biopsy or immediately refer patients with concerning plantar hyperpigmentation to a dermatologist.

Health disparity highlight

The mortality rate for acral melanoma in Black patients is disproportionately high for the following reasons^15,16:

• Patients and health care providers do not expect to see melanoma in Black patients (it truly is rare!), so screening and education on sun protection are limited.
• Benign ethnic melanosis makes it more difficult to distinguish between early acral melanoma and benign skin changes.
• Black patients and other US patient populations with skin of color may be less likely to have health insurance, which contributes to inequities in access to health care. As of 2022, the uninsured rates for nonelderly American Indian and Alaska Native, Hispanic, Native Hawaiian and Other Pacific Islander, Black, and White individuals were 19.1%, 18.0%, 12.7%, 10.0%, and 6.6%, respectively.¹⁷

Multi-institutional registries could improve understanding of acral melanoma in Black patients.⁴ More studies are needed to help differentiate between the dermoscopic finding of PRP in benign ethnic melanosis vs malignant melanoma.

The Comparison

A Plantar hyperpigmentation (benign ethnic melanosis) on the sole of the foot in a 62-year-old man of African descent with deeply pigmented skin. Dermoscopy showed a parallel ridge pattern even though the hyperpigmentation was benign (inset).

B Melanoma in situ with multicomponent hyperpigmentation on the sole of the foot in a 65-year-old Hispanic woman. Dermoscopy revealed a parallel ridge pattern (inset).

Plantar hyperpigmentation (also known as plantar melanosis [increased melanin], volar pigmented macules, benign racial melanosis, acral pigmentation, acral ethnic melanosis, or mottled hyperpigmentation of the plantar surface) is a benign finding in many individuals and is especially prevalent in those with darker skin tones. Acral refers to manifestation on the hands and feet, volar on the palms and soles, and plantar on the soles only. Here, we focus on plantar hyperpigmentation. We use the terms ethnic and racial interchangeably.

It is critically important to differentiate benign hyperpigmentation, which is common in patients with skin of color, from melanoma. Although rare, Black patients in the United States experience high morbidity and mortality from acral melanoma, which often is diagnosed late in the disease course.¹

There are many causes of hyperpigmentation on the plantar surfaces, including benign ethnic melanosis, nevi, melanoma, infections such as syphilis and tinea nigra, conditions such as Peutz-Jeghers syndrome and Laugier-Hunziker syndrome, and postinflammatory hyperpigmentation secondary to atopic dermatitis and psoriasis. We focus on the most common causes, ethnic melanosis and nevi, as well as melanoma, which is the deadliest cause.

Epidemiology

In a 1980 study (N=251), Black Americans had a high incidence of plantar hyperpigmentation, with 52% of affected patients having dark brown skin and 31% having light brown skin.²

The epidemiology of melanoma varies by race/ethnicity. Melanoma in Black individuals is relatively rare, with an annual incidence of approximately 1 in 100,000 individuals.³ However, when individuals with skin of color develop melanoma, they are more likely than their White counterparts to have acral melanoma (acral lentiginous melanoma), one of the deadliest types.¹ In a case series of Black patients with melanoma (N=48) from 2 tertiary care centers in Texas, 30 of 40 primary cutaneous melanomas (75%) were located on acral skin.⁴ Overall, 13 patients developed stage IV disease and 12 died due to disease progression. All patients who developed distant metastases or died of melanoma had acral melanoma.⁴ Individuals of Asian descent also have a high incidence of acral melanoma, as shown in research from Japan.^5-9

Key clinical features in individuals with darker skin tones

Dermoscopy is an evidence-based clinical examination method for earlier diagnosis of cutaneous melanoma, including on acral skin.^10,11 Benign nevi on the volar skin as well as the palms and soles tend to have one of these 3 dermoscopic patterns: parallel furrow, lattice, or irregular fibrillar. The pattern that is most predictive of volar melanoma is the parallel ridge pattern (PRP) (Figures A and B [insets]), which showed a high specificity (99.0%) and very high negative predictive value (97.7%) for malignant melanoma in a Japanese population.⁷ The PRP data from this study cannot be applied reliably to Black individuals, especially because benign ethnic melanosis and other benign conditions can demonstrate PRP.¹² Reliance on the PRP as a diagnostic clue could result in unneccessary biopsies in as many as 50% of Black patients with benign plantar hyperpigmentation.² Furthermore, biopsies of the plantar surface can be painful and cause pain while walking.

It has been suggested that PRP seen on dermoscopy in benign hyperpigmentation such as ethnic melanosis and nevi may preserve the acrosyringia (eccrine gland openings on the ridge), whereas PRP in melanoma may obliterate the acrosyringia.¹³ This observation is based on case reports only and needs further study. However, if validated, it could be a useful diagnostic clue.

Worth noting

In a retrospective cohort study of skin cancer in Black individuals (n=165) at a New York City–based cancer center from 2000 to 2020, 68% of patients were diagnosed with melanomas—80% were the acral subtype and 75% displayed a PRP. However, the surrounding uninvolved background skin, which was visible in most cases, also demonstrated a PRP.¹⁴ Because of the high morbidity and mortality rates of acral melanoma, clinicians should biopsy or immediately refer patients with concerning plantar hyperpigmentation to a dermatologist.

Health disparity highlight

The mortality rate for acral melanoma in Black patients is disproportionately high for the following reasons^15,16:

• Patients and health care providers do not expect to see melanoma in Black patients (it truly is rare!), so screening and education on sun protection are limited.
• Benign ethnic melanosis makes it more difficult to distinguish between early acral melanoma and benign skin changes.
• Black patients and other US patient populations with skin of color may be less likely to have health insurance, which contributes to inequities in access to health care. As of 2022, the uninsured rates for nonelderly American Indian and Alaska Native, Hispanic, Native Hawaiian and Other Pacific Islander, Black, and White individuals were 19.1%, 18.0%, 12.7%, 10.0%, and 6.6%, respectively.¹⁷

Multi-institutional registries could improve understanding of acral melanoma in Black patients.⁴ More studies are needed to help differentiate between the dermoscopic finding of PRP in benign ethnic melanosis vs malignant melanoma.

The Comparison

A Plantar hyperpigmentation (benign ethnic melanosis) on the sole of the foot in a 62-year-old man of African descent with deeply pigmented skin. Dermoscopy showed a parallel ridge pattern even though the hyperpigmentation was benign (inset).

B Melanoma in situ with multicomponent hyperpigmentation on the sole of the foot in a 65-year-old Hispanic woman. Dermoscopy revealed a parallel ridge pattern (inset).

Plantar hyperpigmentation (also known as plantar melanosis [increased melanin], volar pigmented macules, benign racial melanosis, acral pigmentation, acral ethnic melanosis, or mottled hyperpigmentation of the plantar surface) is a benign finding in many individuals and is especially prevalent in those with darker skin tones. Acral refers to manifestation on the hands and feet, volar on the palms and soles, and plantar on the soles only. Here, we focus on plantar hyperpigmentation. We use the terms ethnic and racial interchangeably.

It is critically important to differentiate benign hyperpigmentation, which is common in patients with skin of color, from melanoma. Although rare, Black patients in the United States experience high morbidity and mortality from acral melanoma, which often is diagnosed late in the disease course.¹

There are many causes of hyperpigmentation on the plantar surfaces, including benign ethnic melanosis, nevi, melanoma, infections such as syphilis and tinea nigra, conditions such as Peutz-Jeghers syndrome and Laugier-Hunziker syndrome, and postinflammatory hyperpigmentation secondary to atopic dermatitis and psoriasis. We focus on the most common causes, ethnic melanosis and nevi, as well as melanoma, which is the deadliest cause.

Epidemiology

In a 1980 study (N=251), Black Americans had a high incidence of plantar hyperpigmentation, with 52% of affected patients having dark brown skin and 31% having light brown skin.²

The epidemiology of melanoma varies by race/ethnicity. Melanoma in Black individuals is relatively rare, with an annual incidence of approximately 1 in 100,000 individuals.³ However, when individuals with skin of color develop melanoma, they are more likely than their White counterparts to have acral melanoma (acral lentiginous melanoma), one of the deadliest types.¹ In a case series of Black patients with melanoma (N=48) from 2 tertiary care centers in Texas, 30 of 40 primary cutaneous melanomas (75%) were located on acral skin.⁴ Overall, 13 patients developed stage IV disease and 12 died due to disease progression. All patients who developed distant metastases or died of melanoma had acral melanoma.⁴ Individuals of Asian descent also have a high incidence of acral melanoma, as shown in research from Japan.^5-9

Key clinical features in individuals with darker skin tones

Dermoscopy is an evidence-based clinical examination method for earlier diagnosis of cutaneous melanoma, including on acral skin.^10,11 Benign nevi on the volar skin as well as the palms and soles tend to have one of these 3 dermoscopic patterns: parallel furrow, lattice, or irregular fibrillar. The pattern that is most predictive of volar melanoma is the parallel ridge pattern (PRP) (Figures A and B [insets]), which showed a high specificity (99.0%) and very high negative predictive value (97.7%) for malignant melanoma in a Japanese population.⁷ The PRP data from this study cannot be applied reliably to Black individuals, especially because benign ethnic melanosis and other benign conditions can demonstrate PRP.¹² Reliance on the PRP as a diagnostic clue could result in unneccessary biopsies in as many as 50% of Black patients with benign plantar hyperpigmentation.² Furthermore, biopsies of the plantar surface can be painful and cause pain while walking.

It has been suggested that PRP seen on dermoscopy in benign hyperpigmentation such as ethnic melanosis and nevi may preserve the acrosyringia (eccrine gland openings on the ridge), whereas PRP in melanoma may obliterate the acrosyringia.¹³ This observation is based on case reports only and needs further study. However, if validated, it could be a useful diagnostic clue.

Worth noting

In a retrospective cohort study of skin cancer in Black individuals (n=165) at a New York City–based cancer center from 2000 to 2020, 68% of patients were diagnosed with melanomas—80% were the acral subtype and 75% displayed a PRP. However, the surrounding uninvolved background skin, which was visible in most cases, also demonstrated a PRP.¹⁴ Because of the high morbidity and mortality rates of acral melanoma, clinicians should biopsy or immediately refer patients with concerning plantar hyperpigmentation to a dermatologist.

Health disparity highlight

The mortality rate for acral melanoma in Black patients is disproportionately high for the following reasons^15,16:

• Patients and health care providers do not expect to see melanoma in Black patients (it truly is rare!), so screening and education on sun protection are limited.
• Benign ethnic melanosis makes it more difficult to distinguish between early acral melanoma and benign skin changes.
• Black patients and other US patient populations with skin of color may be less likely to have health insurance, which contributes to inequities in access to health care. As of 2022, the uninsured rates for nonelderly American Indian and Alaska Native, Hispanic, Native Hawaiian and Other Pacific Islander, Black, and White individuals were 19.1%, 18.0%, 12.7%, 10.0%, and 6.6%, respectively.¹⁷

Multi-institutional registries could improve understanding of acral melanoma in Black patients.⁴ More studies are needed to help differentiate between the dermoscopic finding of PRP in benign ethnic melanosis vs malignant melanoma.

To the Editor:

Tinea capitis is a common childhood infection seen worldwide and is more prevalent in children of African descent.¹ Treatment can be effective; however, the diagnosis may be delayed due to variability in presentation, camouflage of scalp scale with ointment, and the diagnostic experience of the provider. A common complication of tinea capitis is the dermatophytid (id) reaction, which commonly manifests as multiple 1- to 2-mm monomorphic papules. We report a case of a papulosquamous variant of an id reaction secondary to tinea capitis.

An 8-year-old African American child presented with annular hyperpigmented patches on the face and trunk of several months’ duration. There was no preceding fever, illness, scalp pruritus, or alopecia according to the patient’s mother. The hyperpigmented patches persisted despite use of hydrocortisone and antifungal creams prescribed by a primary care provider. A fungal culture of a scalp specimen was negative. Physical examination during the initial dermatology visit revealed multiple annular hyperpigmented patches on the trunk and extremities. No plaques were evident; however, the mother reported that when the lesions first developed, they were raised and mildly pruritic. The patient was prescribed triamcinolone ointment 0.1% twice daily as needed for itching, and sun protection was emphasized.

At the follow-up visit weeks later, the patient’s mother reported that the ointment had helped the lesions resolve faster, but new lesions continued to appear. Physical examination at this visit was notable for scattered hyperpigmented patches, annular hyperpigmented plaques, and erythematous plaques on the trunk, arms, and legs, in addition to papulosquamous plaques and hyperpigmented patches on the forehead (Figure 1). Suspicion for tinea capitis was discussed, a repeat scalp fungal culture was performed, and oral terbinafine 250 mg once daily was started empirically. The culture was positive for Trichophyton tonsurans supporting the diagnosis of concomitant tinea capitis. The rash resolved with terbinafine, and annular patches of postinflammatory hyperpigmentation remained.

Dermatophytid reactions are immunologically mediated, disseminated, eczematous eruptions occurring after cutaneous infections or inflammatory skin conditions. Reactions occur days to weeks after exposure to antigens of dermatophytes causing tinea pedis or capitis.²

Common culprits include Microsporum canis and T tonsurans.³ Dermatophytid reactions with tinea capitis exhibit morphologic variability including a symmetric distribution of grouped or diffuse,⁴ pruritic, erythematous or flesh-colored, follicular papules on the trunk, with or without progression to the face, torso, upper extremities, and/or lower extremities.³ Other reported manifestations include erythema multiforme, erythema nodosum,³ or lupuslike lesions, and crops of dyshidrotic vesicles on the hands in the setting of Trichophyton mentagrophytes–induced tinea pedis.⁵

The papulosquamous variant id reaction should be considered in a wider differential that includes psoriasis, nummular eczema, and pityriasis rosea. Unlike psoriasis, the id reaction is not chronic and responds to systemic antifungal therapy. Nummular eczema can be ruled out, though not entirely, by a lack of personal or family history of atopy. The characteristic cleavage lines of pityriasis rosea on the trunk are absent in patients with an id reaction, and there would be no preceding illness or herald patches seen in the id reaction.

Tinea capitis may cause a variety of id manifestations, including the papulosquamous phenotype. This case addresses practice gaps that may lead to delayed diagnosis. It also highlights the importance of recognizing uncommon morphologies, performing repeat cultures of the scalp after a negative fungal culture, and lowering the threshold of suspicion for tinea capitis in the appropriate age group and demographic, specifically pediatric patients of African descent.

To the Editor:

Tinea capitis is a common childhood infection seen worldwide and is more prevalent in children of African descent.¹ Treatment can be effective; however, the diagnosis may be delayed due to variability in presentation, camouflage of scalp scale with ointment, and the diagnostic experience of the provider. A common complication of tinea capitis is the dermatophytid (id) reaction, which commonly manifests as multiple 1- to 2-mm monomorphic papules. We report a case of a papulosquamous variant of an id reaction secondary to tinea capitis.

An 8-year-old African American child presented with annular hyperpigmented patches on the face and trunk of several months’ duration. There was no preceding fever, illness, scalp pruritus, or alopecia according to the patient’s mother. The hyperpigmented patches persisted despite use of hydrocortisone and antifungal creams prescribed by a primary care provider. A fungal culture of a scalp specimen was negative. Physical examination during the initial dermatology visit revealed multiple annular hyperpigmented patches on the trunk and extremities. No plaques were evident; however, the mother reported that when the lesions first developed, they were raised and mildly pruritic. The patient was prescribed triamcinolone ointment 0.1% twice daily as needed for itching, and sun protection was emphasized.

At the follow-up visit weeks later, the patient’s mother reported that the ointment had helped the lesions resolve faster, but new lesions continued to appear. Physical examination at this visit was notable for scattered hyperpigmented patches, annular hyperpigmented plaques, and erythematous plaques on the trunk, arms, and legs, in addition to papulosquamous plaques and hyperpigmented patches on the forehead (Figure 1). Suspicion for tinea capitis was discussed, a repeat scalp fungal culture was performed, and oral terbinafine 250 mg once daily was started empirically. The culture was positive for Trichophyton tonsurans supporting the diagnosis of concomitant tinea capitis. The rash resolved with terbinafine, and annular patches of postinflammatory hyperpigmentation remained.

Dermatophytid reactions are immunologically mediated, disseminated, eczematous eruptions occurring after cutaneous infections or inflammatory skin conditions. Reactions occur days to weeks after exposure to antigens of dermatophytes causing tinea pedis or capitis.²

Common culprits include Microsporum canis and T tonsurans.³ Dermatophytid reactions with tinea capitis exhibit morphologic variability including a symmetric distribution of grouped or diffuse,⁴ pruritic, erythematous or flesh-colored, follicular papules on the trunk, with or without progression to the face, torso, upper extremities, and/or lower extremities.³ Other reported manifestations include erythema multiforme, erythema nodosum,³ or lupuslike lesions, and crops of dyshidrotic vesicles on the hands in the setting of Trichophyton mentagrophytes–induced tinea pedis.⁵

The papulosquamous variant id reaction should be considered in a wider differential that includes psoriasis, nummular eczema, and pityriasis rosea. Unlike psoriasis, the id reaction is not chronic and responds to systemic antifungal therapy. Nummular eczema can be ruled out, though not entirely, by a lack of personal or family history of atopy. The characteristic cleavage lines of pityriasis rosea on the trunk are absent in patients with an id reaction, and there would be no preceding illness or herald patches seen in the id reaction.

Tinea capitis may cause a variety of id manifestations, including the papulosquamous phenotype. This case addresses practice gaps that may lead to delayed diagnosis. It also highlights the importance of recognizing uncommon morphologies, performing repeat cultures of the scalp after a negative fungal culture, and lowering the threshold of suspicion for tinea capitis in the appropriate age group and demographic, specifically pediatric patients of African descent.

To the Editor:

Tinea capitis is a common childhood infection seen worldwide and is more prevalent in children of African descent.¹ Treatment can be effective; however, the diagnosis may be delayed due to variability in presentation, camouflage of scalp scale with ointment, and the diagnostic experience of the provider. A common complication of tinea capitis is the dermatophytid (id) reaction, which commonly manifests as multiple 1- to 2-mm monomorphic papules. We report a case of a papulosquamous variant of an id reaction secondary to tinea capitis.

An 8-year-old African American child presented with annular hyperpigmented patches on the face and trunk of several months’ duration. There was no preceding fever, illness, scalp pruritus, or alopecia according to the patient’s mother. The hyperpigmented patches persisted despite use of hydrocortisone and antifungal creams prescribed by a primary care provider. A fungal culture of a scalp specimen was negative. Physical examination during the initial dermatology visit revealed multiple annular hyperpigmented patches on the trunk and extremities. No plaques were evident; however, the mother reported that when the lesions first developed, they were raised and mildly pruritic. The patient was prescribed triamcinolone ointment 0.1% twice daily as needed for itching, and sun protection was emphasized.

At the follow-up visit weeks later, the patient’s mother reported that the ointment had helped the lesions resolve faster, but new lesions continued to appear. Physical examination at this visit was notable for scattered hyperpigmented patches, annular hyperpigmented plaques, and erythematous plaques on the trunk, arms, and legs, in addition to papulosquamous plaques and hyperpigmented patches on the forehead (Figure 1). Suspicion for tinea capitis was discussed, a repeat scalp fungal culture was performed, and oral terbinafine 250 mg once daily was started empirically. The culture was positive for Trichophyton tonsurans supporting the diagnosis of concomitant tinea capitis. The rash resolved with terbinafine, and annular patches of postinflammatory hyperpigmentation remained.

Dermatophytid reactions are immunologically mediated, disseminated, eczematous eruptions occurring after cutaneous infections or inflammatory skin conditions. Reactions occur days to weeks after exposure to antigens of dermatophytes causing tinea pedis or capitis.²

Common culprits include Microsporum canis and T tonsurans.³ Dermatophytid reactions with tinea capitis exhibit morphologic variability including a symmetric distribution of grouped or diffuse,⁴ pruritic, erythematous or flesh-colored, follicular papules on the trunk, with or without progression to the face, torso, upper extremities, and/or lower extremities.³ Other reported manifestations include erythema multiforme, erythema nodosum,³ or lupuslike lesions, and crops of dyshidrotic vesicles on the hands in the setting of Trichophyton mentagrophytes–induced tinea pedis.⁵

The papulosquamous variant id reaction should be considered in a wider differential that includes psoriasis, nummular eczema, and pityriasis rosea. Unlike psoriasis, the id reaction is not chronic and responds to systemic antifungal therapy. Nummular eczema can be ruled out, though not entirely, by a lack of personal or family history of atopy. The characteristic cleavage lines of pityriasis rosea on the trunk are absent in patients with an id reaction, and there would be no preceding illness or herald patches seen in the id reaction.

Tinea capitis may cause a variety of id manifestations, including the papulosquamous phenotype. This case addresses practice gaps that may lead to delayed diagnosis. It also highlights the importance of recognizing uncommon morphologies, performing repeat cultures of the scalp after a negative fungal culture, and lowering the threshold of suspicion for tinea capitis in the appropriate age group and demographic, specifically pediatric patients of African descent.

Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Melanoma in situ manifesting as longitudinal melanonychia (LM) in a single digit in a Black man. Dermoscopy showed irregular dark bands of brown pigmentation and micro-Hutchinson sign on the cuticle (inset).

B Melanoma manifesting as LM with a prominent Hutchinson sign in a Hispanic man, with variable shades of brown covering more than 50% of the nail width.

C Longitudinal melanonychia of at least 2 nails with a pseudo-Hutchinson sign (pigment on the nail folds in a benign case of LM) in a young Black man demonstrating ethnic/racial melanosis. The longitudinal bands, which were caused by benign melanocytic activation, are more gray than brown and are less than 3 mm wide.

Longitudinal melanonychia (LM) is a pigmented linear band—brown, black, or gray—spanning the length of the nail plate due to the presence of excess melanin, which may be attributed to a benign or malignant process and may warrant further investigation.^1,2 The majority of patients who present with LM are diagnosed with melanocytic activation of the nail matrix due to their inherent darker skin tone or various triggers including trauma, infection, and medications. Longitudinal melanonychia secondary to melanocytic activation often occurs spontaneously in patients with skin of color.³ Less commonly, LM is caused by a nail matrix nevus or lentigo; however, LM may arise secondary to subungual melanoma, a more dangerous cause.

A thorough clinical history including duration, recent changes in LM manifestation, nail trauma, or infection is helpful in evaluating patients with LM; however, a history of nail trauma can be misleading, as nail changes attributed to the trauma may in fact be melanoma. Irregularly spaced vertical lines of pigmentation ranging from brown to black with variations in spacing and width are characteristic of subungual melanoma.⁴ Nail dystrophy, granular hyperpigmentation, and Hutchinson sign (extension of pigmentation to the nail folds) also are worrisome features.⁵ In recent years, dermoscopy has become an important tool in the clinical examination of LM, with the development of criteria based on color and pattern recognition.^5,6 Dermoscopy can be useful in screening potential candidates for biopsy. Although clinical examination and dermoscopy are essential to evaluating LM, the gold-standard diagnostic test when malignancy is suspected is a nail matrix biopsy.^1,2,6,7

Epidemiology

It is not unusual for patients with darker skin tones to develop LM due to melanocytic activation of multiple nails with age. This finding can be seen in approximately 80% of African American individuals, 30% of Japanese individuals, and 50% of Hispanic individuals.² It has even been reported that approximately 100% of Black patients older than 50 years will have evidence of LM.³

In a retrospective analysis, children presenting with LM tend to have a higher prevalence of nail matrix nevi compared to adults (56.1% [60/106] vs 34.3% [23/66]; P=.005).⁸ Involvement of a single digit in children is most likely indicative of a nevus; however, when an adult presents with LM in a single digit, suspicion for subungual melanoma should be raised.^2,3,9

Two separate single-center retrospective studies showed the prevalence of subungual melanoma in patients presenting with melanonychia in Asia. Jin et al10 reported subungual melanoma in 6.2% (17/275) of Korean patients presenting with melanonychia at a general dermatology clinic from 2002 to 2014. Lyu et al⁸ studied LM in 172 Chinese patients in a dermatology clinic from 2018 to 2021 and reported 9% (6/66) of adults (aged ≥18 years) with subungual melanoma, with no reported cases in childhood (aged <18 years).

Although the prevalence of subungual melanoma in patients with LM is low, it is an important diagnosis that should not be missed. In confirmed cases of subungual melanoma, two-thirds of lesions manifested as LM.^3,10,11 Thus, LM arising in an adult in a single digit is more concerning for malignancy.^2,3,7,9

Individuals of African and Asian descent as well as American Indian individuals are at highest risk for subungual melanoma with a poor prognosis compared to other types of melanoma, largely due to diagnosis at an advanced stage of disease.^3,9 In a retrospective study of 25 patients with surgically treated subungual melanoma, the mean recurrence-free survival was 33.6 months. The recurrence-free survival was 66% at 1 year and 40% at 3 years, and the overall survival rate was 37% at 3 years.¹²

Key clinical features in individuals with darker skin tones

• In patients with darker skin tones, LM tends to occur on multiple nails as a result of melanocytic activation.^2,13
• Several longitudinal bands may be noted on the same nail and the pigmentation of the bands may vary. With age, these longitudinal bands typically increase in number and width.¹³
• Pseudo-Hutchinson sign may be present due to ethnic melanosis of the proximal nail fold.^13,14
• Dermoscopic findings of LM in patients with skin of color include wider bands (P=.0125), lower band brightness (P<.032), and higher frequency of changing appearance of bands (P=.0071).¹⁵

Worth noting

When patients present with LM, thorough examination of the nail plate, periungual skin, and distal pulp of all digits on all extremities with adequate lighting is important.² Dermoscopy is useful, and a gel interface helps for examining the nail plates.⁷

Clinicians should be encouraged to biopsy or immediately refer patients with concerning nail unit lesions. Cases of LM most likely are benign, but if some doubt exists, the lesions should be biopsied or tracked closely with clinical and dermoscopic images, with a biopsy if changes occur.¹⁶ In conjunction with evaluation by a qualified clinician, patients also should be encouraged to take photographs, as the evolution of nail changes is a critical part of clinical decision-making on the need for a biopsy or referral.

Health disparity highlight

Despite the disproportionately high mortality rates from subungual melanoma in Black and Hispanic populations,^3,9 studies often do not adequately represent these populations. Although subungual melanoma is rare, a delay in the diagnosis contributes to high morbidity and mortality rates.

Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Melanoma in situ manifesting as longitudinal melanonychia (LM) in a single digit in a Black man. Dermoscopy showed irregular dark bands of brown pigmentation and micro-Hutchinson sign on the cuticle (inset).

B Melanoma manifesting as LM with a prominent Hutchinson sign in a Hispanic man, with variable shades of brown covering more than 50% of the nail width.

C Longitudinal melanonychia of at least 2 nails with a pseudo-Hutchinson sign (pigment on the nail folds in a benign case of LM) in a young Black man demonstrating ethnic/racial melanosis. The longitudinal bands, which were caused by benign melanocytic activation, are more gray than brown and are less than 3 mm wide.

Longitudinal melanonychia (LM) is a pigmented linear band—brown, black, or gray—spanning the length of the nail plate due to the presence of excess melanin, which may be attributed to a benign or malignant process and may warrant further investigation.^1,2 The majority of patients who present with LM are diagnosed with melanocytic activation of the nail matrix due to their inherent darker skin tone or various triggers including trauma, infection, and medications. Longitudinal melanonychia secondary to melanocytic activation often occurs spontaneously in patients with skin of color.³ Less commonly, LM is caused by a nail matrix nevus or lentigo; however, LM may arise secondary to subungual melanoma, a more dangerous cause.

A thorough clinical history including duration, recent changes in LM manifestation, nail trauma, or infection is helpful in evaluating patients with LM; however, a history of nail trauma can be misleading, as nail changes attributed to the trauma may in fact be melanoma. Irregularly spaced vertical lines of pigmentation ranging from brown to black with variations in spacing and width are characteristic of subungual melanoma.⁴ Nail dystrophy, granular hyperpigmentation, and Hutchinson sign (extension of pigmentation to the nail folds) also are worrisome features.⁵ In recent years, dermoscopy has become an important tool in the clinical examination of LM, with the development of criteria based on color and pattern recognition.^5,6 Dermoscopy can be useful in screening potential candidates for biopsy. Although clinical examination and dermoscopy are essential to evaluating LM, the gold-standard diagnostic test when malignancy is suspected is a nail matrix biopsy.^1,2,6,7

Epidemiology

It is not unusual for patients with darker skin tones to develop LM due to melanocytic activation of multiple nails with age. This finding can be seen in approximately 80% of African American individuals, 30% of Japanese individuals, and 50% of Hispanic individuals.² It has even been reported that approximately 100% of Black patients older than 50 years will have evidence of LM.³

In a retrospective analysis, children presenting with LM tend to have a higher prevalence of nail matrix nevi compared to adults (56.1% [60/106] vs 34.3% [23/66]; P=.005).⁸ Involvement of a single digit in children is most likely indicative of a nevus; however, when an adult presents with LM in a single digit, suspicion for subungual melanoma should be raised.^2,3,9

Two separate single-center retrospective studies showed the prevalence of subungual melanoma in patients presenting with melanonychia in Asia. Jin et al10 reported subungual melanoma in 6.2% (17/275) of Korean patients presenting with melanonychia at a general dermatology clinic from 2002 to 2014. Lyu et al⁸ studied LM in 172 Chinese patients in a dermatology clinic from 2018 to 2021 and reported 9% (6/66) of adults (aged ≥18 years) with subungual melanoma, with no reported cases in childhood (aged <18 years).

Although the prevalence of subungual melanoma in patients with LM is low, it is an important diagnosis that should not be missed. In confirmed cases of subungual melanoma, two-thirds of lesions manifested as LM.^3,10,11 Thus, LM arising in an adult in a single digit is more concerning for malignancy.^2,3,7,9

Individuals of African and Asian descent as well as American Indian individuals are at highest risk for subungual melanoma with a poor prognosis compared to other types of melanoma, largely due to diagnosis at an advanced stage of disease.^3,9 In a retrospective study of 25 patients with surgically treated subungual melanoma, the mean recurrence-free survival was 33.6 months. The recurrence-free survival was 66% at 1 year and 40% at 3 years, and the overall survival rate was 37% at 3 years.¹²

Key clinical features in individuals with darker skin tones

• In patients with darker skin tones, LM tends to occur on multiple nails as a result of melanocytic activation.^2,13
• Several longitudinal bands may be noted on the same nail and the pigmentation of the bands may vary. With age, these longitudinal bands typically increase in number and width.¹³
• Pseudo-Hutchinson sign may be present due to ethnic melanosis of the proximal nail fold.^13,14
• Dermoscopic findings of LM in patients with skin of color include wider bands (P=.0125), lower band brightness (P<.032), and higher frequency of changing appearance of bands (P=.0071).¹⁵

Worth noting

When patients present with LM, thorough examination of the nail plate, periungual skin, and distal pulp of all digits on all extremities with adequate lighting is important.² Dermoscopy is useful, and a gel interface helps for examining the nail plates.⁷

Clinicians should be encouraged to biopsy or immediately refer patients with concerning nail unit lesions. Cases of LM most likely are benign, but if some doubt exists, the lesions should be biopsied or tracked closely with clinical and dermoscopic images, with a biopsy if changes occur.¹⁶ In conjunction with evaluation by a qualified clinician, patients also should be encouraged to take photographs, as the evolution of nail changes is a critical part of clinical decision-making on the need for a biopsy or referral.

Health disparity highlight

Despite the disproportionately high mortality rates from subungual melanoma in Black and Hispanic populations,^3,9 studies often do not adequately represent these populations. Although subungual melanoma is rare, a delay in the diagnosis contributes to high morbidity and mortality rates.

Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Melanoma in situ manifesting as longitudinal melanonychia (LM) in a single digit in a Black man. Dermoscopy showed irregular dark bands of brown pigmentation and micro-Hutchinson sign on the cuticle (inset).

B Melanoma manifesting as LM with a prominent Hutchinson sign in a Hispanic man, with variable shades of brown covering more than 50% of the nail width.

C Longitudinal melanonychia of at least 2 nails with a pseudo-Hutchinson sign (pigment on the nail folds in a benign case of LM) in a young Black man demonstrating ethnic/racial melanosis. The longitudinal bands, which were caused by benign melanocytic activation, are more gray than brown and are less than 3 mm wide.

Longitudinal melanonychia (LM) is a pigmented linear band—brown, black, or gray—spanning the length of the nail plate due to the presence of excess melanin, which may be attributed to a benign or malignant process and may warrant further investigation.^1,2 The majority of patients who present with LM are diagnosed with melanocytic activation of the nail matrix due to their inherent darker skin tone or various triggers including trauma, infection, and medications. Longitudinal melanonychia secondary to melanocytic activation often occurs spontaneously in patients with skin of color.³ Less commonly, LM is caused by a nail matrix nevus or lentigo; however, LM may arise secondary to subungual melanoma, a more dangerous cause.

A thorough clinical history including duration, recent changes in LM manifestation, nail trauma, or infection is helpful in evaluating patients with LM; however, a history of nail trauma can be misleading, as nail changes attributed to the trauma may in fact be melanoma. Irregularly spaced vertical lines of pigmentation ranging from brown to black with variations in spacing and width are characteristic of subungual melanoma.⁴ Nail dystrophy, granular hyperpigmentation, and Hutchinson sign (extension of pigmentation to the nail folds) also are worrisome features.⁵ In recent years, dermoscopy has become an important tool in the clinical examination of LM, with the development of criteria based on color and pattern recognition.^5,6 Dermoscopy can be useful in screening potential candidates for biopsy. Although clinical examination and dermoscopy are essential to evaluating LM, the gold-standard diagnostic test when malignancy is suspected is a nail matrix biopsy.^1,2,6,7

Epidemiology

It is not unusual for patients with darker skin tones to develop LM due to melanocytic activation of multiple nails with age. This finding can be seen in approximately 80% of African American individuals, 30% of Japanese individuals, and 50% of Hispanic individuals.² It has even been reported that approximately 100% of Black patients older than 50 years will have evidence of LM.³

In a retrospective analysis, children presenting with LM tend to have a higher prevalence of nail matrix nevi compared to adults (56.1% [60/106] vs 34.3% [23/66]; P=.005).⁸ Involvement of a single digit in children is most likely indicative of a nevus; however, when an adult presents with LM in a single digit, suspicion for subungual melanoma should be raised.^2,3,9

Two separate single-center retrospective studies showed the prevalence of subungual melanoma in patients presenting with melanonychia in Asia. Jin et al10 reported subungual melanoma in 6.2% (17/275) of Korean patients presenting with melanonychia at a general dermatology clinic from 2002 to 2014. Lyu et al⁸ studied LM in 172 Chinese patients in a dermatology clinic from 2018 to 2021 and reported 9% (6/66) of adults (aged ≥18 years) with subungual melanoma, with no reported cases in childhood (aged <18 years).

Although the prevalence of subungual melanoma in patients with LM is low, it is an important diagnosis that should not be missed. In confirmed cases of subungual melanoma, two-thirds of lesions manifested as LM.^3,10,11 Thus, LM arising in an adult in a single digit is more concerning for malignancy.^2,3,7,9

Individuals of African and Asian descent as well as American Indian individuals are at highest risk for subungual melanoma with a poor prognosis compared to other types of melanoma, largely due to diagnosis at an advanced stage of disease.^3,9 In a retrospective study of 25 patients with surgically treated subungual melanoma, the mean recurrence-free survival was 33.6 months. The recurrence-free survival was 66% at 1 year and 40% at 3 years, and the overall survival rate was 37% at 3 years.¹²

Key clinical features in individuals with darker skin tones

• In patients with darker skin tones, LM tends to occur on multiple nails as a result of melanocytic activation.^2,13
• Several longitudinal bands may be noted on the same nail and the pigmentation of the bands may vary. With age, these longitudinal bands typically increase in number and width.¹³
• Pseudo-Hutchinson sign may be present due to ethnic melanosis of the proximal nail fold.^13,14
• Dermoscopic findings of LM in patients with skin of color include wider bands (P=.0125), lower band brightness (P<.032), and higher frequency of changing appearance of bands (P=.0071).¹⁵

Worth noting

When patients present with LM, thorough examination of the nail plate, periungual skin, and distal pulp of all digits on all extremities with adequate lighting is important.² Dermoscopy is useful, and a gel interface helps for examining the nail plates.⁷

Clinicians should be encouraged to biopsy or immediately refer patients with concerning nail unit lesions. Cases of LM most likely are benign, but if some doubt exists, the lesions should be biopsied or tracked closely with clinical and dermoscopic images, with a biopsy if changes occur.¹⁶ In conjunction with evaluation by a qualified clinician, patients also should be encouraged to take photographs, as the evolution of nail changes is a critical part of clinical decision-making on the need for a biopsy or referral.

Health disparity highlight

Despite the disproportionately high mortality rates from subungual melanoma in Black and Hispanic populations,^3,9 studies often do not adequately represent these populations. Although subungual melanoma is rare, a delay in the diagnosis contributes to high morbidity and mortality rates.

THE COMPARISON

A An 11-year-old Hispanic boy with allergic contact dermatitis (ACD) on the abdomen. The geometric nature of the eruption and proximity to the belt buckle were highly suggestive of ACD to nickel; patch testing was not needed.

B A Black woman with ACD on the neck. A punch biopsy demonstrated spongiotic dermatitis that was typical of ACD. The diagnosis was supported by the patient’s history of dermatitis that developed after new products were applied to the hair. The patient declined patch testing.

C A Hispanic man with ACD on hair-bearing areas of the face where hair dye was used. The patient’s history of dermatitis following the application of hair dye was highly suggestive of ACD; patch testing confirmed the allergen was paraphenylenediamine (PPD).

Allergic contact dermatitis (ACD) is an inflammatory condition of the skin caused by an immunologic response to 1 or more identifiable allergens. A delayed-type immune response (type IV hypersensitivity reaction) occurs after the skin is re-exposed to an offending allergen.¹ Severe pruritus is the main symptom of ACD in the early stages, accompanied by erythema, vesicles, and scaling in a distinct pattern corresponding to the allergen’s contact with the skin.² Delayed widespread dermatitis after exposure to an allergen—a phenomenon known as autoeczematization (id reaction)—also may occur.³

The gold-standard diagnostic tool for ACD is patch testing, in which the patient is re-exposed to the suspected contact allergen(s) and observed for the development of dermatitis.⁴ However, ACD can be diagnosed with a detailed patient history including occupation, hobbies, personal care practices, and possible triggers with subsequent rashes. Thorough clinical examination of the skin is paramount. Indicators of possible ACD include dermatitis that persists despite use of appropriate treatment, an unexplained flare of previously quiescent dermatitis, and a diagnosis of dermatitis without a clear cause.¹

Hairdressers, health care workers, and metal workers are at higher risk for ACD.⁵ Occupational ACD has notable socioeconomic implications, as it can result in frequent sick days, inability to perform tasks at work, and in some cases job loss.⁶

Patients with atopic dermatitis have impaired barrier function of the skin, permitting the entrance of allergens and subsequent sensitization.⁷ ACD is a challenge to manage, as complete avoidance of the allergen may not be possible.⁸

Continue to: The underrepresentation of patients...

The underrepresentation of patients with skin of color (SOC) in educational materials as well as socioeconomic health disparities may contribute to the lower rates of diagnosis, patch testing, and treatment of ACD in this patient population.

Epidemiology

An ACD prevalence of 15.2% was reported in a study of 793 Danish patients who underwent skin prick and patch testing.⁹ Alinaghi et al¹⁰ conducted a meta-analysis of 20,107 patients across 28 studies who were patch tested to determine the prevalence of ACD in the general population. The researchers concluded that 20.1% (95% CI, 16.8%-23.7%) of the general population experienced ACD. They analyzed 22 studies to determine the prevalence of ACD based on specific geographic area, including 18,709 individuals from Europe with a prevalence of 19.5% (95% CI, 15.8%-23.4%), 1639 individuals from North America with a prevalence of 20.6% (95% CI, 9.2%-35.2%), and 2 studies from China (no other studies from Asia found) with a prevalence of 20.6% (95% CI, 17.4%-23.9%). Researchers did not find data from studies conducted in Africa or South America.¹⁰

The current available epidemiologic data on ACD are not representative of SOC populations. DeLeo et al¹¹ looked at patch test reaction patterns in association with race and ethnicity in a large sample size (N = 19,457); 92.9% of these patients were White and only 7.1% were Black. Large-scale, inclusive studies are needed, which can only be achieved with increased suspicion for ACD and increased access to patch testing.

ACD is more common in women, with nickel being the most frequently identified allergen (FIGURE A).¹⁰ Personal care products often are linked to ACD (FIGURE B). An analysis of data from the North American Contact Dermatitis Group revealed that the top 5 personal care product allergens were methylisothiazolinone (a preservative), fragrance mix I, balsam of Peru, quaternium-15 (a preservative), and paraphenylenediamine (PPD; a common component of hair dye) (FIGURE C).¹²

There is a paucity of epidemiologic data among various ethnic groups; however, a few studies have suggested that there is no difference in the frequency rates of positive patch test results in Black vs White populations.^11,13,14 One study of patch test results from 114 Black patients and 877 White patients at the Cleveland Clinic Foundation in Ohio demonstrated a similar allergy frequency of 43.0% and 43.6%, respectively.13 However, there were differences in the types of allergen sensitization. Black patients had higher positive patch test rates for PPD than White patients (10.6% vs 4.5%). Black men had a higher frequency of sensitivity to PPD (21.2% vs 4.2%) and imidazolidinyl urea (a formaldehyde-releasing preservative; 9.1% vs 2.6%) compared to White men.¹³

Continue to: Ethnicity and cultural practices...

Ethnicity and cultural practices influence epidemiologic patterns of ACD. Darker hair dyes used in Black patients¹⁴ and deeply pigmented PPD dye found in henna tattoos used in Indian and Black patients¹⁵ may lead to increased sensitization to PPD. ACD due to formaldehyde is more common in White patients, possibly due to more frequent use of formaldehyde-containing moisturizers, shampoos, and creams.¹⁵

Key clinical features in people with darker skin tones

In patients with SOC, the clinical features of ACD vary, posing a diagnostic challenge. Hyperpigmentation, lichenification, and induration are more likely to be seen than the papules, vesicles, and erythematous dermatitis often described in lighter skin tones or acute ACD. Erythema can be difficult to assess on darker skin and may appear violaceous or very faint pink.16

Worth noting

A high index of suspicion is necessary when interpreting patch tests in patients with SOC, as patch test kits use a reading plate with graduated intensities of erythema, papulation, and vesicular reactions to determine the likelihood of ACD. The potential contact allergens are placed on the skin on Day 1 and covered. Then, on Day 3 the allergens are removed. The skin is clinically evaluated using visual assessment and skin palpation. The reactions are graded as negative, irritant reaction, equivocal, weak positive, strong positive, or extreme reaction at around Days 3 and 5 to capture both early and delayed reactions.¹⁷ A patch test may be positive even if obvious signs of erythema are not appreciated as expected.

ACD is more common in women, with nickel being the most frequently identified allergen.

Adjusting the lighting in the examination room, including side lighting, or using a blue background can be helpful in identifying erythema in darker skin tones.^15,16,18 Palpation of the skin also is useful, as even slight texture changes and induration are indicators of a possible skin reaction to the test allergen.¹⁵

Health disparity highlight

Clinical photographs of ACD and patch test results in patients with SOC are not commonplace in the literature. Positive patch test results in patients with darker skin tones vary from those of patients with lighter skin tones, and if the clinician reading the patch test result is not familiar with the findings in darker skin tones, the diagnosis may be delayed or missed.¹⁵

Continue to: Furthermore, Scott et al...

Furthermore, Scott et al¹⁵ highlighted that many dermatology residency training programs have a paucity of SOC education in their curriculum. This lack of representation may contribute to the diagnostic challenges encountered by health care providers.

The lower rates of patch testing in Black patients are likely due to the impact of social determinants of health.

Timely access to health care and education as well as economic stability are essential for the successful management of patients with ACD. Some individuals with SOC have been disproportionately affected by social determinants of health. Rodriguez-Homs et al¹⁹ demonstrated that the distance needed to travel to a clinic and the poverty rate of the county the patient lives in play a role in referral to a clinician specializing in contact dermatitis.

A retrospective registry review of 2310 patients undergoing patch testing at the Massachusetts General Hospital in Boston revealed that 2.5% were Black, 5.5% were Latinx, 8.3% were Asian, and the remaining 83.7% were White.²⁰ Qian et al²¹ also looked at patch testing patterns among various sociodemographic groups (N = 1,107,530) and found that 69% of patients were White and 59% were female. Rates of patch testing among patients who were Black, lesser educated, male, lower income, and younger (children ages 0-12 years) were significantly lower than for other groups when ACD was suspected (P < .0001).²¹ The lower rates of patch testing in patients with SOC may be due to low suspicion of diagnosis, low referral rates due to limited medical insurance, and financial instability, as well as other socioeconomic factors.²⁰

Tamazian et al¹⁶ reviewed pediatric populations at 13 US centers and found that Black children received patch testing less frequently than White and Hispanic children. Another review of pediatric patch testing in patients with SOC found that a less comprehensive panel of allergens was used in this population.²²

The key to resolution of ACD is removal of the offending antigen, and if patients are not being tested, then they risk having a prolonged and complicated course of ACD with a poor prognosis. Patients with SOC also experience greater negative psychosocial impact due to ACD disease burden.^21,23 The lower rates of patch testing in Black patients cannot solely be attributed to difficulty diagnosing ACD in darker skin tones; it is likely due to the impact of social determinants of health. Alleviating health disparities will improve patient outcomes and quality of life.

THE COMPARISON

A An 11-year-old Hispanic boy with allergic contact dermatitis (ACD) on the abdomen. The geometric nature of the eruption and proximity to the belt buckle were highly suggestive of ACD to nickel; patch testing was not needed.

B A Black woman with ACD on the neck. A punch biopsy demonstrated spongiotic dermatitis that was typical of ACD. The diagnosis was supported by the patient’s history of dermatitis that developed after new products were applied to the hair. The patient declined patch testing.

C A Hispanic man with ACD on hair-bearing areas of the face where hair dye was used. The patient’s history of dermatitis following the application of hair dye was highly suggestive of ACD; patch testing confirmed the allergen was paraphenylenediamine (PPD).

Allergic contact dermatitis (ACD) is an inflammatory condition of the skin caused by an immunologic response to 1 or more identifiable allergens. A delayed-type immune response (type IV hypersensitivity reaction) occurs after the skin is re-exposed to an offending allergen.¹ Severe pruritus is the main symptom of ACD in the early stages, accompanied by erythema, vesicles, and scaling in a distinct pattern corresponding to the allergen’s contact with the skin.² Delayed widespread dermatitis after exposure to an allergen—a phenomenon known as autoeczematization (id reaction)—also may occur.³

The gold-standard diagnostic tool for ACD is patch testing, in which the patient is re-exposed to the suspected contact allergen(s) and observed for the development of dermatitis.⁴ However, ACD can be diagnosed with a detailed patient history including occupation, hobbies, personal care practices, and possible triggers with subsequent rashes. Thorough clinical examination of the skin is paramount. Indicators of possible ACD include dermatitis that persists despite use of appropriate treatment, an unexplained flare of previously quiescent dermatitis, and a diagnosis of dermatitis without a clear cause.¹

Hairdressers, health care workers, and metal workers are at higher risk for ACD.⁵ Occupational ACD has notable socioeconomic implications, as it can result in frequent sick days, inability to perform tasks at work, and in some cases job loss.⁶

Patients with atopic dermatitis have impaired barrier function of the skin, permitting the entrance of allergens and subsequent sensitization.⁷ ACD is a challenge to manage, as complete avoidance of the allergen may not be possible.⁸

Continue to: The underrepresentation of patients...

The underrepresentation of patients with skin of color (SOC) in educational materials as well as socioeconomic health disparities may contribute to the lower rates of diagnosis, patch testing, and treatment of ACD in this patient population.

Epidemiology

An ACD prevalence of 15.2% was reported in a study of 793 Danish patients who underwent skin prick and patch testing.⁹ Alinaghi et al¹⁰ conducted a meta-analysis of 20,107 patients across 28 studies who were patch tested to determine the prevalence of ACD in the general population. The researchers concluded that 20.1% (95% CI, 16.8%-23.7%) of the general population experienced ACD. They analyzed 22 studies to determine the prevalence of ACD based on specific geographic area, including 18,709 individuals from Europe with a prevalence of 19.5% (95% CI, 15.8%-23.4%), 1639 individuals from North America with a prevalence of 20.6% (95% CI, 9.2%-35.2%), and 2 studies from China (no other studies from Asia found) with a prevalence of 20.6% (95% CI, 17.4%-23.9%). Researchers did not find data from studies conducted in Africa or South America.¹⁰

The current available epidemiologic data on ACD are not representative of SOC populations. DeLeo et al¹¹ looked at patch test reaction patterns in association with race and ethnicity in a large sample size (N = 19,457); 92.9% of these patients were White and only 7.1% were Black. Large-scale, inclusive studies are needed, which can only be achieved with increased suspicion for ACD and increased access to patch testing.

ACD is more common in women, with nickel being the most frequently identified allergen (FIGURE A).¹⁰ Personal care products often are linked to ACD (FIGURE B). An analysis of data from the North American Contact Dermatitis Group revealed that the top 5 personal care product allergens were methylisothiazolinone (a preservative), fragrance mix I, balsam of Peru, quaternium-15 (a preservative), and paraphenylenediamine (PPD; a common component of hair dye) (FIGURE C).¹²

There is a paucity of epidemiologic data among various ethnic groups; however, a few studies have suggested that there is no difference in the frequency rates of positive patch test results in Black vs White populations.^11,13,14 One study of patch test results from 114 Black patients and 877 White patients at the Cleveland Clinic Foundation in Ohio demonstrated a similar allergy frequency of 43.0% and 43.6%, respectively.13 However, there were differences in the types of allergen sensitization. Black patients had higher positive patch test rates for PPD than White patients (10.6% vs 4.5%). Black men had a higher frequency of sensitivity to PPD (21.2% vs 4.2%) and imidazolidinyl urea (a formaldehyde-releasing preservative; 9.1% vs 2.6%) compared to White men.¹³

Continue to: Ethnicity and cultural practices...

Ethnicity and cultural practices influence epidemiologic patterns of ACD. Darker hair dyes used in Black patients¹⁴ and deeply pigmented PPD dye found in henna tattoos used in Indian and Black patients¹⁵ may lead to increased sensitization to PPD. ACD due to formaldehyde is more common in White patients, possibly due to more frequent use of formaldehyde-containing moisturizers, shampoos, and creams.¹⁵

Key clinical features in people with darker skin tones

In patients with SOC, the clinical features of ACD vary, posing a diagnostic challenge. Hyperpigmentation, lichenification, and induration are more likely to be seen than the papules, vesicles, and erythematous dermatitis often described in lighter skin tones or acute ACD. Erythema can be difficult to assess on darker skin and may appear violaceous or very faint pink.16

Worth noting

A high index of suspicion is necessary when interpreting patch tests in patients with SOC, as patch test kits use a reading plate with graduated intensities of erythema, papulation, and vesicular reactions to determine the likelihood of ACD. The potential contact allergens are placed on the skin on Day 1 and covered. Then, on Day 3 the allergens are removed. The skin is clinically evaluated using visual assessment and skin palpation. The reactions are graded as negative, irritant reaction, equivocal, weak positive, strong positive, or extreme reaction at around Days 3 and 5 to capture both early and delayed reactions.¹⁷ A patch test may be positive even if obvious signs of erythema are not appreciated as expected.

ACD is more common in women, with nickel being the most frequently identified allergen.

Adjusting the lighting in the examination room, including side lighting, or using a blue background can be helpful in identifying erythema in darker skin tones.^15,16,18 Palpation of the skin also is useful, as even slight texture changes and induration are indicators of a possible skin reaction to the test allergen.¹⁵

Health disparity highlight

Clinical photographs of ACD and patch test results in patients with SOC are not commonplace in the literature. Positive patch test results in patients with darker skin tones vary from those of patients with lighter skin tones, and if the clinician reading the patch test result is not familiar with the findings in darker skin tones, the diagnosis may be delayed or missed.¹⁵

Continue to: Furthermore, Scott et al...

Furthermore, Scott et al¹⁵ highlighted that many dermatology residency training programs have a paucity of SOC education in their curriculum. This lack of representation may contribute to the diagnostic challenges encountered by health care providers.

The lower rates of patch testing in Black patients are likely due to the impact of social determinants of health.

Timely access to health care and education as well as economic stability are essential for the successful management of patients with ACD. Some individuals with SOC have been disproportionately affected by social determinants of health. Rodriguez-Homs et al¹⁹ demonstrated that the distance needed to travel to a clinic and the poverty rate of the county the patient lives in play a role in referral to a clinician specializing in contact dermatitis.

A retrospective registry review of 2310 patients undergoing patch testing at the Massachusetts General Hospital in Boston revealed that 2.5% were Black, 5.5% were Latinx, 8.3% were Asian, and the remaining 83.7% were White.²⁰ Qian et al²¹ also looked at patch testing patterns among various sociodemographic groups (N = 1,107,530) and found that 69% of patients were White and 59% were female. Rates of patch testing among patients who were Black, lesser educated, male, lower income, and younger (children ages 0-12 years) were significantly lower than for other groups when ACD was suspected (P < .0001).²¹ The lower rates of patch testing in patients with SOC may be due to low suspicion of diagnosis, low referral rates due to limited medical insurance, and financial instability, as well as other socioeconomic factors.²⁰

Tamazian et al¹⁶ reviewed pediatric populations at 13 US centers and found that Black children received patch testing less frequently than White and Hispanic children. Another review of pediatric patch testing in patients with SOC found that a less comprehensive panel of allergens was used in this population.²²

The key to resolution of ACD is removal of the offending antigen, and if patients are not being tested, then they risk having a prolonged and complicated course of ACD with a poor prognosis. Patients with SOC also experience greater negative psychosocial impact due to ACD disease burden.^21,23 The lower rates of patch testing in Black patients cannot solely be attributed to difficulty diagnosing ACD in darker skin tones; it is likely due to the impact of social determinants of health. Alleviating health disparities will improve patient outcomes and quality of life.

THE COMPARISON

A An 11-year-old Hispanic boy with allergic contact dermatitis (ACD) on the abdomen. The geometric nature of the eruption and proximity to the belt buckle were highly suggestive of ACD to nickel; patch testing was not needed.

B A Black woman with ACD on the neck. A punch biopsy demonstrated spongiotic dermatitis that was typical of ACD. The diagnosis was supported by the patient’s history of dermatitis that developed after new products were applied to the hair. The patient declined patch testing.

C A Hispanic man with ACD on hair-bearing areas of the face where hair dye was used. The patient’s history of dermatitis following the application of hair dye was highly suggestive of ACD; patch testing confirmed the allergen was paraphenylenediamine (PPD).

Allergic contact dermatitis (ACD) is an inflammatory condition of the skin caused by an immunologic response to 1 or more identifiable allergens. A delayed-type immune response (type IV hypersensitivity reaction) occurs after the skin is re-exposed to an offending allergen.¹ Severe pruritus is the main symptom of ACD in the early stages, accompanied by erythema, vesicles, and scaling in a distinct pattern corresponding to the allergen’s contact with the skin.² Delayed widespread dermatitis after exposure to an allergen—a phenomenon known as autoeczematization (id reaction)—also may occur.³

The gold-standard diagnostic tool for ACD is patch testing, in which the patient is re-exposed to the suspected contact allergen(s) and observed for the development of dermatitis.⁴ However, ACD can be diagnosed with a detailed patient history including occupation, hobbies, personal care practices, and possible triggers with subsequent rashes. Thorough clinical examination of the skin is paramount. Indicators of possible ACD include dermatitis that persists despite use of appropriate treatment, an unexplained flare of previously quiescent dermatitis, and a diagnosis of dermatitis without a clear cause.¹

Hairdressers, health care workers, and metal workers are at higher risk for ACD.⁵ Occupational ACD has notable socioeconomic implications, as it can result in frequent sick days, inability to perform tasks at work, and in some cases job loss.⁶

Patients with atopic dermatitis have impaired barrier function of the skin, permitting the entrance of allergens and subsequent sensitization.⁷ ACD is a challenge to manage, as complete avoidance of the allergen may not be possible.⁸

Continue to: The underrepresentation of patients...

The underrepresentation of patients with skin of color (SOC) in educational materials as well as socioeconomic health disparities may contribute to the lower rates of diagnosis, patch testing, and treatment of ACD in this patient population.

Epidemiology

An ACD prevalence of 15.2% was reported in a study of 793 Danish patients who underwent skin prick and patch testing.⁹ Alinaghi et al¹⁰ conducted a meta-analysis of 20,107 patients across 28 studies who were patch tested to determine the prevalence of ACD in the general population. The researchers concluded that 20.1% (95% CI, 16.8%-23.7%) of the general population experienced ACD. They analyzed 22 studies to determine the prevalence of ACD based on specific geographic area, including 18,709 individuals from Europe with a prevalence of 19.5% (95% CI, 15.8%-23.4%), 1639 individuals from North America with a prevalence of 20.6% (95% CI, 9.2%-35.2%), and 2 studies from China (no other studies from Asia found) with a prevalence of 20.6% (95% CI, 17.4%-23.9%). Researchers did not find data from studies conducted in Africa or South America.¹⁰

The current available epidemiologic data on ACD are not representative of SOC populations. DeLeo et al¹¹ looked at patch test reaction patterns in association with race and ethnicity in a large sample size (N = 19,457); 92.9% of these patients were White and only 7.1% were Black. Large-scale, inclusive studies are needed, which can only be achieved with increased suspicion for ACD and increased access to patch testing.

ACD is more common in women, with nickel being the most frequently identified allergen (FIGURE A).¹⁰ Personal care products often are linked to ACD (FIGURE B). An analysis of data from the North American Contact Dermatitis Group revealed that the top 5 personal care product allergens were methylisothiazolinone (a preservative), fragrance mix I, balsam of Peru, quaternium-15 (a preservative), and paraphenylenediamine (PPD; a common component of hair dye) (FIGURE C).¹²

There is a paucity of epidemiologic data among various ethnic groups; however, a few studies have suggested that there is no difference in the frequency rates of positive patch test results in Black vs White populations.^11,13,14 One study of patch test results from 114 Black patients and 877 White patients at the Cleveland Clinic Foundation in Ohio demonstrated a similar allergy frequency of 43.0% and 43.6%, respectively.13 However, there were differences in the types of allergen sensitization. Black patients had higher positive patch test rates for PPD than White patients (10.6% vs 4.5%). Black men had a higher frequency of sensitivity to PPD (21.2% vs 4.2%) and imidazolidinyl urea (a formaldehyde-releasing preservative; 9.1% vs 2.6%) compared to White men.¹³

Continue to: Ethnicity and cultural practices...

Ethnicity and cultural practices influence epidemiologic patterns of ACD. Darker hair dyes used in Black patients¹⁴ and deeply pigmented PPD dye found in henna tattoos used in Indian and Black patients¹⁵ may lead to increased sensitization to PPD. ACD due to formaldehyde is more common in White patients, possibly due to more frequent use of formaldehyde-containing moisturizers, shampoos, and creams.¹⁵

Key clinical features in people with darker skin tones

In patients with SOC, the clinical features of ACD vary, posing a diagnostic challenge. Hyperpigmentation, lichenification, and induration are more likely to be seen than the papules, vesicles, and erythematous dermatitis often described in lighter skin tones or acute ACD. Erythema can be difficult to assess on darker skin and may appear violaceous or very faint pink.16

Worth noting

A high index of suspicion is necessary when interpreting patch tests in patients with SOC, as patch test kits use a reading plate with graduated intensities of erythema, papulation, and vesicular reactions to determine the likelihood of ACD. The potential contact allergens are placed on the skin on Day 1 and covered. Then, on Day 3 the allergens are removed. The skin is clinically evaluated using visual assessment and skin palpation. The reactions are graded as negative, irritant reaction, equivocal, weak positive, strong positive, or extreme reaction at around Days 3 and 5 to capture both early and delayed reactions.¹⁷ A patch test may be positive even if obvious signs of erythema are not appreciated as expected.

ACD is more common in women, with nickel being the most frequently identified allergen.

Adjusting the lighting in the examination room, including side lighting, or using a blue background can be helpful in identifying erythema in darker skin tones.^15,16,18 Palpation of the skin also is useful, as even slight texture changes and induration are indicators of a possible skin reaction to the test allergen.¹⁵

Health disparity highlight

Clinical photographs of ACD and patch test results in patients with SOC are not commonplace in the literature. Positive patch test results in patients with darker skin tones vary from those of patients with lighter skin tones, and if the clinician reading the patch test result is not familiar with the findings in darker skin tones, the diagnosis may be delayed or missed.¹⁵

Continue to: Furthermore, Scott et al...

Furthermore, Scott et al¹⁵ highlighted that many dermatology residency training programs have a paucity of SOC education in their curriculum. This lack of representation may contribute to the diagnostic challenges encountered by health care providers.

The lower rates of patch testing in Black patients are likely due to the impact of social determinants of health.

Timely access to health care and education as well as economic stability are essential for the successful management of patients with ACD. Some individuals with SOC have been disproportionately affected by social determinants of health. Rodriguez-Homs et al¹⁹ demonstrated that the distance needed to travel to a clinic and the poverty rate of the county the patient lives in play a role in referral to a clinician specializing in contact dermatitis.

A retrospective registry review of 2310 patients undergoing patch testing at the Massachusetts General Hospital in Boston revealed that 2.5% were Black, 5.5% were Latinx, 8.3% were Asian, and the remaining 83.7% were White.²⁰ Qian et al²¹ also looked at patch testing patterns among various sociodemographic groups (N = 1,107,530) and found that 69% of patients were White and 59% were female. Rates of patch testing among patients who were Black, lesser educated, male, lower income, and younger (children ages 0-12 years) were significantly lower than for other groups when ACD was suspected (P < .0001).²¹ The lower rates of patch testing in patients with SOC may be due to low suspicion of diagnosis, low referral rates due to limited medical insurance, and financial instability, as well as other socioeconomic factors.²⁰

Tamazian et al¹⁶ reviewed pediatric populations at 13 US centers and found that Black children received patch testing less frequently than White and Hispanic children. Another review of pediatric patch testing in patients with SOC found that a less comprehensive panel of allergens was used in this population.²²

The key to resolution of ACD is removal of the offending antigen, and if patients are not being tested, then they risk having a prolonged and complicated course of ACD with a poor prognosis. Patients with SOC also experience greater negative psychosocial impact due to ACD disease burden.^21,23 The lower rates of patch testing in Black patients cannot solely be attributed to difficulty diagnosing ACD in darker skin tones; it is likely due to the impact of social determinants of health. Alleviating health disparities will improve patient outcomes and quality of life.