Diversity in Medicine

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

Prevalence and Epidemiology

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

AD in Black Adolescents

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

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

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

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

Diagnosis

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

Treatment of AD

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

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

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

Treatment of AV in Patients With AD

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

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

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

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

Impact of Athletics on AD in Black Adolescents

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

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

Use of Cosmetics for AD

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

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

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

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

Alternative Therapies for AD

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

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

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

Final Thoughts

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

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

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

Prevalence and Epidemiology

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

AD in Black Adolescents

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

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

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

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

Diagnosis

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

Treatment of AD

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

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

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

Treatment of AV in Patients With AD

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

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

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

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

Impact of Athletics on AD in Black Adolescents

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

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

Use of Cosmetics for AD

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

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

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

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

Alternative Therapies for AD

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

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

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

Final Thoughts

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

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

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

Prevalence and Epidemiology

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

AD in Black Adolescents

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

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

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

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

Diagnosis

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

Treatment of AD

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

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

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

Treatment of AV in Patients With AD

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

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

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

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

Impact of Athletics on AD in Black Adolescents

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

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

Use of Cosmetics for AD

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

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

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

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

Alternative Therapies for AD

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

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

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

Final Thoughts

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

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

Over the last 5 years, there has been an important dialogue among dermatologists about diversity in our specialty that has shifted the mind-set of the dermatology community and highlighted an intent to build a diverse workforce. It is important to reflect on this effort and acknowledge the progress that has been made. Additionally, it also is important to envision what our ideal specialty will look like 10 years from now and to discuss specific ways that we can achieve that vision for the future of dermatology.

At the 2015 Annual Meeting of the American Academy of Dermatology (AAD), Bruce E. Wintroub, MD, highlighted the importance of diversity in dermatology when he presented the Clarence S. Livingood lecture.¹ His discussion was followed by a call to action from Pandya et al² in 2016, which described the lack of diversity in our specialty (the second least diverse specialty in medicine) and proposed specific steps that can be taken by individuals and organizations to address the issue. In line with this effort, the AAD’s Diversity Task Force, Diversity Mentorship Program,³ and Diversity Champion Initiative were created. The latter program enlisted dermatology residency programs across the country to select a diversity champion who would lead efforts to increase diversity in each participating department, including mentorship of underrepresented-in-medicine college and medical students. The AAD’s 2019 Diversity Champion Workshop⁴ (September 12–13, 2019) will be held for the first time prior to the Association of Professors of Dermatology Annual Meeting (September 13–14, 2019) in an attempt to scale up the Diversity Champion Initiative. This workshop has galvanized widespread support and will be collaboratively hosted by the AAD, Association of Professors of Dermatology, Skin of Color Society, Society for Investigative Dermatology, and Women’s Dermatologic Society.

Current diversity efforts have largely focused on increasing representation in the dermatology workforce. A publication in 2017 challenged the tenets of dermatology resident selection and advocated for holistic review of residency program applicants as one way to address the lack of diversity in dermatology.⁵ This viewpoint highlighted that dermatology’s traditional focus on US Medical Licensing Examination scores and Alpha Omega Alpha Honor Medical Society membership leads to bias^6-8; the viewpoint proposed several ways to change the resident selection process to enhance diversity.⁵ A recent proposal to eliminate numerical scores on the US Medical Licensing Examination Step 1 and move to a pass/fail grading system aligns well with this viewpoint.⁹ Defining best practices to perform holistic reviews is an ongoing effort and challenge for many programs, one that will be discussed at the AAD’s 2019 Diversity Champion Workshop. Implementing best practices will require individual residency programs to develop review processes tailored to departmental resources and strengths. Achieving increased representation must be an active process starting with an explicit commitment to improving diversity.

Through these efforts, we are poised to improve our specialty; however, it is critical to recognize that simply increasing the number of underrepresented dermatologists is not enough to improve diversity in dermatology. What does meaningful change look like? In 10 years, we hope that, in addition to a more inclusive workforce, we will see expanded diversity efforts beyond race and ethnicity; improved cultural competence within dermatology departments and organizations that creates more inclusive places to work, learn, and practice medicine; intentional broader representation in dermatology leadership; high-quality, evidence-based, inclusive, and culturally competent education, patient care, and research; and equal and improved outcomes for all of our patients, particularly those who traditionally experience health care disparities. To this end, ensuring diversity in research and publications is paramount. Academic journals should be actively working to include articles in the literature that help us better understand health care differences, including research that examines the presentations of skin disease in a broad spectrum of study populations, as well as to spotlight and solicit content from diverse voices. Inclusion of a diverse range of participants in research based on human subjects should be a requirement for publication, which would ensure more generalizable data. Diversity in clinical trials is improving,¹⁰ but more effort should be devoted to further increasing diversity in medical research. In particular, we need to broaden the inclusivity of dermatology research efforts and outcomes data to include more patients with skin of color as well as other underrepresented groups, thus helping to improve our understanding of the differential effects of certain interventions.

We also must educate trainees and practicing dermatologists to better understand the diagnosis and management of skin diseases in all populations; to this end, it is essential to develop a culturally competent curriculum and continuing medical education on diseases of the skin and hair that affect patients with skin of color as well as cutaneous conditions that present in groups such as sexual and gender minorities.^11,12 All dermatologists—not just the experts in academic skin of color and other specialty clinics—should have expertise in the dermatologic care of diverse patients.

We have made notable and important strides with regard to diversity in dermatology by beginning this conversation, identifying problems, coming up with solutions, and implementing them.¹³ This progress has been made relatively quickly and is commendable; however, we have more work to do before our specialty is inclusive of underrepresented-in-medicine physicians and provides excellent care to all patients.

Over the last 5 years, there has been an important dialogue among dermatologists about diversity in our specialty that has shifted the mind-set of the dermatology community and highlighted an intent to build a diverse workforce. It is important to reflect on this effort and acknowledge the progress that has been made. Additionally, it also is important to envision what our ideal specialty will look like 10 years from now and to discuss specific ways that we can achieve that vision for the future of dermatology.

At the 2015 Annual Meeting of the American Academy of Dermatology (AAD), Bruce E. Wintroub, MD, highlighted the importance of diversity in dermatology when he presented the Clarence S. Livingood lecture.¹ His discussion was followed by a call to action from Pandya et al² in 2016, which described the lack of diversity in our specialty (the second least diverse specialty in medicine) and proposed specific steps that can be taken by individuals and organizations to address the issue. In line with this effort, the AAD’s Diversity Task Force, Diversity Mentorship Program,³ and Diversity Champion Initiative were created. The latter program enlisted dermatology residency programs across the country to select a diversity champion who would lead efforts to increase diversity in each participating department, including mentorship of underrepresented-in-medicine college and medical students. The AAD’s 2019 Diversity Champion Workshop⁴ (September 12–13, 2019) will be held for the first time prior to the Association of Professors of Dermatology Annual Meeting (September 13–14, 2019) in an attempt to scale up the Diversity Champion Initiative. This workshop has galvanized widespread support and will be collaboratively hosted by the AAD, Association of Professors of Dermatology, Skin of Color Society, Society for Investigative Dermatology, and Women’s Dermatologic Society.

Current diversity efforts have largely focused on increasing representation in the dermatology workforce. A publication in 2017 challenged the tenets of dermatology resident selection and advocated for holistic review of residency program applicants as one way to address the lack of diversity in dermatology.⁵ This viewpoint highlighted that dermatology’s traditional focus on US Medical Licensing Examination scores and Alpha Omega Alpha Honor Medical Society membership leads to bias^6-8; the viewpoint proposed several ways to change the resident selection process to enhance diversity.⁵ A recent proposal to eliminate numerical scores on the US Medical Licensing Examination Step 1 and move to a pass/fail grading system aligns well with this viewpoint.⁹ Defining best practices to perform holistic reviews is an ongoing effort and challenge for many programs, one that will be discussed at the AAD’s 2019 Diversity Champion Workshop. Implementing best practices will require individual residency programs to develop review processes tailored to departmental resources and strengths. Achieving increased representation must be an active process starting with an explicit commitment to improving diversity.

Through these efforts, we are poised to improve our specialty; however, it is critical to recognize that simply increasing the number of underrepresented dermatologists is not enough to improve diversity in dermatology. What does meaningful change look like? In 10 years, we hope that, in addition to a more inclusive workforce, we will see expanded diversity efforts beyond race and ethnicity; improved cultural competence within dermatology departments and organizations that creates more inclusive places to work, learn, and practice medicine; intentional broader representation in dermatology leadership; high-quality, evidence-based, inclusive, and culturally competent education, patient care, and research; and equal and improved outcomes for all of our patients, particularly those who traditionally experience health care disparities. To this end, ensuring diversity in research and publications is paramount. Academic journals should be actively working to include articles in the literature that help us better understand health care differences, including research that examines the presentations of skin disease in a broad spectrum of study populations, as well as to spotlight and solicit content from diverse voices. Inclusion of a diverse range of participants in research based on human subjects should be a requirement for publication, which would ensure more generalizable data. Diversity in clinical trials is improving,¹⁰ but more effort should be devoted to further increasing diversity in medical research. In particular, we need to broaden the inclusivity of dermatology research efforts and outcomes data to include more patients with skin of color as well as other underrepresented groups, thus helping to improve our understanding of the differential effects of certain interventions.

We also must educate trainees and practicing dermatologists to better understand the diagnosis and management of skin diseases in all populations; to this end, it is essential to develop a culturally competent curriculum and continuing medical education on diseases of the skin and hair that affect patients with skin of color as well as cutaneous conditions that present in groups such as sexual and gender minorities.^11,12 All dermatologists—not just the experts in academic skin of color and other specialty clinics—should have expertise in the dermatologic care of diverse patients.

We have made notable and important strides with regard to diversity in dermatology by beginning this conversation, identifying problems, coming up with solutions, and implementing them.¹³ This progress has been made relatively quickly and is commendable; however, we have more work to do before our specialty is inclusive of underrepresented-in-medicine physicians and provides excellent care to all patients.

Over the last 5 years, there has been an important dialogue among dermatologists about diversity in our specialty that has shifted the mind-set of the dermatology community and highlighted an intent to build a diverse workforce. It is important to reflect on this effort and acknowledge the progress that has been made. Additionally, it also is important to envision what our ideal specialty will look like 10 years from now and to discuss specific ways that we can achieve that vision for the future of dermatology.

At the 2015 Annual Meeting of the American Academy of Dermatology (AAD), Bruce E. Wintroub, MD, highlighted the importance of diversity in dermatology when he presented the Clarence S. Livingood lecture.¹ His discussion was followed by a call to action from Pandya et al² in 2016, which described the lack of diversity in our specialty (the second least diverse specialty in medicine) and proposed specific steps that can be taken by individuals and organizations to address the issue. In line with this effort, the AAD’s Diversity Task Force, Diversity Mentorship Program,³ and Diversity Champion Initiative were created. The latter program enlisted dermatology residency programs across the country to select a diversity champion who would lead efforts to increase diversity in each participating department, including mentorship of underrepresented-in-medicine college and medical students. The AAD’s 2019 Diversity Champion Workshop⁴ (September 12–13, 2019) will be held for the first time prior to the Association of Professors of Dermatology Annual Meeting (September 13–14, 2019) in an attempt to scale up the Diversity Champion Initiative. This workshop has galvanized widespread support and will be collaboratively hosted by the AAD, Association of Professors of Dermatology, Skin of Color Society, Society for Investigative Dermatology, and Women’s Dermatologic Society.

Current diversity efforts have largely focused on increasing representation in the dermatology workforce. A publication in 2017 challenged the tenets of dermatology resident selection and advocated for holistic review of residency program applicants as one way to address the lack of diversity in dermatology.⁵ This viewpoint highlighted that dermatology’s traditional focus on US Medical Licensing Examination scores and Alpha Omega Alpha Honor Medical Society membership leads to bias^6-8; the viewpoint proposed several ways to change the resident selection process to enhance diversity.⁵ A recent proposal to eliminate numerical scores on the US Medical Licensing Examination Step 1 and move to a pass/fail grading system aligns well with this viewpoint.⁹ Defining best practices to perform holistic reviews is an ongoing effort and challenge for many programs, one that will be discussed at the AAD’s 2019 Diversity Champion Workshop. Implementing best practices will require individual residency programs to develop review processes tailored to departmental resources and strengths. Achieving increased representation must be an active process starting with an explicit commitment to improving diversity.

Through these efforts, we are poised to improve our specialty; however, it is critical to recognize that simply increasing the number of underrepresented dermatologists is not enough to improve diversity in dermatology. What does meaningful change look like? In 10 years, we hope that, in addition to a more inclusive workforce, we will see expanded diversity efforts beyond race and ethnicity; improved cultural competence within dermatology departments and organizations that creates more inclusive places to work, learn, and practice medicine; intentional broader representation in dermatology leadership; high-quality, evidence-based, inclusive, and culturally competent education, patient care, and research; and equal and improved outcomes for all of our patients, particularly those who traditionally experience health care disparities. To this end, ensuring diversity in research and publications is paramount. Academic journals should be actively working to include articles in the literature that help us better understand health care differences, including research that examines the presentations of skin disease in a broad spectrum of study populations, as well as to spotlight and solicit content from diverse voices. Inclusion of a diverse range of participants in research based on human subjects should be a requirement for publication, which would ensure more generalizable data. Diversity in clinical trials is improving,¹⁰ but more effort should be devoted to further increasing diversity in medical research. In particular, we need to broaden the inclusivity of dermatology research efforts and outcomes data to include more patients with skin of color as well as other underrepresented groups, thus helping to improve our understanding of the differential effects of certain interventions.

We also must educate trainees and practicing dermatologists to better understand the diagnosis and management of skin diseases in all populations; to this end, it is essential to develop a culturally competent curriculum and continuing medical education on diseases of the skin and hair that affect patients with skin of color as well as cutaneous conditions that present in groups such as sexual and gender minorities.^11,12 All dermatologists—not just the experts in academic skin of color and other specialty clinics—should have expertise in the dermatologic care of diverse patients.

We have made notable and important strides with regard to diversity in dermatology by beginning this conversation, identifying problems, coming up with solutions, and implementing them.¹³ This progress has been made relatively quickly and is commendable; however, we have more work to do before our specialty is inclusive of underrepresented-in-medicine physicians and provides excellent care to all patients.

Rosacea is a chronic inflammatory cutaneous disorder that affects the vasculature and pilosebaceous units of the face. Delayed and misdiagnosed rosacea in the SOC population has led to increased morbidity in this patient population. ^1-3 It is characterized by facial flushing and warmth, erythema, telangiectasia, papules, and pustules. The 4 major subtypes include erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea. ⁴ Granulomatous rosacea is considered to be a unique variant of rosacea. Until recently, rosacea was thought to predominately affect lighter-skinned individuals of Celtic and northern European origin. ^5,6 A paucity of studies and case reports in the literature have contributed to the commonly held belief that rosacea occurs infrequently in patients with skin of color (SOC). ¹ A PubMed search of articles indexed for MEDLINE revealed 32 results using the terms skin of color and rosacea vs 3786 using the term rosacea alone. It is possible that the nuance involved in appreciating erythema or other clinical manifestations of rosacea in SOC patients has led to underdiagnosis. Alternatively, these patients may be unaware that their symptoms represent a disease process and do not seek treatment. Many patients with darker skin will have endured rosacea for months or even years because the disease has been unrecognized or misdiagnosed. ^6-8 Another factor possibly accounting for the perception that rosacea occurs infrequently in patients with SOC is misdiagnosis of rosacea as other diseases that are known to occur more commonly in the SOC population. Dermatologists should be aware that rosacea can affect SOC patients and that there are several rosacea mimickers to be considered and excluded when making the rosacea diagnosis in this patient population. To promote accurate and timely diagnosis of rosacea, we review several possible rosacea mimickers in SOC patients and highlight the distinguishing features.

Epidemiology

In 2018, a meta-analysis of published studies on rosacea estimated the global prevalence in all adults to be 5.46%.⁹ A multicenter study across 6 cities in Colombia identified 291 outpatients with rosacea; of them, 12.4% had either Fitzpatrick skin types IV or V.¹⁰ A study of 2743 Angolan adults with Fitzpatrick skin types V and VI reported that only 0.4% of patients had a diagnosis of rosacea.¹¹ A Saudi study of 50 dark-skinned female patients with rosacea revealed 40% (20/50), 18% (9/50), and 42% (21/50) were Fitzpatrick skin types IV, V, and VI, respectively.¹² The prevalence of rosacea in SOC patients in the United States is less defined. Data from the US National Ambulatory Medical Care Survey (1993-2010) of 31.5 million rosacea visits showed that 2% of rosacea patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino.⁸

Clinical Features

Each of the 4 major rosacea subtypes can present in the SOC population. The granulomatous variant has been predominantly reported in black patients.¹³ This predilection has been attributed to either an increased susceptibility in black patients to develop this variant or a delay in diagnosis of earlier phases of inflammatory rosacea.⁷

In a Saudi study (N=50), severe erythematotelangiectatic rosacea was diagnosed in 42% (21/50) of patients, with the majority having Fitzpatrick skin type IV. The severe papulopustular subtype was seen in 14% (7/50) of patients, with 20% (10/50) and 14% (7/50) having Fitzpatrick skin types IV and VI, respectively.¹² In a Tunisian study (N=244), erythematotelangiectatic rosacea was seen in 12% of patients, papulopustular rosacea in 69%, phymatous rosacea in 4%, and ocular rosacea in 16%. Less frequently, the granulomatous variant was seen in 3% of patients, and steroid rosacea was noted in 12% patients.¹⁴

Recognizing the signs of rosacea may be a challenge, particularly erythema and telangiectasia. Tips for making an accurate diagnosis include use of adequate lighting, blanching of the skin (Figure 1), photography of the affected area against a dark blue background, and dermatoscopic examination.³ Furthermore, a thorough medical history, especially when evaluating the presence of facial erythema and identifying triggers, may help reach the correct diagnosis. Careful examination of the distribution of papules and pustules as well as the morphology and color of the papules in SOC patients also may provide diagnostic clues.

Differential Diagnosis and Distinguishing Features

Several disorders are included in the differential diagnosis of rosacea and may confound a correct rosacea diagnosis, including systemic lupus erythematosus (SLE), seborrheic dermatitis, dermatomyositis, acne vulgaris, sarcoidosis, and steroid dermatitis. Many of these disorders also occur more commonly in patients with SOC; therefore, it is important to clearly distinguish these entities from rosacea in this population.

Systemic Lupus Erythematosus
Systemic lupus erythematosus is an autoimmune disease that commonly presents with erythema as well as erythematous inflammatory facial lesions similar to rosacea. The classic clinical appearance of SLE is the butterfly or malar rash, an erythematous macular eruption on the malar region of the face that also may involve the nose. This rash can appear similar to rosacea; however, the malar rash classically spares the nasolabial folds, while erythema of rosacea often involves this anatomic boundary. Although the facial erythema in both SLE and early stages of rosacea may be patchy and similar in presentation, the presence of papules and pustules rarely occurs in SLE and may help to differentiate SLE from certain variants of rosacea.¹⁵

Seborrheic Dermatitis
Seborrheic dermatitis is a frequent cause of facial erythema linked to the Malassezia yeast species in susceptible individuals. Seborrheic dermatitis has a notable prevalence in women of African descent and often is considered normal by these patients.²¹ Rosacea and seborrheic dermatitis are relatively common dermatoses and therefore can present concurrently. In both diseases, facial erythema may be difficult to discern upon cursory inspection. Seborrheic dermatitis may be distinguished from rosacea by the clinical appearance of erythematous patches and plaques involving the scalp, anterior and posterior hairlines, preauricular and postauricular areas, and medial eyebrows. Both seborrheic dermatitis and rosacea may involve the nasolabial folds, but the presence of scale in seborrheic dermatitis is a distinguishing feature. Scale may vary in appearance from thick, greasy, and yellowish to fine, thin, and whitish.²² In contrast to rosacea, the erythematous lesions of seborrheic dermatitis often are annular in configuration. Furthermore, postinflammatory hypopigmentation and, to a lesser extent, postinflammatory hyperpigmentation are key clinical components of seborrheic dermatitis in SOC patients but are not as commonly observed in rosacea.

Dermatomyositis
Dermatomyositis is a systemic autoimmune disease characterized by progressive and symmetric proximal musculoskeletal weakness and cutaneous findings. Facial erythema in the malar and nasolabial folds can be seen in patients with dermatomyositis¹⁸; however, the facial erythema seen in dermatomyositis, known as heliotrope rash, has a violaceous dusky quality and also involves the periorbital region. The violaceous hue and periorbital involvement are distinguishing features from rosacea. Okiyama et al²³ described facial macular violaceous erythema with scale and edema in Japanese patients with dermatomyositis on the nasolabial folds, eyebrows, chin, cheeks, and ears; they also described mild atrophy with telangiectasia. Other clinical signs to help distinguish rosacea from dermatomyositis are the presence of edema of the face and extremities, Gottron papules, and poikiloderma. Dermatomyositis is a disease that affects all races; however, it is 4 times more common in black vs white patients,²⁴ making it even more important to be able to distinguish between these conditions.

Acne Vulgaris
Acne vulgaris, the most commonly diagnosed dermatosis in patients with SOC, is characterized by papules, pustules, cysts, nodules, open and closed comedones, and hyperpigmented macules on the face, chest, and back.^25,26 The absence of comedonal lesions and the presence of hyperpigmented macules distinguishes acne vulgaris from rosacea in this population.¹ In addition, the absence of telangiectasia and flushing are important distinguishing factors when making the diagnosis of acne vulgaris.

Sarcoidosis
Sarcoidosis is a multisystem inflammatory disease characterized histologically by the presence of noncaseating granulomas in sites such as the lungs, lymph nodes, eyes, nervous system, liver, spleen, heart, and skin.²⁷ Cutaneous sarcoidosis is known as a great mimicker of many other dermatoses, as it may present with multiple morphologic features. Cutaneous sarcoidosis most typically presents as papules, but nodules, plaques, lupus pernio, subcutaneous infiltrates, and infiltration of scars also have been identified.²⁸ Sarcoid papules typically are 1 to 5 mm in size on the face, neck, and periorbital skin²⁹; they are initially orange or yellow-brown in color, turn brownish red or violaceous, then involute to form faint macules.³⁰ Papular lesions may either resolve or evolve into plaques, particularly on the extremities, face, scalp, back, and buttocks. Additionally, there are a few case reports of patients with cutaneous sarcoidosis presenting with large bulbous nasal masses initially thought to be rhinophyma.^31-33 Finally, it may be difficult to distinguish sarcoidosis from granulomatous rosacea, which is characterized by firm yellow, brown, violaceous, red, or flesh-colored monomorphic papules or nodules affecting the perioral, periocular, medial, and/or lateral areas of the face (Figure 2).^4,34 Patients also can have unilateral disease.³⁵ Patients with granulomatous rosacea lack flushing and erythema as seen in more characteristic presentations of rosacea. They may report pain, pruritus, or burning, or they may be asymptomatic.³⁶ Features that distinguish granulomatous rosacea from sarcoidosis include the absence of nodules, plaques, lupus pernio, subcutaneous infiltrates, and infiltration of scars. Clinical, histological, and radiographic evaluation are necessary to make the diagnosis of sarcoidosis over rosacea.

Final Thoughts

Rosacea has features common to many other facial dermatoses, making the diagnosis challenging, particularly in patients with SOC. This difficulty in diagnosis may contribute to an underestimation of the prevalence of this disease in SOC patients. An understanding of rosacea, its nuances in clinical appearance, and its mimickers in SOC patients is important in making an accurate diagnosis.

References

Rosacea is a chronic inflammatory cutaneous disorder that affects the vasculature and pilosebaceous units of the face. Delayed and misdiagnosed rosacea in the SOC population has led to increased morbidity in this patient population. ^1-3 It is characterized by facial flushing and warmth, erythema, telangiectasia, papules, and pustules. The 4 major subtypes include erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea. ⁴ Granulomatous rosacea is considered to be a unique variant of rosacea. Until recently, rosacea was thought to predominately affect lighter-skinned individuals of Celtic and northern European origin. ^5,6 A paucity of studies and case reports in the literature have contributed to the commonly held belief that rosacea occurs infrequently in patients with skin of color (SOC). ¹ A PubMed search of articles indexed for MEDLINE revealed 32 results using the terms skin of color and rosacea vs 3786 using the term rosacea alone. It is possible that the nuance involved in appreciating erythema or other clinical manifestations of rosacea in SOC patients has led to underdiagnosis. Alternatively, these patients may be unaware that their symptoms represent a disease process and do not seek treatment. Many patients with darker skin will have endured rosacea for months or even years because the disease has been unrecognized or misdiagnosed. ^6-8 Another factor possibly accounting for the perception that rosacea occurs infrequently in patients with SOC is misdiagnosis of rosacea as other diseases that are known to occur more commonly in the SOC population. Dermatologists should be aware that rosacea can affect SOC patients and that there are several rosacea mimickers to be considered and excluded when making the rosacea diagnosis in this patient population. To promote accurate and timely diagnosis of rosacea, we review several possible rosacea mimickers in SOC patients and highlight the distinguishing features.

Epidemiology

In 2018, a meta-analysis of published studies on rosacea estimated the global prevalence in all adults to be 5.46%.⁹ A multicenter study across 6 cities in Colombia identified 291 outpatients with rosacea; of them, 12.4% had either Fitzpatrick skin types IV or V.¹⁰ A study of 2743 Angolan adults with Fitzpatrick skin types V and VI reported that only 0.4% of patients had a diagnosis of rosacea.¹¹ A Saudi study of 50 dark-skinned female patients with rosacea revealed 40% (20/50), 18% (9/50), and 42% (21/50) were Fitzpatrick skin types IV, V, and VI, respectively.¹² The prevalence of rosacea in SOC patients in the United States is less defined. Data from the US National Ambulatory Medical Care Survey (1993-2010) of 31.5 million rosacea visits showed that 2% of rosacea patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino.⁸

Clinical Features

Each of the 4 major rosacea subtypes can present in the SOC population. The granulomatous variant has been predominantly reported in black patients.¹³ This predilection has been attributed to either an increased susceptibility in black patients to develop this variant or a delay in diagnosis of earlier phases of inflammatory rosacea.⁷

In a Saudi study (N=50), severe erythematotelangiectatic rosacea was diagnosed in 42% (21/50) of patients, with the majority having Fitzpatrick skin type IV. The severe papulopustular subtype was seen in 14% (7/50) of patients, with 20% (10/50) and 14% (7/50) having Fitzpatrick skin types IV and VI, respectively.¹² In a Tunisian study (N=244), erythematotelangiectatic rosacea was seen in 12% of patients, papulopustular rosacea in 69%, phymatous rosacea in 4%, and ocular rosacea in 16%. Less frequently, the granulomatous variant was seen in 3% of patients, and steroid rosacea was noted in 12% patients.¹⁴

Recognizing the signs of rosacea may be a challenge, particularly erythema and telangiectasia. Tips for making an accurate diagnosis include use of adequate lighting, blanching of the skin (Figure 1), photography of the affected area against a dark blue background, and dermatoscopic examination.³ Furthermore, a thorough medical history, especially when evaluating the presence of facial erythema and identifying triggers, may help reach the correct diagnosis. Careful examination of the distribution of papules and pustules as well as the morphology and color of the papules in SOC patients also may provide diagnostic clues.

Differential Diagnosis and Distinguishing Features

Several disorders are included in the differential diagnosis of rosacea and may confound a correct rosacea diagnosis, including systemic lupus erythematosus (SLE), seborrheic dermatitis, dermatomyositis, acne vulgaris, sarcoidosis, and steroid dermatitis. Many of these disorders also occur more commonly in patients with SOC; therefore, it is important to clearly distinguish these entities from rosacea in this population.

Systemic Lupus Erythematosus
Systemic lupus erythematosus is an autoimmune disease that commonly presents with erythema as well as erythematous inflammatory facial lesions similar to rosacea. The classic clinical appearance of SLE is the butterfly or malar rash, an erythematous macular eruption on the malar region of the face that also may involve the nose. This rash can appear similar to rosacea; however, the malar rash classically spares the nasolabial folds, while erythema of rosacea often involves this anatomic boundary. Although the facial erythema in both SLE and early stages of rosacea may be patchy and similar in presentation, the presence of papules and pustules rarely occurs in SLE and may help to differentiate SLE from certain variants of rosacea.¹⁵

Seborrheic Dermatitis
Seborrheic dermatitis is a frequent cause of facial erythema linked to the Malassezia yeast species in susceptible individuals. Seborrheic dermatitis has a notable prevalence in women of African descent and often is considered normal by these patients.²¹ Rosacea and seborrheic dermatitis are relatively common dermatoses and therefore can present concurrently. In both diseases, facial erythema may be difficult to discern upon cursory inspection. Seborrheic dermatitis may be distinguished from rosacea by the clinical appearance of erythematous patches and plaques involving the scalp, anterior and posterior hairlines, preauricular and postauricular areas, and medial eyebrows. Both seborrheic dermatitis and rosacea may involve the nasolabial folds, but the presence of scale in seborrheic dermatitis is a distinguishing feature. Scale may vary in appearance from thick, greasy, and yellowish to fine, thin, and whitish.²² In contrast to rosacea, the erythematous lesions of seborrheic dermatitis often are annular in configuration. Furthermore, postinflammatory hypopigmentation and, to a lesser extent, postinflammatory hyperpigmentation are key clinical components of seborrheic dermatitis in SOC patients but are not as commonly observed in rosacea.

Dermatomyositis
Dermatomyositis is a systemic autoimmune disease characterized by progressive and symmetric proximal musculoskeletal weakness and cutaneous findings. Facial erythema in the malar and nasolabial folds can be seen in patients with dermatomyositis¹⁸; however, the facial erythema seen in dermatomyositis, known as heliotrope rash, has a violaceous dusky quality and also involves the periorbital region. The violaceous hue and periorbital involvement are distinguishing features from rosacea. Okiyama et al²³ described facial macular violaceous erythema with scale and edema in Japanese patients with dermatomyositis on the nasolabial folds, eyebrows, chin, cheeks, and ears; they also described mild atrophy with telangiectasia. Other clinical signs to help distinguish rosacea from dermatomyositis are the presence of edema of the face and extremities, Gottron papules, and poikiloderma. Dermatomyositis is a disease that affects all races; however, it is 4 times more common in black vs white patients,²⁴ making it even more important to be able to distinguish between these conditions.

Acne Vulgaris
Acne vulgaris, the most commonly diagnosed dermatosis in patients with SOC, is characterized by papules, pustules, cysts, nodules, open and closed comedones, and hyperpigmented macules on the face, chest, and back.^25,26 The absence of comedonal lesions and the presence of hyperpigmented macules distinguishes acne vulgaris from rosacea in this population.¹ In addition, the absence of telangiectasia and flushing are important distinguishing factors when making the diagnosis of acne vulgaris.

Sarcoidosis
Sarcoidosis is a multisystem inflammatory disease characterized histologically by the presence of noncaseating granulomas in sites such as the lungs, lymph nodes, eyes, nervous system, liver, spleen, heart, and skin.²⁷ Cutaneous sarcoidosis is known as a great mimicker of many other dermatoses, as it may present with multiple morphologic features. Cutaneous sarcoidosis most typically presents as papules, but nodules, plaques, lupus pernio, subcutaneous infiltrates, and infiltration of scars also have been identified.²⁸ Sarcoid papules typically are 1 to 5 mm in size on the face, neck, and periorbital skin²⁹; they are initially orange or yellow-brown in color, turn brownish red or violaceous, then involute to form faint macules.³⁰ Papular lesions may either resolve or evolve into plaques, particularly on the extremities, face, scalp, back, and buttocks. Additionally, there are a few case reports of patients with cutaneous sarcoidosis presenting with large bulbous nasal masses initially thought to be rhinophyma.^31-33 Finally, it may be difficult to distinguish sarcoidosis from granulomatous rosacea, which is characterized by firm yellow, brown, violaceous, red, or flesh-colored monomorphic papules or nodules affecting the perioral, periocular, medial, and/or lateral areas of the face (Figure 2).^4,34 Patients also can have unilateral disease.³⁵ Patients with granulomatous rosacea lack flushing and erythema as seen in more characteristic presentations of rosacea. They may report pain, pruritus, or burning, or they may be asymptomatic.³⁶ Features that distinguish granulomatous rosacea from sarcoidosis include the absence of nodules, plaques, lupus pernio, subcutaneous infiltrates, and infiltration of scars. Clinical, histological, and radiographic evaluation are necessary to make the diagnosis of sarcoidosis over rosacea.

Final Thoughts

Rosacea has features common to many other facial dermatoses, making the diagnosis challenging, particularly in patients with SOC. This difficulty in diagnosis may contribute to an underestimation of the prevalence of this disease in SOC patients. An understanding of rosacea, its nuances in clinical appearance, and its mimickers in SOC patients is important in making an accurate diagnosis.

References

Rosacea is a chronic inflammatory cutaneous disorder that affects the vasculature and pilosebaceous units of the face. Delayed and misdiagnosed rosacea in the SOC population has led to increased morbidity in this patient population. ^1-3 It is characterized by facial flushing and warmth, erythema, telangiectasia, papules, and pustules. The 4 major subtypes include erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea. ⁴ Granulomatous rosacea is considered to be a unique variant of rosacea. Until recently, rosacea was thought to predominately affect lighter-skinned individuals of Celtic and northern European origin. ^5,6 A paucity of studies and case reports in the literature have contributed to the commonly held belief that rosacea occurs infrequently in patients with skin of color (SOC). ¹ A PubMed search of articles indexed for MEDLINE revealed 32 results using the terms skin of color and rosacea vs 3786 using the term rosacea alone. It is possible that the nuance involved in appreciating erythema or other clinical manifestations of rosacea in SOC patients has led to underdiagnosis. Alternatively, these patients may be unaware that their symptoms represent a disease process and do not seek treatment. Many patients with darker skin will have endured rosacea for months or even years because the disease has been unrecognized or misdiagnosed. ^6-8 Another factor possibly accounting for the perception that rosacea occurs infrequently in patients with SOC is misdiagnosis of rosacea as other diseases that are known to occur more commonly in the SOC population. Dermatologists should be aware that rosacea can affect SOC patients and that there are several rosacea mimickers to be considered and excluded when making the rosacea diagnosis in this patient population. To promote accurate and timely diagnosis of rosacea, we review several possible rosacea mimickers in SOC patients and highlight the distinguishing features.

Epidemiology

In 2018, a meta-analysis of published studies on rosacea estimated the global prevalence in all adults to be 5.46%.⁹ A multicenter study across 6 cities in Colombia identified 291 outpatients with rosacea; of them, 12.4% had either Fitzpatrick skin types IV or V.¹⁰ A study of 2743 Angolan adults with Fitzpatrick skin types V and VI reported that only 0.4% of patients had a diagnosis of rosacea.¹¹ A Saudi study of 50 dark-skinned female patients with rosacea revealed 40% (20/50), 18% (9/50), and 42% (21/50) were Fitzpatrick skin types IV, V, and VI, respectively.¹² The prevalence of rosacea in SOC patients in the United States is less defined. Data from the US National Ambulatory Medical Care Survey (1993-2010) of 31.5 million rosacea visits showed that 2% of rosacea patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino.⁸

Clinical Features

Each of the 4 major rosacea subtypes can present in the SOC population. The granulomatous variant has been predominantly reported in black patients.¹³ This predilection has been attributed to either an increased susceptibility in black patients to develop this variant or a delay in diagnosis of earlier phases of inflammatory rosacea.⁷

In a Saudi study (N=50), severe erythematotelangiectatic rosacea was diagnosed in 42% (21/50) of patients, with the majority having Fitzpatrick skin type IV. The severe papulopustular subtype was seen in 14% (7/50) of patients, with 20% (10/50) and 14% (7/50) having Fitzpatrick skin types IV and VI, respectively.¹² In a Tunisian study (N=244), erythematotelangiectatic rosacea was seen in 12% of patients, papulopustular rosacea in 69%, phymatous rosacea in 4%, and ocular rosacea in 16%. Less frequently, the granulomatous variant was seen in 3% of patients, and steroid rosacea was noted in 12% patients.¹⁴

Recognizing the signs of rosacea may be a challenge, particularly erythema and telangiectasia. Tips for making an accurate diagnosis include use of adequate lighting, blanching of the skin (Figure 1), photography of the affected area against a dark blue background, and dermatoscopic examination.³ Furthermore, a thorough medical history, especially when evaluating the presence of facial erythema and identifying triggers, may help reach the correct diagnosis. Careful examination of the distribution of papules and pustules as well as the morphology and color of the papules in SOC patients also may provide diagnostic clues.

Differential Diagnosis and Distinguishing Features

Several disorders are included in the differential diagnosis of rosacea and may confound a correct rosacea diagnosis, including systemic lupus erythematosus (SLE), seborrheic dermatitis, dermatomyositis, acne vulgaris, sarcoidosis, and steroid dermatitis. Many of these disorders also occur more commonly in patients with SOC; therefore, it is important to clearly distinguish these entities from rosacea in this population.

Systemic Lupus Erythematosus
Systemic lupus erythematosus is an autoimmune disease that commonly presents with erythema as well as erythematous inflammatory facial lesions similar to rosacea. The classic clinical appearance of SLE is the butterfly or malar rash, an erythematous macular eruption on the malar region of the face that also may involve the nose. This rash can appear similar to rosacea; however, the malar rash classically spares the nasolabial folds, while erythema of rosacea often involves this anatomic boundary. Although the facial erythema in both SLE and early stages of rosacea may be patchy and similar in presentation, the presence of papules and pustules rarely occurs in SLE and may help to differentiate SLE from certain variants of rosacea.¹⁵

Seborrheic Dermatitis
Seborrheic dermatitis is a frequent cause of facial erythema linked to the Malassezia yeast species in susceptible individuals. Seborrheic dermatitis has a notable prevalence in women of African descent and often is considered normal by these patients.²¹ Rosacea and seborrheic dermatitis are relatively common dermatoses and therefore can present concurrently. In both diseases, facial erythema may be difficult to discern upon cursory inspection. Seborrheic dermatitis may be distinguished from rosacea by the clinical appearance of erythematous patches and plaques involving the scalp, anterior and posterior hairlines, preauricular and postauricular areas, and medial eyebrows. Both seborrheic dermatitis and rosacea may involve the nasolabial folds, but the presence of scale in seborrheic dermatitis is a distinguishing feature. Scale may vary in appearance from thick, greasy, and yellowish to fine, thin, and whitish.²² In contrast to rosacea, the erythematous lesions of seborrheic dermatitis often are annular in configuration. Furthermore, postinflammatory hypopigmentation and, to a lesser extent, postinflammatory hyperpigmentation are key clinical components of seborrheic dermatitis in SOC patients but are not as commonly observed in rosacea.

Dermatomyositis
Dermatomyositis is a systemic autoimmune disease characterized by progressive and symmetric proximal musculoskeletal weakness and cutaneous findings. Facial erythema in the malar and nasolabial folds can be seen in patients with dermatomyositis¹⁸; however, the facial erythema seen in dermatomyositis, known as heliotrope rash, has a violaceous dusky quality and also involves the periorbital region. The violaceous hue and periorbital involvement are distinguishing features from rosacea. Okiyama et al²³ described facial macular violaceous erythema with scale and edema in Japanese patients with dermatomyositis on the nasolabial folds, eyebrows, chin, cheeks, and ears; they also described mild atrophy with telangiectasia. Other clinical signs to help distinguish rosacea from dermatomyositis are the presence of edema of the face and extremities, Gottron papules, and poikiloderma. Dermatomyositis is a disease that affects all races; however, it is 4 times more common in black vs white patients,²⁴ making it even more important to be able to distinguish between these conditions.

Acne Vulgaris
Acne vulgaris, the most commonly diagnosed dermatosis in patients with SOC, is characterized by papules, pustules, cysts, nodules, open and closed comedones, and hyperpigmented macules on the face, chest, and back.^25,26 The absence of comedonal lesions and the presence of hyperpigmented macules distinguishes acne vulgaris from rosacea in this population.¹ In addition, the absence of telangiectasia and flushing are important distinguishing factors when making the diagnosis of acne vulgaris.

Sarcoidosis
Sarcoidosis is a multisystem inflammatory disease characterized histologically by the presence of noncaseating granulomas in sites such as the lungs, lymph nodes, eyes, nervous system, liver, spleen, heart, and skin.²⁷ Cutaneous sarcoidosis is known as a great mimicker of many other dermatoses, as it may present with multiple morphologic features. Cutaneous sarcoidosis most typically presents as papules, but nodules, plaques, lupus pernio, subcutaneous infiltrates, and infiltration of scars also have been identified.²⁸ Sarcoid papules typically are 1 to 5 mm in size on the face, neck, and periorbital skin²⁹; they are initially orange or yellow-brown in color, turn brownish red or violaceous, then involute to form faint macules.³⁰ Papular lesions may either resolve or evolve into plaques, particularly on the extremities, face, scalp, back, and buttocks. Additionally, there are a few case reports of patients with cutaneous sarcoidosis presenting with large bulbous nasal masses initially thought to be rhinophyma.^31-33 Finally, it may be difficult to distinguish sarcoidosis from granulomatous rosacea, which is characterized by firm yellow, brown, violaceous, red, or flesh-colored monomorphic papules or nodules affecting the perioral, periocular, medial, and/or lateral areas of the face (Figure 2).^4,34 Patients also can have unilateral disease.³⁵ Patients with granulomatous rosacea lack flushing and erythema as seen in more characteristic presentations of rosacea. They may report pain, pruritus, or burning, or they may be asymptomatic.³⁶ Features that distinguish granulomatous rosacea from sarcoidosis include the absence of nodules, plaques, lupus pernio, subcutaneous infiltrates, and infiltration of scars. Clinical, histological, and radiographic evaluation are necessary to make the diagnosis of sarcoidosis over rosacea.

Final Thoughts

Rosacea has features common to many other facial dermatoses, making the diagnosis challenging, particularly in patients with SOC. This difficulty in diagnosis may contribute to an underestimation of the prevalence of this disease in SOC patients. An understanding of rosacea, its nuances in clinical appearance, and its mimickers in SOC patients is important in making an accurate diagnosis.

References

As the rest of the industrialized world has seen a decline in maternal mortality, the United States has seen a substantial rise over the last 30 years (FIGURE).¹ It is estimated that more than 60% of these pregnancy-related deaths are preventable. Additionally, substantial disparities exist, with African-American women 3 to 4 times more likely to die of pregnancy-related complications than white women.¹

A good first step

The Preventing Maternal Deaths Act was passed by the 115th Congress and signed into law December 2018 in an effort to support and expand maternal mortality review committees (MMRCs) on a state level while allowing the Centers for Disease Control and Prevention (CDC) to further study disparities within maternal mortality. Although these efforts are a good first step to help reduce maternal mortality, more needs to be done to quell this growing epidemic.

We must now improve care access

One strategy to aid in decreasing maternal morbidity and mortality is to improve affordable access to medical care. Medicaid is the largest single payer of maternity care in the United States, covering 42.6% of births. Currently, in many states, Medicaid coverage only lasts until a woman is 60 days postpartum.² Although 31 states, including the District of Columbia, have adopted Medicaid expansion programs to allow women to extend coverage beyond those 60 days, offering these programs is not a federal law. In the 19 remaining states with no extension options, the vast majority of women will lose their Medicaid coverage just after they are 2 months postpartum and will have no alternative health insurance coverage.²

Why does this coverage cutoff matter? Pregnancy-related deaths are defined as up to 12 months postpartum. A report reviewing 9 MMRCs found that 38% of pregnancy-related deaths occurred while a woman was pregnant, 45% of deaths occurred within 42 days of delivery, and 18% from 43 days to 1 year after delivery.³ Additionally, nearly half of women with Medicaid do not come to their 6-week postpartum visit (for a variety of reasons), missing a critical opportunity to address health concerns.² Of the deaths that occurred in this later postpartum period, leading causes were cardiomyopathy (32%), mental health conditions (16%), and embolism (11%).³ Prevention and management of these conditions require regular follow-up with an ObGyn, as well as potentially from subspecialists in cardiology, psychiatry, hematology, and other subspecialties. Women not having access to affordable health care during the critical postpartum period greatly increases their risk of death or severe morbidity.

An important next step beyond the Preventing Maternal Deaths Act is to extend Medicaid coverage to 12 months postpartum for all women everywhere. MMRCs have concluded that extending coverage would ensure that “medical and behavioral health conditions [could be] managed and treated before becoming progressively severe.”³ This would presumably help decrease the risk of pregnancy-related death and address worsening morbidity. Additionally, the postpartum period is a well-established time of increased stress and can be an overwhelming and emotional time for many new mothers, especially for those with limited resources for childcare, transportation, stable housing, etc.⁶ Providing and ensuring ongoing medical care would substantially improve the lives and health of women and the health of their families.

We, as a country, need to make changes

Every step of the way, a woman faces challenges to safely and affordably access health care. Providing access to insurance coverage for 12 months postpartum can help to decrease our country’s rising maternal mortality and morbidity rates.

Take action

Congresswoman Robin Kelly (D-IL) and Senator Dick Durbin (D-IL) have introduced the MOMMA Act (H.R. 1897/S. 916) to help address the rising maternal mortality rate.

This Act would:

• Expand Medicaid coverage to 1 year postpartum.
• Work with the CDC to uniformly collect data to accurately assess maternal mortality and morbidity.
• Ensure the sharing of best practices of care across hospital systems.
• Focus on culturally-competent care to address implicit bias among health care workers.
• Support and expand the Alliance for Innovation on Maternal Health (AIM)—a data-driven initiative to implement safety protocols in hospitals across the country.

To call or contact your representative to co-sponsor this bill, click here. To review if your Congressperson is a co-sponsor, click here. To review if your Senator is a co-sponsor, click here.
 

As the rest of the industrialized world has seen a decline in maternal mortality, the United States has seen a substantial rise over the last 30 years (FIGURE).¹ It is estimated that more than 60% of these pregnancy-related deaths are preventable. Additionally, substantial disparities exist, with African-American women 3 to 4 times more likely to die of pregnancy-related complications than white women.¹

A good first step

The Preventing Maternal Deaths Act was passed by the 115th Congress and signed into law December 2018 in an effort to support and expand maternal mortality review committees (MMRCs) on a state level while allowing the Centers for Disease Control and Prevention (CDC) to further study disparities within maternal mortality. Although these efforts are a good first step to help reduce maternal mortality, more needs to be done to quell this growing epidemic.

We must now improve care access

One strategy to aid in decreasing maternal morbidity and mortality is to improve affordable access to medical care. Medicaid is the largest single payer of maternity care in the United States, covering 42.6% of births. Currently, in many states, Medicaid coverage only lasts until a woman is 60 days postpartum.² Although 31 states, including the District of Columbia, have adopted Medicaid expansion programs to allow women to extend coverage beyond those 60 days, offering these programs is not a federal law. In the 19 remaining states with no extension options, the vast majority of women will lose their Medicaid coverage just after they are 2 months postpartum and will have no alternative health insurance coverage.²

Why does this coverage cutoff matter? Pregnancy-related deaths are defined as up to 12 months postpartum. A report reviewing 9 MMRCs found that 38% of pregnancy-related deaths occurred while a woman was pregnant, 45% of deaths occurred within 42 days of delivery, and 18% from 43 days to 1 year after delivery.³ Additionally, nearly half of women with Medicaid do not come to their 6-week postpartum visit (for a variety of reasons), missing a critical opportunity to address health concerns.² Of the deaths that occurred in this later postpartum period, leading causes were cardiomyopathy (32%), mental health conditions (16%), and embolism (11%).³ Prevention and management of these conditions require regular follow-up with an ObGyn, as well as potentially from subspecialists in cardiology, psychiatry, hematology, and other subspecialties. Women not having access to affordable health care during the critical postpartum period greatly increases their risk of death or severe morbidity.

An important next step beyond the Preventing Maternal Deaths Act is to extend Medicaid coverage to 12 months postpartum for all women everywhere. MMRCs have concluded that extending coverage would ensure that “medical and behavioral health conditions [could be] managed and treated before becoming progressively severe.”³ This would presumably help decrease the risk of pregnancy-related death and address worsening morbidity. Additionally, the postpartum period is a well-established time of increased stress and can be an overwhelming and emotional time for many new mothers, especially for those with limited resources for childcare, transportation, stable housing, etc.⁶ Providing and ensuring ongoing medical care would substantially improve the lives and health of women and the health of their families.

We, as a country, need to make changes

Every step of the way, a woman faces challenges to safely and affordably access health care. Providing access to insurance coverage for 12 months postpartum can help to decrease our country’s rising maternal mortality and morbidity rates.

Take action

Congresswoman Robin Kelly (D-IL) and Senator Dick Durbin (D-IL) have introduced the MOMMA Act (H.R. 1897/S. 916) to help address the rising maternal mortality rate.

This Act would:

• Expand Medicaid coverage to 1 year postpartum.
• Work with the CDC to uniformly collect data to accurately assess maternal mortality and morbidity.
• Ensure the sharing of best practices of care across hospital systems.
• Focus on culturally-competent care to address implicit bias among health care workers.
• Support and expand the Alliance for Innovation on Maternal Health (AIM)—a data-driven initiative to implement safety protocols in hospitals across the country.

To call or contact your representative to co-sponsor this bill, click here. To review if your Congressperson is a co-sponsor, click here. To review if your Senator is a co-sponsor, click here.
 

As the rest of the industrialized world has seen a decline in maternal mortality, the United States has seen a substantial rise over the last 30 years (FIGURE).¹ It is estimated that more than 60% of these pregnancy-related deaths are preventable. Additionally, substantial disparities exist, with African-American women 3 to 4 times more likely to die of pregnancy-related complications than white women.¹

A good first step

The Preventing Maternal Deaths Act was passed by the 115th Congress and signed into law December 2018 in an effort to support and expand maternal mortality review committees (MMRCs) on a state level while allowing the Centers for Disease Control and Prevention (CDC) to further study disparities within maternal mortality. Although these efforts are a good first step to help reduce maternal mortality, more needs to be done to quell this growing epidemic.

We must now improve care access

One strategy to aid in decreasing maternal morbidity and mortality is to improve affordable access to medical care. Medicaid is the largest single payer of maternity care in the United States, covering 42.6% of births. Currently, in many states, Medicaid coverage only lasts until a woman is 60 days postpartum.² Although 31 states, including the District of Columbia, have adopted Medicaid expansion programs to allow women to extend coverage beyond those 60 days, offering these programs is not a federal law. In the 19 remaining states with no extension options, the vast majority of women will lose their Medicaid coverage just after they are 2 months postpartum and will have no alternative health insurance coverage.²

Why does this coverage cutoff matter? Pregnancy-related deaths are defined as up to 12 months postpartum. A report reviewing 9 MMRCs found that 38% of pregnancy-related deaths occurred while a woman was pregnant, 45% of deaths occurred within 42 days of delivery, and 18% from 43 days to 1 year after delivery.³ Additionally, nearly half of women with Medicaid do not come to their 6-week postpartum visit (for a variety of reasons), missing a critical opportunity to address health concerns.² Of the deaths that occurred in this later postpartum period, leading causes were cardiomyopathy (32%), mental health conditions (16%), and embolism (11%).³ Prevention and management of these conditions require regular follow-up with an ObGyn, as well as potentially from subspecialists in cardiology, psychiatry, hematology, and other subspecialties. Women not having access to affordable health care during the critical postpartum period greatly increases their risk of death or severe morbidity.

An important next step beyond the Preventing Maternal Deaths Act is to extend Medicaid coverage to 12 months postpartum for all women everywhere. MMRCs have concluded that extending coverage would ensure that “medical and behavioral health conditions [could be] managed and treated before becoming progressively severe.”³ This would presumably help decrease the risk of pregnancy-related death and address worsening morbidity. Additionally, the postpartum period is a well-established time of increased stress and can be an overwhelming and emotional time for many new mothers, especially for those with limited resources for childcare, transportation, stable housing, etc.⁶ Providing and ensuring ongoing medical care would substantially improve the lives and health of women and the health of their families.

We, as a country, need to make changes

Every step of the way, a woman faces challenges to safely and affordably access health care. Providing access to insurance coverage for 12 months postpartum can help to decrease our country’s rising maternal mortality and morbidity rates.

Take action

Congresswoman Robin Kelly (D-IL) and Senator Dick Durbin (D-IL) have introduced the MOMMA Act (H.R. 1897/S. 916) to help address the rising maternal mortality rate.

This Act would:

• Expand Medicaid coverage to 1 year postpartum.
• Work with the CDC to uniformly collect data to accurately assess maternal mortality and morbidity.
• Ensure the sharing of best practices of care across hospital systems.
• Focus on culturally-competent care to address implicit bias among health care workers.
• Support and expand the Alliance for Innovation on Maternal Health (AIM)—a data-driven initiative to implement safety protocols in hospitals across the country.

To call or contact your representative to co-sponsor this bill, click here. To review if your Congressperson is a co-sponsor, click here. To review if your Senator is a co-sponsor, click here.
 

Acral lentiginous melanoma (ALM) is a rare subtype of melanoma that occurs on the palms, soles, and nail apparatus. Unlike more common types of melanoma, ALM occurs on sun-protected areas of the skin and has distinct clinical, histologic, and genetic features. Acral lentiginous melanoma accounts for a larger proportion of melanomas in individuals with skin of color and has a worse prognosis and recurrence rate than other forms of melanoma.

Population Trends in Skin of Color

Much of the literature on malignant melanoma historically has involved non-Hispanic white patients, but the incidence in lighter-skinned populations has been increasing steadily over the last few decades.¹ Although ALM can occur in any race, it disproportionately affects skin of color populations; ALM accounts for only 0.8% to 1% of all melanomas in white populations, but it constitutes 4% to 58% of melanomas in ethnic populations and is the most common melanoma subtype among black Americans.^2-5 Acral lentiginous melanoma also is associated with a worse prognosis compared to other subtypes, which may indicate a more aggressive biological nature⁶ but also may point toward socioeconomic and cultural barriers (eg, low income or education levels, lack of insurance, lower health literacy), leading to disparities in access to care and diagnosis at advanced stages.⁵

Similarly, the distribution of acral melanocytic nevi appears to demonstrate an association with ethnicity and skin pigmentation. Although skin of color patients have fewer nevi than non-Hispanic whites, the proportion of acral melanocytic nevi tends to be greater.^6,7 Given its grim prognosis, accurately differentiating ALM from acral nevi is of utmost importance.

Diagnostic Challenges of Acral Lesions

Due to the unique nature of the surfaces of acral sites, melanocytic lesions on the palms, soles, and nail apparatus present many diagnostic challenges. It can be difficult to distinguish acral melanoma from benign lesions using the naked eye alone. Volar surfaces are characterized by the presence of dermatoglyphics, and pigment deposition along ridges and furrows create particular dermoscopic patterns exclusive to these sites.⁸ Thus, dermoscopy can be useful on acral surfaces, but the dermoscopic features are different from those on the rest of the body and must be learned separately.

In addition, nearly half of patients are unaware of their acral lesions.⁶ Acral surfaces may not always be examined by clinicians during total-body skin examinations, leading to further possibility of overlooking a lesion. Obtaining biopsies on glabrous skin or nails also is challenging because they can be more painful and hemostasis can be more difficult, especially in the nail. Acral melanomas also may be amelanotic, including those at subungual sites. Although the overall incidence of amelanotic ALM is low, approximately 20% to 28% of amelanotic melanomas in Asian patients are located on acral sites.⁹ Due to these challenges, acral lesions may be overlooked or misdiagnosed as warts,¹⁰ tinea pedis,¹¹ or traumatic ulcers.¹²

Dermoscopic Patterns of Acral Volar Skin

Dermoscopy is a useful noninvasive tool for distinguishing between benign and malignant acral melanocytic lesions, and its efficacy in improving diagnostic accuracy and decreasing unnecessary biopsies is well-established in the literature.^13,14 Acral dermoscopy allows for visualization of pigment along the dermatoglyphics that constitute the characteristic dermoscopic patterns.

Acral Lentiginous Melanoma
The hallmark dermoscopic pattern and most important finding of ALM is the parallel ridge pattern, characterized by parallel linear pigmentation along the ridges of dermatoglyphics. In the early phases of malignancy, the pattern appears light brown and involves most of the lesion; as the tumor develops, increasing melanin production results in focal areas of the parallel ridge pattern with darker bands.^15,16 The sensitivity and specificity of a parallel ridge pattern for diagnosing early ALM has been shown to be 86% and 99%, respectively.^15,16

A pattern of irregular diffuse pigmentation also can be observed in more advanced ALM. Dermoscopy may reveal a structureless pattern (ie, lack of identifiable structures or patterns) in a background of tan-black coloration due to more exuberant melanocyte proliferation along the epidermis.¹⁵ Sensitivity and specificity of this dermoscopic finding for invasive lesions is high at 94% and 97%, respectively.^16,17 Interestingly, once ALM lesions have advanced even further, conventional melanoma-associated structures (ie, blue-white veil, polymorphous blood vessels, ulceration, irregular dots/globules or streaks) or atypical forms of typically benign acral dermoscopic patterns may be observed.¹⁵

Per a 3-step diagnostic algorithm created by Koga and Saida,¹⁸ a suspected acral lesion should first be evaluated for a parallel ridge pattern to determine the need for biopsy, as it is seen in approximately two-thirds of ALMs.¹⁹ If no parallel ridge pattern is observed, the lesion should then be checked for any of the typical dermoscopic patterns seen in benign acral nevi (eg, parallel furrow, latticelike, or fibrillar patterns).¹⁸ The maximum diameter should be measured only if the lesion does not exhibit any of the typical dermoscopic patterns. If the lesion’s diameter is greater than 7 mm in diameter, it should be biopsied; if the diameter is less than 7 mm, it should have regular clinical and dermoscopic follow-up.¹⁸

In 2015, Lallas et al²⁰ developed the BRAAFF checklist, a scoring system of 6 variables: blotches, ridge pattern, asymmetry of structures, asymmetry of colors, parallel furrow pattern, and fibrillar pattern. The checklist also was shown to substantially improve diagnostic accuracy of dermoscopy for ALM, with sensitivity and specificity at 93.1% and 86.7%, respectively.²⁰

Acquired Acral Nevi
Three classic dermoscopic patterns are associated with acquired acral nevi: parallel furrow pattern, latticelike pattern, and fibrillar pattern.^15,21 Approximately three-quarters of all acquired acral nevi exhibit one of these patterns, roughly half exhibiting parallel furrow with tan-brown bandlike pigmentation along dermatoglyphic grooves.^16,17

Latticelike patterns also are characterized by brown parallel lines along the sulci of dermatoglyphics but additionally have multiple intersecting lines. Thus, this pattern can be considered a variant of the parallel furrow pattern.¹⁵ The crisscross markings can be predominantly found in the plantar arch.²² This dermoscopic pattern comprises 15% to 25% of all acral nevi.²¹

Fibrillar pattern accounts for 10% to 20% of all acral melanocytic nevi.²¹ Dermoscopically, these lesions demonstrate parallel filamentous streaks that cross dermatoglyphics obliquely. The fibrillar pattern is predominantly found on weight-bearing areas of the sole,²² which likely is explained by pressure causing slanting of melanin columns in the horny layer.²³ The fibrillar pattern has been shown to be the benign acral dermoscopic pattern that is most commonly misdiagnosed, with higher reported rates of biopsy.²⁴

Acral Congenital Melanocytic Nevi
Congenital melanocytic nevi (CMN) present at birth or appear during the first few weeks of life. Congenital melanocytic nevi can vary widely in size, shape, and color, and they are occasionally biopsied in cases of larger diameter or dermoscopic atypia to differentiate from melanoma.²⁵ Congenital melanocytic nevi also can occur on acral volar surfaces. Possible dermoscopic patterns include parallel furrow or fibrillar patterns as well as a crista dotted pattern, defined as evenly spaced dots/globules on the ridges near the openings of eccrine ducts.²⁶ A more commonly observed dermoscopic pattern in acral CMN is a combination of the crista dotted and parallel furrow patterns, known as the peas-in-a-pod pattern. Changes in the clinical appearance and dermoscopic features of an acral CMN are possible over time; some lesions also may fade with age.²⁶

Final Thoughts

Acral lentiginous melanoma is a rare but potentially aggressive melanoma subtype that accounts for a larger proportion of melanomas in patients with skin of color than in white patients. Dermoscopy of acral volar skin provides invaluable diagnostic information and allows for better management of acral melanocytic lesions. Dermoscopic patterns such as the parallel ridge, parallel furrow, latticelike, fibrillar, and peas-in-a-pod patterns are unique to acral sites and can be used to differentiate between ALMs, acquired nevi, or CMNs.

Acral lentiginous melanoma (ALM) is a rare subtype of melanoma that occurs on the palms, soles, and nail apparatus. Unlike more common types of melanoma, ALM occurs on sun-protected areas of the skin and has distinct clinical, histologic, and genetic features. Acral lentiginous melanoma accounts for a larger proportion of melanomas in individuals with skin of color and has a worse prognosis and recurrence rate than other forms of melanoma.

Population Trends in Skin of Color

Much of the literature on malignant melanoma historically has involved non-Hispanic white patients, but the incidence in lighter-skinned populations has been increasing steadily over the last few decades.¹ Although ALM can occur in any race, it disproportionately affects skin of color populations; ALM accounts for only 0.8% to 1% of all melanomas in white populations, but it constitutes 4% to 58% of melanomas in ethnic populations and is the most common melanoma subtype among black Americans.^2-5 Acral lentiginous melanoma also is associated with a worse prognosis compared to other subtypes, which may indicate a more aggressive biological nature⁶ but also may point toward socioeconomic and cultural barriers (eg, low income or education levels, lack of insurance, lower health literacy), leading to disparities in access to care and diagnosis at advanced stages.⁵

Similarly, the distribution of acral melanocytic nevi appears to demonstrate an association with ethnicity and skin pigmentation. Although skin of color patients have fewer nevi than non-Hispanic whites, the proportion of acral melanocytic nevi tends to be greater.^6,7 Given its grim prognosis, accurately differentiating ALM from acral nevi is of utmost importance.

Diagnostic Challenges of Acral Lesions

Due to the unique nature of the surfaces of acral sites, melanocytic lesions on the palms, soles, and nail apparatus present many diagnostic challenges. It can be difficult to distinguish acral melanoma from benign lesions using the naked eye alone. Volar surfaces are characterized by the presence of dermatoglyphics, and pigment deposition along ridges and furrows create particular dermoscopic patterns exclusive to these sites.⁸ Thus, dermoscopy can be useful on acral surfaces, but the dermoscopic features are different from those on the rest of the body and must be learned separately.

In addition, nearly half of patients are unaware of their acral lesions.⁶ Acral surfaces may not always be examined by clinicians during total-body skin examinations, leading to further possibility of overlooking a lesion. Obtaining biopsies on glabrous skin or nails also is challenging because they can be more painful and hemostasis can be more difficult, especially in the nail. Acral melanomas also may be amelanotic, including those at subungual sites. Although the overall incidence of amelanotic ALM is low, approximately 20% to 28% of amelanotic melanomas in Asian patients are located on acral sites.⁹ Due to these challenges, acral lesions may be overlooked or misdiagnosed as warts,¹⁰ tinea pedis,¹¹ or traumatic ulcers.¹²

Dermoscopic Patterns of Acral Volar Skin

Dermoscopy is a useful noninvasive tool for distinguishing between benign and malignant acral melanocytic lesions, and its efficacy in improving diagnostic accuracy and decreasing unnecessary biopsies is well-established in the literature.^13,14 Acral dermoscopy allows for visualization of pigment along the dermatoglyphics that constitute the characteristic dermoscopic patterns.

Acral Lentiginous Melanoma
The hallmark dermoscopic pattern and most important finding of ALM is the parallel ridge pattern, characterized by parallel linear pigmentation along the ridges of dermatoglyphics. In the early phases of malignancy, the pattern appears light brown and involves most of the lesion; as the tumor develops, increasing melanin production results in focal areas of the parallel ridge pattern with darker bands.^15,16 The sensitivity and specificity of a parallel ridge pattern for diagnosing early ALM has been shown to be 86% and 99%, respectively.^15,16

A pattern of irregular diffuse pigmentation also can be observed in more advanced ALM. Dermoscopy may reveal a structureless pattern (ie, lack of identifiable structures or patterns) in a background of tan-black coloration due to more exuberant melanocyte proliferation along the epidermis.¹⁵ Sensitivity and specificity of this dermoscopic finding for invasive lesions is high at 94% and 97%, respectively.^16,17 Interestingly, once ALM lesions have advanced even further, conventional melanoma-associated structures (ie, blue-white veil, polymorphous blood vessels, ulceration, irregular dots/globules or streaks) or atypical forms of typically benign acral dermoscopic patterns may be observed.¹⁵

Per a 3-step diagnostic algorithm created by Koga and Saida,¹⁸ a suspected acral lesion should first be evaluated for a parallel ridge pattern to determine the need for biopsy, as it is seen in approximately two-thirds of ALMs.¹⁹ If no parallel ridge pattern is observed, the lesion should then be checked for any of the typical dermoscopic patterns seen in benign acral nevi (eg, parallel furrow, latticelike, or fibrillar patterns).¹⁸ The maximum diameter should be measured only if the lesion does not exhibit any of the typical dermoscopic patterns. If the lesion’s diameter is greater than 7 mm in diameter, it should be biopsied; if the diameter is less than 7 mm, it should have regular clinical and dermoscopic follow-up.¹⁸

In 2015, Lallas et al²⁰ developed the BRAAFF checklist, a scoring system of 6 variables: blotches, ridge pattern, asymmetry of structures, asymmetry of colors, parallel furrow pattern, and fibrillar pattern. The checklist also was shown to substantially improve diagnostic accuracy of dermoscopy for ALM, with sensitivity and specificity at 93.1% and 86.7%, respectively.²⁰

Acquired Acral Nevi
Three classic dermoscopic patterns are associated with acquired acral nevi: parallel furrow pattern, latticelike pattern, and fibrillar pattern.^15,21 Approximately three-quarters of all acquired acral nevi exhibit one of these patterns, roughly half exhibiting parallel furrow with tan-brown bandlike pigmentation along dermatoglyphic grooves.^16,17

Latticelike patterns also are characterized by brown parallel lines along the sulci of dermatoglyphics but additionally have multiple intersecting lines. Thus, this pattern can be considered a variant of the parallel furrow pattern.¹⁵ The crisscross markings can be predominantly found in the plantar arch.²² This dermoscopic pattern comprises 15% to 25% of all acral nevi.²¹

Fibrillar pattern accounts for 10% to 20% of all acral melanocytic nevi.²¹ Dermoscopically, these lesions demonstrate parallel filamentous streaks that cross dermatoglyphics obliquely. The fibrillar pattern is predominantly found on weight-bearing areas of the sole,²² which likely is explained by pressure causing slanting of melanin columns in the horny layer.²³ The fibrillar pattern has been shown to be the benign acral dermoscopic pattern that is most commonly misdiagnosed, with higher reported rates of biopsy.²⁴

Acral Congenital Melanocytic Nevi
Congenital melanocytic nevi (CMN) present at birth or appear during the first few weeks of life. Congenital melanocytic nevi can vary widely in size, shape, and color, and they are occasionally biopsied in cases of larger diameter or dermoscopic atypia to differentiate from melanoma.²⁵ Congenital melanocytic nevi also can occur on acral volar surfaces. Possible dermoscopic patterns include parallel furrow or fibrillar patterns as well as a crista dotted pattern, defined as evenly spaced dots/globules on the ridges near the openings of eccrine ducts.²⁶ A more commonly observed dermoscopic pattern in acral CMN is a combination of the crista dotted and parallel furrow patterns, known as the peas-in-a-pod pattern. Changes in the clinical appearance and dermoscopic features of an acral CMN are possible over time; some lesions also may fade with age.²⁶

Final Thoughts

Acral lentiginous melanoma is a rare but potentially aggressive melanoma subtype that accounts for a larger proportion of melanomas in patients with skin of color than in white patients. Dermoscopy of acral volar skin provides invaluable diagnostic information and allows for better management of acral melanocytic lesions. Dermoscopic patterns such as the parallel ridge, parallel furrow, latticelike, fibrillar, and peas-in-a-pod patterns are unique to acral sites and can be used to differentiate between ALMs, acquired nevi, or CMNs.

Acral lentiginous melanoma (ALM) is a rare subtype of melanoma that occurs on the palms, soles, and nail apparatus. Unlike more common types of melanoma, ALM occurs on sun-protected areas of the skin and has distinct clinical, histologic, and genetic features. Acral lentiginous melanoma accounts for a larger proportion of melanomas in individuals with skin of color and has a worse prognosis and recurrence rate than other forms of melanoma.

Population Trends in Skin of Color

Much of the literature on malignant melanoma historically has involved non-Hispanic white patients, but the incidence in lighter-skinned populations has been increasing steadily over the last few decades.¹ Although ALM can occur in any race, it disproportionately affects skin of color populations; ALM accounts for only 0.8% to 1% of all melanomas in white populations, but it constitutes 4% to 58% of melanomas in ethnic populations and is the most common melanoma subtype among black Americans.^2-5 Acral lentiginous melanoma also is associated with a worse prognosis compared to other subtypes, which may indicate a more aggressive biological nature⁶ but also may point toward socioeconomic and cultural barriers (eg, low income or education levels, lack of insurance, lower health literacy), leading to disparities in access to care and diagnosis at advanced stages.⁵

Similarly, the distribution of acral melanocytic nevi appears to demonstrate an association with ethnicity and skin pigmentation. Although skin of color patients have fewer nevi than non-Hispanic whites, the proportion of acral melanocytic nevi tends to be greater.^6,7 Given its grim prognosis, accurately differentiating ALM from acral nevi is of utmost importance.

Diagnostic Challenges of Acral Lesions

Due to the unique nature of the surfaces of acral sites, melanocytic lesions on the palms, soles, and nail apparatus present many diagnostic challenges. It can be difficult to distinguish acral melanoma from benign lesions using the naked eye alone. Volar surfaces are characterized by the presence of dermatoglyphics, and pigment deposition along ridges and furrows create particular dermoscopic patterns exclusive to these sites.⁸ Thus, dermoscopy can be useful on acral surfaces, but the dermoscopic features are different from those on the rest of the body and must be learned separately.

In addition, nearly half of patients are unaware of their acral lesions.⁶ Acral surfaces may not always be examined by clinicians during total-body skin examinations, leading to further possibility of overlooking a lesion. Obtaining biopsies on glabrous skin or nails also is challenging because they can be more painful and hemostasis can be more difficult, especially in the nail. Acral melanomas also may be amelanotic, including those at subungual sites. Although the overall incidence of amelanotic ALM is low, approximately 20% to 28% of amelanotic melanomas in Asian patients are located on acral sites.⁹ Due to these challenges, acral lesions may be overlooked or misdiagnosed as warts,¹⁰ tinea pedis,¹¹ or traumatic ulcers.¹²

Dermoscopic Patterns of Acral Volar Skin

Dermoscopy is a useful noninvasive tool for distinguishing between benign and malignant acral melanocytic lesions, and its efficacy in improving diagnostic accuracy and decreasing unnecessary biopsies is well-established in the literature.^13,14 Acral dermoscopy allows for visualization of pigment along the dermatoglyphics that constitute the characteristic dermoscopic patterns.

Acral Lentiginous Melanoma
The hallmark dermoscopic pattern and most important finding of ALM is the parallel ridge pattern, characterized by parallel linear pigmentation along the ridges of dermatoglyphics. In the early phases of malignancy, the pattern appears light brown and involves most of the lesion; as the tumor develops, increasing melanin production results in focal areas of the parallel ridge pattern with darker bands.^15,16 The sensitivity and specificity of a parallel ridge pattern for diagnosing early ALM has been shown to be 86% and 99%, respectively.^15,16

A pattern of irregular diffuse pigmentation also can be observed in more advanced ALM. Dermoscopy may reveal a structureless pattern (ie, lack of identifiable structures or patterns) in a background of tan-black coloration due to more exuberant melanocyte proliferation along the epidermis.¹⁵ Sensitivity and specificity of this dermoscopic finding for invasive lesions is high at 94% and 97%, respectively.^16,17 Interestingly, once ALM lesions have advanced even further, conventional melanoma-associated structures (ie, blue-white veil, polymorphous blood vessels, ulceration, irregular dots/globules or streaks) or atypical forms of typically benign acral dermoscopic patterns may be observed.¹⁵

Per a 3-step diagnostic algorithm created by Koga and Saida,¹⁸ a suspected acral lesion should first be evaluated for a parallel ridge pattern to determine the need for biopsy, as it is seen in approximately two-thirds of ALMs.¹⁹ If no parallel ridge pattern is observed, the lesion should then be checked for any of the typical dermoscopic patterns seen in benign acral nevi (eg, parallel furrow, latticelike, or fibrillar patterns).¹⁸ The maximum diameter should be measured only if the lesion does not exhibit any of the typical dermoscopic patterns. If the lesion’s diameter is greater than 7 mm in diameter, it should be biopsied; if the diameter is less than 7 mm, it should have regular clinical and dermoscopic follow-up.¹⁸

In 2015, Lallas et al²⁰ developed the BRAAFF checklist, a scoring system of 6 variables: blotches, ridge pattern, asymmetry of structures, asymmetry of colors, parallel furrow pattern, and fibrillar pattern. The checklist also was shown to substantially improve diagnostic accuracy of dermoscopy for ALM, with sensitivity and specificity at 93.1% and 86.7%, respectively.²⁰

Acquired Acral Nevi
Three classic dermoscopic patterns are associated with acquired acral nevi: parallel furrow pattern, latticelike pattern, and fibrillar pattern.^15,21 Approximately three-quarters of all acquired acral nevi exhibit one of these patterns, roughly half exhibiting parallel furrow with tan-brown bandlike pigmentation along dermatoglyphic grooves.^16,17

Latticelike patterns also are characterized by brown parallel lines along the sulci of dermatoglyphics but additionally have multiple intersecting lines. Thus, this pattern can be considered a variant of the parallel furrow pattern.¹⁵ The crisscross markings can be predominantly found in the plantar arch.²² This dermoscopic pattern comprises 15% to 25% of all acral nevi.²¹

Fibrillar pattern accounts for 10% to 20% of all acral melanocytic nevi.²¹ Dermoscopically, these lesions demonstrate parallel filamentous streaks that cross dermatoglyphics obliquely. The fibrillar pattern is predominantly found on weight-bearing areas of the sole,²² which likely is explained by pressure causing slanting of melanin columns in the horny layer.²³ The fibrillar pattern has been shown to be the benign acral dermoscopic pattern that is most commonly misdiagnosed, with higher reported rates of biopsy.²⁴

Acral Congenital Melanocytic Nevi
Congenital melanocytic nevi (CMN) present at birth or appear during the first few weeks of life. Congenital melanocytic nevi can vary widely in size, shape, and color, and they are occasionally biopsied in cases of larger diameter or dermoscopic atypia to differentiate from melanoma.²⁵ Congenital melanocytic nevi also can occur on acral volar surfaces. Possible dermoscopic patterns include parallel furrow or fibrillar patterns as well as a crista dotted pattern, defined as evenly spaced dots/globules on the ridges near the openings of eccrine ducts.²⁶ A more commonly observed dermoscopic pattern in acral CMN is a combination of the crista dotted and parallel furrow patterns, known as the peas-in-a-pod pattern. Changes in the clinical appearance and dermoscopic features of an acral CMN are possible over time; some lesions also may fade with age.²⁶

Final Thoughts

Acral lentiginous melanoma is a rare but potentially aggressive melanoma subtype that accounts for a larger proportion of melanomas in patients with skin of color than in white patients. Dermoscopy of acral volar skin provides invaluable diagnostic information and allows for better management of acral melanocytic lesions. Dermoscopic patterns such as the parallel ridge, parallel furrow, latticelike, fibrillar, and peas-in-a-pod patterns are unique to acral sites and can be used to differentiate between ALMs, acquired nevi, or CMNs.

Postnflammatory hyperpigmentation (PIH) is an acquired hypermelanosis that can occur in children and adults following an inflammatory cutaneous disease or trauma. Postinflammatory hyperpigmentation may last for months to even years. Although PIH may occur in all skin types, it is more common and presents with greater severity and intensity in individuals with skin of color. By the year 2050, 1 in 3 US residents is projected to be Hispanic.¹ It is projected that by 2044, non-Hispanic white individuals (all ages) will make up less than 50% of the US population.² Currently, the majority of the US residents younger than 18 years are minorities. The majority minority population in the United States already exists in those younger than 18 years and is predicted to occur in the adult population by 2044.²

Effective treatment options and management strategies for PIH in adults with skin of color have been described in the literature.³ Due to a paucity of research, the approach to management of PIH in children with skin of color has been based on clinical experience and lessons learned from adult patients. This article focuses on management of PIH in pediatric patients with skin of color, which includes black/African American, African-Caribbean, Hispanic, Asian, Pacific Islander, and American Indian individuals.

Underlying Inflammatory Dermatoses Resulting in PIH

There are numerous conditions that may result in PIH, including but not limited to atopic dermatitis (AD), acne, arthropod bites, and injuries to the skin. Postinflammatory hyperpigmentation may have more of a psychological impact than the inciting disease or injury itself. The most important step in the approach to managing PIH is treating the underlying inflammatory condition that caused the pigmentation.

Parents/guardians may report a chief concern of dark spots, manchas (stains), blemishes, or stains on the skin, often with no mention of a coexisting inflammatory dermatosis. Parents/guardians of children with skin of color often have personally experienced PIH and may be determined to shield their children from similar angst associated with the condition. Although physicians may see just another pediatric patient with PIH, the child’s parents/guardians may see a condition that will be readily perceptible during major life events, such as the child’s prom or even his/her wedding day. Promptly diagnosing and instituting early treatment of inflammatory conditions associated with PIH may accelerate resolution and prevent worsening of the pigmentation.³

Select inflammatory dermatoses that are common in children with skin of color and may lead to PIH are highlighted below. Although this list is not comprehensive, the approach and management strategies should prompt creation of plans that keep PIH in mind when treating primary inflammatory skin diseases.

Atopic Dermatitis
Atopic dermatitis may induce PIH or hypopigmentation of the skin in children with skin of color. Developing a plan for AD flare prevention, as well as management of mild, moderate, and severe AD flares, is imperative in pediatric patients. Prevention plans should include gentle skin care, twice-daily application of emollients to the full body, and reduction of Staphylococcus aureus loads on the skin. The treatment action plan for mild to moderate flares may include topical corticosteroids, immunomodulators, and nonsteroidal agents. Treatment options for severe AD or patients who were unsuccessfully treated with other therapies may include phototherapy, biologics, and methotrexate, among others.⁴ Creating action plans for AD flares is a vital step in the prevention of PIH in patients with skin of color. Additionally, PIH should not be considered a sign of AD treatment failure.

Acne
Acne is a common skin disorder seen in patients with skin of color.⁵ A prospective observational study found that 34.3% of 683 children aged 9 to 14 years in a pediatric ambulatory clinic had acne.⁶ The number of preadolescents with acne is growing. Most cases are not associated with underlying endocrinopathy.⁷ With the growing population of children with skin of color in the United States along with the increasing childhood acne rate and subsequent inherent risk for hyperpigmentation, early acne interventions should be considered in pediatric acne patients with skin of color to reduce the impact of PIH in those at risk.

In a survey study of 313 adult acne patients with skin of color, 37.2% reported the presence of dark marks lasting 4 months or longer.⁵ Regardless of the severity of the acne, treatment should be initiated as tolerated in those with PIH. Adolescent acne patients with skin of color may develop PIH that is more severe and longer lasting than the acne itself.

The foundation for treatment of acne in adolescent skin of color patients is the same as those without skin of color, including topical retinoids, topical antibiotics, oral antibiotics, and isotretinoin when needed. Topical tretinoin, adapalene, azelaic acid, and tazarotene not only treat acne but also are a valuable part of the treatment armamentarium for PIH. Several studies in adults with skin of color have demonstrated improvement of PIH from the use of topical retinoids alone.^8-10 Despite wanting to treat the acne aggressively, special guidance should be given to prevent retinoid dermatitis, which may lead to PIH.¹⁰ Demonstrating the application of the topical acne medications, discussing how to avoid potential side effects, and giving permission to skip applications, if needed, may empower families to make adjustments between visits to limit irritation that might prompt further PIH. Incorporating α-hydroxy acid–based cleansers, α-hydroxy acid–based chemical peels, or salicylic acid chemical peels may be warranted in the setting of intense PIH. Selecting treatments that not only help the inflammatory disease leading to the PIH but also can help improve the pigmentation are preferred; however, the risks and benefits have to be weighed because many treatments that work well for PIH also may cause irritation, leading to new or worsening PIH.

Arthropod Bites
Arthropod bites cause inflamed pruritic papules and nodules, and the resulting PIH in those with darker skin types may be quite dramatic. Parents/guardians should be instructed to have a low-potency topical corticosteroid on hand to use on bites for a few days when they appear, which will not only help with the inflammation associated with the bite but also will help decrease pruritus and subsequently skin injury from scratching. In homes with pets, checking animals routinely for fleas and other infestations is helpful. In the setting of repeated arthropod bites in the spring and summer, applying bug repellant with 10% to 30% DEET (N,N-diethyl-meta-toluamide) on the child’s clothing and exposed body areas before playing outside or in the morning before school or camp may prevent some bites. There are DEET alternatives, such as picaridin, that may be used. Product instructions should be followed when using insect repellants in the pediatric population.¹¹

PIH Management Strategies

Gentle Skin Care Routine
There are misconceptions that areas of hyperpigmentation on the skin are caused by dirt and that scrubbing the skin harder may help to lighten the affected areas. Parents/guardians may report that the child’s skin looks dirty or, in the setting of acne, view dirt as the cause of the skin condition, which may prompt the patient to scrub the skin and the friction further worsens the PIH. Use of daily gentle cleansers and moisturizers is advised to keep the skin moisturized and free of further potential irritation and dryness that may prompt scratching or flares of the underlying condition.

Photoprotection
During the treatment course for PIH, using sun protection is helpful to prevent further darkening of the PIH areas. Sun protection may be in the form of broad-spectrum sunscreen, hats, or sun-protective clothing. Patients should be encouraged to apply sunscreen daily and to reapply every 2 hours and after water-based activities.¹² For pediatric and adolescent populations, practicing sun-protective behaviors before school or outdoor activities also should be advised, as many families only think about sun protection in the setting of sunny vacation activities. Research has demonstrated that individuals with skin of color may not realize that they can be affected by skin cancer,¹³ thus they may not have any experience selecting, applying, or regularly using sunscreens. Products that do not leave a white hue on the skin are suggested for adolescents who may be sensitive about their appearance following sunscreen application.

Skin Lightening Treatments

Although the most important therapy for PIH is to treat the underlying inflammatory conditions, some parents/guardians may desire additional options due to the extent of involvement of the PIH, its psychological impact on the child, or adverse effect on the child’s quality of life.¹⁴ In adolescents, incorporating an α-hydroxy acid–based cleanser, glycolic acid chemical peels, salicylic acid chemical peels, and topical cosmeceuticals may be warranted in the setting of intense PIH and acne. However, irritation may lead to further dyspigmentation.

Topical ammonium lactate 12% is lactic acid neutralized with ammonium hydroxide that is formulated as a lotion or a cream. It is used to hydrate dry skin and may decrease corneocyte cohesion.¹⁵ Topical ammonium lactate also has been used anecdotally for PIH on the body during periods of watchful waiting.

Topical hydroquinone, the gold standard for treating hyperpigmentation,^3,16 is not approved in children, but some parents/guardians elect to utilize hydroquinone off label to accelerate the clearing of distressing PIH in adolescents. Careful consideration including a discussion of potential risks and alternatives (eg, watchful waiting) should be highlighted.

In the setting of chronic inflammatory conditions that recur and remit, potentially irritating topical treatments should be used only during periods when symptoms of inflammation such as itching or erythema are absent.

Conclusion

Despite the best management efforts, PIH in some patients with skin of color may be present for months to years. In the pediatric skin of color population, treatment of the underlying inflammatory condition, gentle skin care, use of photoprotection, and time may be all that is needed for PIH resolution. With their parent/guardians’ consent, adolescents distressed by PIH may decide to pursue more aggressive, potentially irritating treatments. Above all, the most important management in the setting of PIH is to treat the underlying inflammatory condition causing the PIH and set reasonable expectations. For challenging cases, pediatric dermatologists with special expertise in treating pediatric and adolescent patients with skin of color may be consulted.

Postnflammatory hyperpigmentation (PIH) is an acquired hypermelanosis that can occur in children and adults following an inflammatory cutaneous disease or trauma. Postinflammatory hyperpigmentation may last for months to even years. Although PIH may occur in all skin types, it is more common and presents with greater severity and intensity in individuals with skin of color. By the year 2050, 1 in 3 US residents is projected to be Hispanic.¹ It is projected that by 2044, non-Hispanic white individuals (all ages) will make up less than 50% of the US population.² Currently, the majority of the US residents younger than 18 years are minorities. The majority minority population in the United States already exists in those younger than 18 years and is predicted to occur in the adult population by 2044.²

Effective treatment options and management strategies for PIH in adults with skin of color have been described in the literature.³ Due to a paucity of research, the approach to management of PIH in children with skin of color has been based on clinical experience and lessons learned from adult patients. This article focuses on management of PIH in pediatric patients with skin of color, which includes black/African American, African-Caribbean, Hispanic, Asian, Pacific Islander, and American Indian individuals.

Underlying Inflammatory Dermatoses Resulting in PIH

There are numerous conditions that may result in PIH, including but not limited to atopic dermatitis (AD), acne, arthropod bites, and injuries to the skin. Postinflammatory hyperpigmentation may have more of a psychological impact than the inciting disease or injury itself. The most important step in the approach to managing PIH is treating the underlying inflammatory condition that caused the pigmentation.

Parents/guardians may report a chief concern of dark spots, manchas (stains), blemishes, or stains on the skin, often with no mention of a coexisting inflammatory dermatosis. Parents/guardians of children with skin of color often have personally experienced PIH and may be determined to shield their children from similar angst associated with the condition. Although physicians may see just another pediatric patient with PIH, the child’s parents/guardians may see a condition that will be readily perceptible during major life events, such as the child’s prom or even his/her wedding day. Promptly diagnosing and instituting early treatment of inflammatory conditions associated with PIH may accelerate resolution and prevent worsening of the pigmentation.³

Select inflammatory dermatoses that are common in children with skin of color and may lead to PIH are highlighted below. Although this list is not comprehensive, the approach and management strategies should prompt creation of plans that keep PIH in mind when treating primary inflammatory skin diseases.

Atopic Dermatitis
Atopic dermatitis may induce PIH or hypopigmentation of the skin in children with skin of color. Developing a plan for AD flare prevention, as well as management of mild, moderate, and severe AD flares, is imperative in pediatric patients. Prevention plans should include gentle skin care, twice-daily application of emollients to the full body, and reduction of Staphylococcus aureus loads on the skin. The treatment action plan for mild to moderate flares may include topical corticosteroids, immunomodulators, and nonsteroidal agents. Treatment options for severe AD or patients who were unsuccessfully treated with other therapies may include phototherapy, biologics, and methotrexate, among others.⁴ Creating action plans for AD flares is a vital step in the prevention of PIH in patients with skin of color. Additionally, PIH should not be considered a sign of AD treatment failure.

Acne
Acne is a common skin disorder seen in patients with skin of color.⁵ A prospective observational study found that 34.3% of 683 children aged 9 to 14 years in a pediatric ambulatory clinic had acne.⁶ The number of preadolescents with acne is growing. Most cases are not associated with underlying endocrinopathy.⁷ With the growing population of children with skin of color in the United States along with the increasing childhood acne rate and subsequent inherent risk for hyperpigmentation, early acne interventions should be considered in pediatric acne patients with skin of color to reduce the impact of PIH in those at risk.

In a survey study of 313 adult acne patients with skin of color, 37.2% reported the presence of dark marks lasting 4 months or longer.⁵ Regardless of the severity of the acne, treatment should be initiated as tolerated in those with PIH. Adolescent acne patients with skin of color may develop PIH that is more severe and longer lasting than the acne itself.

The foundation for treatment of acne in adolescent skin of color patients is the same as those without skin of color, including topical retinoids, topical antibiotics, oral antibiotics, and isotretinoin when needed. Topical tretinoin, adapalene, azelaic acid, and tazarotene not only treat acne but also are a valuable part of the treatment armamentarium for PIH. Several studies in adults with skin of color have demonstrated improvement of PIH from the use of topical retinoids alone.^8-10 Despite wanting to treat the acne aggressively, special guidance should be given to prevent retinoid dermatitis, which may lead to PIH.¹⁰ Demonstrating the application of the topical acne medications, discussing how to avoid potential side effects, and giving permission to skip applications, if needed, may empower families to make adjustments between visits to limit irritation that might prompt further PIH. Incorporating α-hydroxy acid–based cleansers, α-hydroxy acid–based chemical peels, or salicylic acid chemical peels may be warranted in the setting of intense PIH. Selecting treatments that not only help the inflammatory disease leading to the PIH but also can help improve the pigmentation are preferred; however, the risks and benefits have to be weighed because many treatments that work well for PIH also may cause irritation, leading to new or worsening PIH.

Arthropod Bites
Arthropod bites cause inflamed pruritic papules and nodules, and the resulting PIH in those with darker skin types may be quite dramatic. Parents/guardians should be instructed to have a low-potency topical corticosteroid on hand to use on bites for a few days when they appear, which will not only help with the inflammation associated with the bite but also will help decrease pruritus and subsequently skin injury from scratching. In homes with pets, checking animals routinely for fleas and other infestations is helpful. In the setting of repeated arthropod bites in the spring and summer, applying bug repellant with 10% to 30% DEET (N,N-diethyl-meta-toluamide) on the child’s clothing and exposed body areas before playing outside or in the morning before school or camp may prevent some bites. There are DEET alternatives, such as picaridin, that may be used. Product instructions should be followed when using insect repellants in the pediatric population.¹¹

PIH Management Strategies

Gentle Skin Care Routine
There are misconceptions that areas of hyperpigmentation on the skin are caused by dirt and that scrubbing the skin harder may help to lighten the affected areas. Parents/guardians may report that the child’s skin looks dirty or, in the setting of acne, view dirt as the cause of the skin condition, which may prompt the patient to scrub the skin and the friction further worsens the PIH. Use of daily gentle cleansers and moisturizers is advised to keep the skin moisturized and free of further potential irritation and dryness that may prompt scratching or flares of the underlying condition.

Photoprotection
During the treatment course for PIH, using sun protection is helpful to prevent further darkening of the PIH areas. Sun protection may be in the form of broad-spectrum sunscreen, hats, or sun-protective clothing. Patients should be encouraged to apply sunscreen daily and to reapply every 2 hours and after water-based activities.¹² For pediatric and adolescent populations, practicing sun-protective behaviors before school or outdoor activities also should be advised, as many families only think about sun protection in the setting of sunny vacation activities. Research has demonstrated that individuals with skin of color may not realize that they can be affected by skin cancer,¹³ thus they may not have any experience selecting, applying, or regularly using sunscreens. Products that do not leave a white hue on the skin are suggested for adolescents who may be sensitive about their appearance following sunscreen application.

Skin Lightening Treatments

Although the most important therapy for PIH is to treat the underlying inflammatory conditions, some parents/guardians may desire additional options due to the extent of involvement of the PIH, its psychological impact on the child, or adverse effect on the child’s quality of life.¹⁴ In adolescents, incorporating an α-hydroxy acid–based cleanser, glycolic acid chemical peels, salicylic acid chemical peels, and topical cosmeceuticals may be warranted in the setting of intense PIH and acne. However, irritation may lead to further dyspigmentation.

Topical ammonium lactate 12% is lactic acid neutralized with ammonium hydroxide that is formulated as a lotion or a cream. It is used to hydrate dry skin and may decrease corneocyte cohesion.¹⁵ Topical ammonium lactate also has been used anecdotally for PIH on the body during periods of watchful waiting.

Topical hydroquinone, the gold standard for treating hyperpigmentation,^3,16 is not approved in children, but some parents/guardians elect to utilize hydroquinone off label to accelerate the clearing of distressing PIH in adolescents. Careful consideration including a discussion of potential risks and alternatives (eg, watchful waiting) should be highlighted.

In the setting of chronic inflammatory conditions that recur and remit, potentially irritating topical treatments should be used only during periods when symptoms of inflammation such as itching or erythema are absent.

Conclusion

Despite the best management efforts, PIH in some patients with skin of color may be present for months to years. In the pediatric skin of color population, treatment of the underlying inflammatory condition, gentle skin care, use of photoprotection, and time may be all that is needed for PIH resolution. With their parent/guardians’ consent, adolescents distressed by PIH may decide to pursue more aggressive, potentially irritating treatments. Above all, the most important management in the setting of PIH is to treat the underlying inflammatory condition causing the PIH and set reasonable expectations. For challenging cases, pediatric dermatologists with special expertise in treating pediatric and adolescent patients with skin of color may be consulted.

Postnflammatory hyperpigmentation (PIH) is an acquired hypermelanosis that can occur in children and adults following an inflammatory cutaneous disease or trauma. Postinflammatory hyperpigmentation may last for months to even years. Although PIH may occur in all skin types, it is more common and presents with greater severity and intensity in individuals with skin of color. By the year 2050, 1 in 3 US residents is projected to be Hispanic.¹ It is projected that by 2044, non-Hispanic white individuals (all ages) will make up less than 50% of the US population.² Currently, the majority of the US residents younger than 18 years are minorities. The majority minority population in the United States already exists in those younger than 18 years and is predicted to occur in the adult population by 2044.²

Effective treatment options and management strategies for PIH in adults with skin of color have been described in the literature.³ Due to a paucity of research, the approach to management of PIH in children with skin of color has been based on clinical experience and lessons learned from adult patients. This article focuses on management of PIH in pediatric patients with skin of color, which includes black/African American, African-Caribbean, Hispanic, Asian, Pacific Islander, and American Indian individuals.

Underlying Inflammatory Dermatoses Resulting in PIH

There are numerous conditions that may result in PIH, including but not limited to atopic dermatitis (AD), acne, arthropod bites, and injuries to the skin. Postinflammatory hyperpigmentation may have more of a psychological impact than the inciting disease or injury itself. The most important step in the approach to managing PIH is treating the underlying inflammatory condition that caused the pigmentation.

Parents/guardians may report a chief concern of dark spots, manchas (stains), blemishes, or stains on the skin, often with no mention of a coexisting inflammatory dermatosis. Parents/guardians of children with skin of color often have personally experienced PIH and may be determined to shield their children from similar angst associated with the condition. Although physicians may see just another pediatric patient with PIH, the child’s parents/guardians may see a condition that will be readily perceptible during major life events, such as the child’s prom or even his/her wedding day. Promptly diagnosing and instituting early treatment of inflammatory conditions associated with PIH may accelerate resolution and prevent worsening of the pigmentation.³

Select inflammatory dermatoses that are common in children with skin of color and may lead to PIH are highlighted below. Although this list is not comprehensive, the approach and management strategies should prompt creation of plans that keep PIH in mind when treating primary inflammatory skin diseases.

Atopic Dermatitis
Atopic dermatitis may induce PIH or hypopigmentation of the skin in children with skin of color. Developing a plan for AD flare prevention, as well as management of mild, moderate, and severe AD flares, is imperative in pediatric patients. Prevention plans should include gentle skin care, twice-daily application of emollients to the full body, and reduction of Staphylococcus aureus loads on the skin. The treatment action plan for mild to moderate flares may include topical corticosteroids, immunomodulators, and nonsteroidal agents. Treatment options for severe AD or patients who were unsuccessfully treated with other therapies may include phototherapy, biologics, and methotrexate, among others.⁴ Creating action plans for AD flares is a vital step in the prevention of PIH in patients with skin of color. Additionally, PIH should not be considered a sign of AD treatment failure.

Acne
Acne is a common skin disorder seen in patients with skin of color.⁵ A prospective observational study found that 34.3% of 683 children aged 9 to 14 years in a pediatric ambulatory clinic had acne.⁶ The number of preadolescents with acne is growing. Most cases are not associated with underlying endocrinopathy.⁷ With the growing population of children with skin of color in the United States along with the increasing childhood acne rate and subsequent inherent risk for hyperpigmentation, early acne interventions should be considered in pediatric acne patients with skin of color to reduce the impact of PIH in those at risk.

In a survey study of 313 adult acne patients with skin of color, 37.2% reported the presence of dark marks lasting 4 months or longer.⁵ Regardless of the severity of the acne, treatment should be initiated as tolerated in those with PIH. Adolescent acne patients with skin of color may develop PIH that is more severe and longer lasting than the acne itself.

The foundation for treatment of acne in adolescent skin of color patients is the same as those without skin of color, including topical retinoids, topical antibiotics, oral antibiotics, and isotretinoin when needed. Topical tretinoin, adapalene, azelaic acid, and tazarotene not only treat acne but also are a valuable part of the treatment armamentarium for PIH. Several studies in adults with skin of color have demonstrated improvement of PIH from the use of topical retinoids alone.^8-10 Despite wanting to treat the acne aggressively, special guidance should be given to prevent retinoid dermatitis, which may lead to PIH.¹⁰ Demonstrating the application of the topical acne medications, discussing how to avoid potential side effects, and giving permission to skip applications, if needed, may empower families to make adjustments between visits to limit irritation that might prompt further PIH. Incorporating α-hydroxy acid–based cleansers, α-hydroxy acid–based chemical peels, or salicylic acid chemical peels may be warranted in the setting of intense PIH. Selecting treatments that not only help the inflammatory disease leading to the PIH but also can help improve the pigmentation are preferred; however, the risks and benefits have to be weighed because many treatments that work well for PIH also may cause irritation, leading to new or worsening PIH.

Arthropod Bites
Arthropod bites cause inflamed pruritic papules and nodules, and the resulting PIH in those with darker skin types may be quite dramatic. Parents/guardians should be instructed to have a low-potency topical corticosteroid on hand to use on bites for a few days when they appear, which will not only help with the inflammation associated with the bite but also will help decrease pruritus and subsequently skin injury from scratching. In homes with pets, checking animals routinely for fleas and other infestations is helpful. In the setting of repeated arthropod bites in the spring and summer, applying bug repellant with 10% to 30% DEET (N,N-diethyl-meta-toluamide) on the child’s clothing and exposed body areas before playing outside or in the morning before school or camp may prevent some bites. There are DEET alternatives, such as picaridin, that may be used. Product instructions should be followed when using insect repellants in the pediatric population.¹¹

PIH Management Strategies

Gentle Skin Care Routine
There are misconceptions that areas of hyperpigmentation on the skin are caused by dirt and that scrubbing the skin harder may help to lighten the affected areas. Parents/guardians may report that the child’s skin looks dirty or, in the setting of acne, view dirt as the cause of the skin condition, which may prompt the patient to scrub the skin and the friction further worsens the PIH. Use of daily gentle cleansers and moisturizers is advised to keep the skin moisturized and free of further potential irritation and dryness that may prompt scratching or flares of the underlying condition.

Photoprotection
During the treatment course for PIH, using sun protection is helpful to prevent further darkening of the PIH areas. Sun protection may be in the form of broad-spectrum sunscreen, hats, or sun-protective clothing. Patients should be encouraged to apply sunscreen daily and to reapply every 2 hours and after water-based activities.¹² For pediatric and adolescent populations, practicing sun-protective behaviors before school or outdoor activities also should be advised, as many families only think about sun protection in the setting of sunny vacation activities. Research has demonstrated that individuals with skin of color may not realize that they can be affected by skin cancer,¹³ thus they may not have any experience selecting, applying, or regularly using sunscreens. Products that do not leave a white hue on the skin are suggested for adolescents who may be sensitive about their appearance following sunscreen application.

Skin Lightening Treatments

Although the most important therapy for PIH is to treat the underlying inflammatory conditions, some parents/guardians may desire additional options due to the extent of involvement of the PIH, its psychological impact on the child, or adverse effect on the child’s quality of life.¹⁴ In adolescents, incorporating an α-hydroxy acid–based cleanser, glycolic acid chemical peels, salicylic acid chemical peels, and topical cosmeceuticals may be warranted in the setting of intense PIH and acne. However, irritation may lead to further dyspigmentation.

Topical ammonium lactate 12% is lactic acid neutralized with ammonium hydroxide that is formulated as a lotion or a cream. It is used to hydrate dry skin and may decrease corneocyte cohesion.¹⁵ Topical ammonium lactate also has been used anecdotally for PIH on the body during periods of watchful waiting.

Topical hydroquinone, the gold standard for treating hyperpigmentation,^3,16 is not approved in children, but some parents/guardians elect to utilize hydroquinone off label to accelerate the clearing of distressing PIH in adolescents. Careful consideration including a discussion of potential risks and alternatives (eg, watchful waiting) should be highlighted.

In the setting of chronic inflammatory conditions that recur and remit, potentially irritating topical treatments should be used only during periods when symptoms of inflammation such as itching or erythema are absent.

Conclusion

Despite the best management efforts, PIH in some patients with skin of color may be present for months to years. In the pediatric skin of color population, treatment of the underlying inflammatory condition, gentle skin care, use of photoprotection, and time may be all that is needed for PIH resolution. With their parent/guardians’ consent, adolescents distressed by PIH may decide to pursue more aggressive, potentially irritating treatments. Above all, the most important management in the setting of PIH is to treat the underlying inflammatory condition causing the PIH and set reasonable expectations. For challenging cases, pediatric dermatologists with special expertise in treating pediatric and adolescent patients with skin of color may be consulted.

Frontal fibrosing alopecia (FFA) has been reported in association with lichen planus pigmentosus (LPP) and facial papules.^1-3 Lichen planus pigmentosus is a variant of lichen planus that causes hyperpigmentation of the face, neck, and/or intertriginous areas that may be useful as a clinical indicator in the development of FFA.¹ Facial papules in association with FFA are secondary to fibrosed vellus hairs.^2,3 Currently, reports of concomitant FFA, LPP, and facial papules in women with skin of color are limited in the literature. This case series includes 5 women of color (Hispanic and black) who presented to our clinic with FFA and various cutaneous associations. A review of the current literature on cutaneous associations of FFA also is provided.

Case Reports

Patient 1
A 50-year-old Hispanic woman who was previously presumed to have melasma by an outside physician presented with pruritus of the scalp and eyebrows of 1 month’s duration. Physical examination revealed decreased frontal scalp hair density with perifollicular erythema and scale with thinning of the lateral eyebrows. Hyperpigmented coalesced macules (Figure 1A) and erythematous perifollicular papules were noted along the temples and on the perioral skin. Depressed forehead and temporal veins also were noted (Figure 1B). A biopsy of the scalp demonstrated perifollicular and perivascular lymphocytic inflammation and fibrosed hair follicles, and a biopsy of the perioral skin demonstrated perivascular lymphocytic inflammation with melanophages in the papillary dermis. A diagnosis of FFA with LPP was established with these biopsies.

Patient 2
A 61-year-old black woman presented with asymptomatic hair loss along the frontal hairline for an unknown duration. On physical examination the frontal scalp and lateral eyebrows demonstrated decreased hair density with loss of follicular ostia. Fine, flesh-colored, monomorphic papules were scattered along the forehead and temples, and ill-defined brown pigmentation was present along the forehead, temples, and cheeks. Biopsy of the frontal scalp demonstrated patchy lichenoid inflammation with decreased number of follicles with replacement by follicular scars, confirming the diagnosis of FFA.

Patient 3
A 47-year-old Hispanic woman presented with hair loss of the frontal scalp and bilateral eyebrows with associated burning of 2 years’ duration. Physical examination demonstrated recession of the frontotemporal hairline with scattered lone hairs and thinning of the eyebrows. Innumerable flesh-colored papules were present on the forehead and temples (Figure 2A). Glabellar and eyebrow erythema was noted (Figure 2B). Biopsy of the frontal scalp demonstrated decreased terminal anagen hair follicles with perifollicular lymphoid infiltrate and fibrosis, consistent with a diagnosis of FFA. The patient was started on oral hydroxychloroquine 400 mg once daily, and 3 months later hyperpigmentation of the forehead and perioral skin was noted. The patient reported that she had facial hyperpigmentation prior to starting hydroxychloroquine and declined a biopsy.

Patient 4
A 40-year-old black woman presented with brown pruritic macles of the face, neck, arms, and forearms of 4 years’ duration. She also reported hair loss on the frontal and occipital scalp, eyebrows, and arms. On physical examination, ill-defined brown macules and patches were noted on the neck (Figure 3), face, arms, and forearms. Decreased hair density was noted on the frontal and occipital scalp with follicular dropout and perifollicular hyperpigmentation. Biopsy of the scalp demonstrated perivascular lymphocytic inflammation with sparse anagen follicles and fibrous tracts, and biopsy of the neck revealed superficial perivascular inflammation with numerous melanophages in the upper dermis; these histopathologic findings were consistent with FFA and LPP, respectively.

Patient 5
A 46-year-old black woman with history of hair loss presented with hyperpigmentation of the face and neck of 2 years’ duration. On physical examination decreased hair density of the frontal and vertex scalp and lateral eyebrows was noted. Flesh-colored papules were noted on the forehead and cheeks, and confluent dark brown patches were present on the temples and neck. Three punch biopsies were performed. Biopsy of the scalp revealed lymphocytic inflammation with surrounding fibroplasia with overlapping features of FFA and central centrifugal cicatricial alopecia (Figure 4). Biopsy of the neck revealed vacuolar interface dermatitis. Additionally, biopsy of a facial papule revealed lichenoid inflammation involving a vellus hair follicle. Clinical and histopathological correlation confirmed the diagnosis of FFA with LPP and facial papules.

Comment

Current understanding of FFA as a progressive, lymphocytic, scarring alopecia has expanded in recent years. Clinical observation suggests that the incidence of FFA is increasing⁴; however more epidemiologic data are needed. Frontal fibrosing alopecia presents clinically with symmetrical frontotemporal hair loss with lone hairs. Trichoscopy reveals perifollicular hyperkeratosis, perifollicular erythema, and follicular plugging in 72%, 66%, and 44% of cases, respectively.⁵ In one study (N=242), patients were classified into 3 clinical patterns of FFA: pattern I (linear) showed bandlike loss of frontal hair with normal density directly behind the hairline; pattern II (diffuse) showed loss of density behind the frontal hairline; and pattern III (double line) showed a pseudo–“fringe sign” appearance. The majority of patients were classified as either pattern I or II, with pattern II predicting a poorer prognosis.⁶

rontal fibrosing alopecia is increasingly recognized in men, with prevalence as high as 5%.¹ Facial hair involvement, particularly of the upper lip and sideburns, is an important consideration in men.⁷ Most studies suggest that 80% to 90% of affected women are postmenopausal,⁸ though a case series presented by Dlova¹ identified 27% of affected women as postmenopausal. The coexistence of premature menopause and hysterectomy in FFA patients suggests a hormonal contribution, but this association is still poorly understood.⁸ Epidemiologic data on ethnicity in FFA are sparse but suggest that white individuals are more likely to be affected. Frontal fibrosing alopecia also may be misdiagnosed as traction alopecia in Hispanic and black patients.⁸

It is prudent for physicians to assess for and recognize clinical clues to severe forms of FFA. A 2014 multicenter review of 355 patients identified 3 clinical entities that predicted more severe forms of FFA: eyelash loss (madarosis), loss of body hair, and facial papules.⁸ Madarosis occurs due to perifollicular inflammation and fibrosis of eyelash hair follicles. Similarly, perifollicular inflammation of body hair was present in 24% of patients (N=86), most commonly of the axillary and pubic hair. Facial papules form due to facial vellus hair inflammation and fibrosis and were identified in 14% of patients (N=49).⁸ These clinical findings may allow providers to predict more extensive clinical involvement of FFA.

Frontal fibrosing alopecia and LPP occur concomitantly in up 54% of patients, more commonly in darker-skinned patients.^1,9,10 Lichen planus pigmentosus frequently occurs on the face and neck, most commonly in a diffuse pattern, though reticulated and macular patterns also have been identified.¹¹ In some patients, LPP precedes the development of FFA and may be useful as a herald sign¹; therefore, it is important for dermatologists to evaluate for signs of FFA when evaluating those with LPP. Thorough evaluation in patients with skin of color also is important because FFA may be misdiagnosed as traction alopecia.

Additional cutaneous associations of FFA include eyebrow loss, glabellar red dots, and prominent frontal veins. Eyebrow loss occurs secondary to fibrosis of eyebrow hair follicles and has been found in 40% to 80% of patients with FFA; it is thought to be associated with milder forms of FFA.⁸ Glabellar red dots correlate with histopathologic lymphocytic inflammation of vellus hair follicles.¹² Additionally, frontal vein prominence has been described in FFA and is thought to be secondary to atrophy in this scarring process, perhaps worsened by local steroid treatments.¹³ Mucocutaneous lichen planus, rosacea, thyroid disease, vitiligo, and other autoimmune disorders also have been reported in patients with FFA.¹⁴

Conclusion

Concomitant FFA, LPP, and facial papules have been rarely reported and exemplify the spectrum of cutaneous associations with FFA, particularly in individuals with skin of color. Clinical variants and associations of FFA are broad, including predictors of poorer prognosis such as eyelash loss and vellus hair involvement seen as facial papules. Lichen planus pigmentosus is well described in association with FFA and may serve as a herald sign that frontal hair loss should not be mistaken for traction alopecia in early stages. Eyebrow loss is thought to represent milder disease. It is important for dermatologists to be aware of these findings to understand the breadth of this disease and for appropriate evaluation and management of patients with FFA.

Frontal fibrosing alopecia (FFA) has been reported in association with lichen planus pigmentosus (LPP) and facial papules.^1-3 Lichen planus pigmentosus is a variant of lichen planus that causes hyperpigmentation of the face, neck, and/or intertriginous areas that may be useful as a clinical indicator in the development of FFA.¹ Facial papules in association with FFA are secondary to fibrosed vellus hairs.^2,3 Currently, reports of concomitant FFA, LPP, and facial papules in women with skin of color are limited in the literature. This case series includes 5 women of color (Hispanic and black) who presented to our clinic with FFA and various cutaneous associations. A review of the current literature on cutaneous associations of FFA also is provided.

Case Reports

Patient 1
A 50-year-old Hispanic woman who was previously presumed to have melasma by an outside physician presented with pruritus of the scalp and eyebrows of 1 month’s duration. Physical examination revealed decreased frontal scalp hair density with perifollicular erythema and scale with thinning of the lateral eyebrows. Hyperpigmented coalesced macules (Figure 1A) and erythematous perifollicular papules were noted along the temples and on the perioral skin. Depressed forehead and temporal veins also were noted (Figure 1B). A biopsy of the scalp demonstrated perifollicular and perivascular lymphocytic inflammation and fibrosed hair follicles, and a biopsy of the perioral skin demonstrated perivascular lymphocytic inflammation with melanophages in the papillary dermis. A diagnosis of FFA with LPP was established with these biopsies.

Patient 2
A 61-year-old black woman presented with asymptomatic hair loss along the frontal hairline for an unknown duration. On physical examination the frontal scalp and lateral eyebrows demonstrated decreased hair density with loss of follicular ostia. Fine, flesh-colored, monomorphic papules were scattered along the forehead and temples, and ill-defined brown pigmentation was present along the forehead, temples, and cheeks. Biopsy of the frontal scalp demonstrated patchy lichenoid inflammation with decreased number of follicles with replacement by follicular scars, confirming the diagnosis of FFA.

Patient 3
A 47-year-old Hispanic woman presented with hair loss of the frontal scalp and bilateral eyebrows with associated burning of 2 years’ duration. Physical examination demonstrated recession of the frontotemporal hairline with scattered lone hairs and thinning of the eyebrows. Innumerable flesh-colored papules were present on the forehead and temples (Figure 2A). Glabellar and eyebrow erythema was noted (Figure 2B). Biopsy of the frontal scalp demonstrated decreased terminal anagen hair follicles with perifollicular lymphoid infiltrate and fibrosis, consistent with a diagnosis of FFA. The patient was started on oral hydroxychloroquine 400 mg once daily, and 3 months later hyperpigmentation of the forehead and perioral skin was noted. The patient reported that she had facial hyperpigmentation prior to starting hydroxychloroquine and declined a biopsy.

Patient 4
A 40-year-old black woman presented with brown pruritic macles of the face, neck, arms, and forearms of 4 years’ duration. She also reported hair loss on the frontal and occipital scalp, eyebrows, and arms. On physical examination, ill-defined brown macules and patches were noted on the neck (Figure 3), face, arms, and forearms. Decreased hair density was noted on the frontal and occipital scalp with follicular dropout and perifollicular hyperpigmentation. Biopsy of the scalp demonstrated perivascular lymphocytic inflammation with sparse anagen follicles and fibrous tracts, and biopsy of the neck revealed superficial perivascular inflammation with numerous melanophages in the upper dermis; these histopathologic findings were consistent with FFA and LPP, respectively.

Patient 5
A 46-year-old black woman with history of hair loss presented with hyperpigmentation of the face and neck of 2 years’ duration. On physical examination decreased hair density of the frontal and vertex scalp and lateral eyebrows was noted. Flesh-colored papules were noted on the forehead and cheeks, and confluent dark brown patches were present on the temples and neck. Three punch biopsies were performed. Biopsy of the scalp revealed lymphocytic inflammation with surrounding fibroplasia with overlapping features of FFA and central centrifugal cicatricial alopecia (Figure 4). Biopsy of the neck revealed vacuolar interface dermatitis. Additionally, biopsy of a facial papule revealed lichenoid inflammation involving a vellus hair follicle. Clinical and histopathological correlation confirmed the diagnosis of FFA with LPP and facial papules.

Comment

Current understanding of FFA as a progressive, lymphocytic, scarring alopecia has expanded in recent years. Clinical observation suggests that the incidence of FFA is increasing⁴; however more epidemiologic data are needed. Frontal fibrosing alopecia presents clinically with symmetrical frontotemporal hair loss with lone hairs. Trichoscopy reveals perifollicular hyperkeratosis, perifollicular erythema, and follicular plugging in 72%, 66%, and 44% of cases, respectively.⁵ In one study (N=242), patients were classified into 3 clinical patterns of FFA: pattern I (linear) showed bandlike loss of frontal hair with normal density directly behind the hairline; pattern II (diffuse) showed loss of density behind the frontal hairline; and pattern III (double line) showed a pseudo–“fringe sign” appearance. The majority of patients were classified as either pattern I or II, with pattern II predicting a poorer prognosis.⁶

rontal fibrosing alopecia is increasingly recognized in men, with prevalence as high as 5%.¹ Facial hair involvement, particularly of the upper lip and sideburns, is an important consideration in men.⁷ Most studies suggest that 80% to 90% of affected women are postmenopausal,⁸ though a case series presented by Dlova¹ identified 27% of affected women as postmenopausal. The coexistence of premature menopause and hysterectomy in FFA patients suggests a hormonal contribution, but this association is still poorly understood.⁸ Epidemiologic data on ethnicity in FFA are sparse but suggest that white individuals are more likely to be affected. Frontal fibrosing alopecia also may be misdiagnosed as traction alopecia in Hispanic and black patients.⁸

It is prudent for physicians to assess for and recognize clinical clues to severe forms of FFA. A 2014 multicenter review of 355 patients identified 3 clinical entities that predicted more severe forms of FFA: eyelash loss (madarosis), loss of body hair, and facial papules.⁸ Madarosis occurs due to perifollicular inflammation and fibrosis of eyelash hair follicles. Similarly, perifollicular inflammation of body hair was present in 24% of patients (N=86), most commonly of the axillary and pubic hair. Facial papules form due to facial vellus hair inflammation and fibrosis and were identified in 14% of patients (N=49).⁸ These clinical findings may allow providers to predict more extensive clinical involvement of FFA.

Frontal fibrosing alopecia and LPP occur concomitantly in up 54% of patients, more commonly in darker-skinned patients.^1,9,10 Lichen planus pigmentosus frequently occurs on the face and neck, most commonly in a diffuse pattern, though reticulated and macular patterns also have been identified.¹¹ In some patients, LPP precedes the development of FFA and may be useful as a herald sign¹; therefore, it is important for dermatologists to evaluate for signs of FFA when evaluating those with LPP. Thorough evaluation in patients with skin of color also is important because FFA may be misdiagnosed as traction alopecia.

Additional cutaneous associations of FFA include eyebrow loss, glabellar red dots, and prominent frontal veins. Eyebrow loss occurs secondary to fibrosis of eyebrow hair follicles and has been found in 40% to 80% of patients with FFA; it is thought to be associated with milder forms of FFA.⁸ Glabellar red dots correlate with histopathologic lymphocytic inflammation of vellus hair follicles.¹² Additionally, frontal vein prominence has been described in FFA and is thought to be secondary to atrophy in this scarring process, perhaps worsened by local steroid treatments.¹³ Mucocutaneous lichen planus, rosacea, thyroid disease, vitiligo, and other autoimmune disorders also have been reported in patients with FFA.¹⁴

Conclusion

Concomitant FFA, LPP, and facial papules have been rarely reported and exemplify the spectrum of cutaneous associations with FFA, particularly in individuals with skin of color. Clinical variants and associations of FFA are broad, including predictors of poorer prognosis such as eyelash loss and vellus hair involvement seen as facial papules. Lichen planus pigmentosus is well described in association with FFA and may serve as a herald sign that frontal hair loss should not be mistaken for traction alopecia in early stages. Eyebrow loss is thought to represent milder disease. It is important for dermatologists to be aware of these findings to understand the breadth of this disease and for appropriate evaluation and management of patients with FFA.

Frontal fibrosing alopecia (FFA) has been reported in association with lichen planus pigmentosus (LPP) and facial papules.^1-3 Lichen planus pigmentosus is a variant of lichen planus that causes hyperpigmentation of the face, neck, and/or intertriginous areas that may be useful as a clinical indicator in the development of FFA.¹ Facial papules in association with FFA are secondary to fibrosed vellus hairs.^2,3 Currently, reports of concomitant FFA, LPP, and facial papules in women with skin of color are limited in the literature. This case series includes 5 women of color (Hispanic and black) who presented to our clinic with FFA and various cutaneous associations. A review of the current literature on cutaneous associations of FFA also is provided.

Case Reports

Patient 1
A 50-year-old Hispanic woman who was previously presumed to have melasma by an outside physician presented with pruritus of the scalp and eyebrows of 1 month’s duration. Physical examination revealed decreased frontal scalp hair density with perifollicular erythema and scale with thinning of the lateral eyebrows. Hyperpigmented coalesced macules (Figure 1A) and erythematous perifollicular papules were noted along the temples and on the perioral skin. Depressed forehead and temporal veins also were noted (Figure 1B). A biopsy of the scalp demonstrated perifollicular and perivascular lymphocytic inflammation and fibrosed hair follicles, and a biopsy of the perioral skin demonstrated perivascular lymphocytic inflammation with melanophages in the papillary dermis. A diagnosis of FFA with LPP was established with these biopsies.

Patient 2
A 61-year-old black woman presented with asymptomatic hair loss along the frontal hairline for an unknown duration. On physical examination the frontal scalp and lateral eyebrows demonstrated decreased hair density with loss of follicular ostia. Fine, flesh-colored, monomorphic papules were scattered along the forehead and temples, and ill-defined brown pigmentation was present along the forehead, temples, and cheeks. Biopsy of the frontal scalp demonstrated patchy lichenoid inflammation with decreased number of follicles with replacement by follicular scars, confirming the diagnosis of FFA.

Patient 3
A 47-year-old Hispanic woman presented with hair loss of the frontal scalp and bilateral eyebrows with associated burning of 2 years’ duration. Physical examination demonstrated recession of the frontotemporal hairline with scattered lone hairs and thinning of the eyebrows. Innumerable flesh-colored papules were present on the forehead and temples (Figure 2A). Glabellar and eyebrow erythema was noted (Figure 2B). Biopsy of the frontal scalp demonstrated decreased terminal anagen hair follicles with perifollicular lymphoid infiltrate and fibrosis, consistent with a diagnosis of FFA. The patient was started on oral hydroxychloroquine 400 mg once daily, and 3 months later hyperpigmentation of the forehead and perioral skin was noted. The patient reported that she had facial hyperpigmentation prior to starting hydroxychloroquine and declined a biopsy.

Patient 4
A 40-year-old black woman presented with brown pruritic macles of the face, neck, arms, and forearms of 4 years’ duration. She also reported hair loss on the frontal and occipital scalp, eyebrows, and arms. On physical examination, ill-defined brown macules and patches were noted on the neck (Figure 3), face, arms, and forearms. Decreased hair density was noted on the frontal and occipital scalp with follicular dropout and perifollicular hyperpigmentation. Biopsy of the scalp demonstrated perivascular lymphocytic inflammation with sparse anagen follicles and fibrous tracts, and biopsy of the neck revealed superficial perivascular inflammation with numerous melanophages in the upper dermis; these histopathologic findings were consistent with FFA and LPP, respectively.

Patient 5
A 46-year-old black woman with history of hair loss presented with hyperpigmentation of the face and neck of 2 years’ duration. On physical examination decreased hair density of the frontal and vertex scalp and lateral eyebrows was noted. Flesh-colored papules were noted on the forehead and cheeks, and confluent dark brown patches were present on the temples and neck. Three punch biopsies were performed. Biopsy of the scalp revealed lymphocytic inflammation with surrounding fibroplasia with overlapping features of FFA and central centrifugal cicatricial alopecia (Figure 4). Biopsy of the neck revealed vacuolar interface dermatitis. Additionally, biopsy of a facial papule revealed lichenoid inflammation involving a vellus hair follicle. Clinical and histopathological correlation confirmed the diagnosis of FFA with LPP and facial papules.

Comment

Current understanding of FFA as a progressive, lymphocytic, scarring alopecia has expanded in recent years. Clinical observation suggests that the incidence of FFA is increasing⁴; however more epidemiologic data are needed. Frontal fibrosing alopecia presents clinically with symmetrical frontotemporal hair loss with lone hairs. Trichoscopy reveals perifollicular hyperkeratosis, perifollicular erythema, and follicular plugging in 72%, 66%, and 44% of cases, respectively.⁵ In one study (N=242), patients were classified into 3 clinical patterns of FFA: pattern I (linear) showed bandlike loss of frontal hair with normal density directly behind the hairline; pattern II (diffuse) showed loss of density behind the frontal hairline; and pattern III (double line) showed a pseudo–“fringe sign” appearance. The majority of patients were classified as either pattern I or II, with pattern II predicting a poorer prognosis.⁶

rontal fibrosing alopecia is increasingly recognized in men, with prevalence as high as 5%.¹ Facial hair involvement, particularly of the upper lip and sideburns, is an important consideration in men.⁷ Most studies suggest that 80% to 90% of affected women are postmenopausal,⁸ though a case series presented by Dlova¹ identified 27% of affected women as postmenopausal. The coexistence of premature menopause and hysterectomy in FFA patients suggests a hormonal contribution, but this association is still poorly understood.⁸ Epidemiologic data on ethnicity in FFA are sparse but suggest that white individuals are more likely to be affected. Frontal fibrosing alopecia also may be misdiagnosed as traction alopecia in Hispanic and black patients.⁸

It is prudent for physicians to assess for and recognize clinical clues to severe forms of FFA. A 2014 multicenter review of 355 patients identified 3 clinical entities that predicted more severe forms of FFA: eyelash loss (madarosis), loss of body hair, and facial papules.⁸ Madarosis occurs due to perifollicular inflammation and fibrosis of eyelash hair follicles. Similarly, perifollicular inflammation of body hair was present in 24% of patients (N=86), most commonly of the axillary and pubic hair. Facial papules form due to facial vellus hair inflammation and fibrosis and were identified in 14% of patients (N=49).⁸ These clinical findings may allow providers to predict more extensive clinical involvement of FFA.

Frontal fibrosing alopecia and LPP occur concomitantly in up 54% of patients, more commonly in darker-skinned patients.^1,9,10 Lichen planus pigmentosus frequently occurs on the face and neck, most commonly in a diffuse pattern, though reticulated and macular patterns also have been identified.¹¹ In some patients, LPP precedes the development of FFA and may be useful as a herald sign¹; therefore, it is important for dermatologists to evaluate for signs of FFA when evaluating those with LPP. Thorough evaluation in patients with skin of color also is important because FFA may be misdiagnosed as traction alopecia.

Additional cutaneous associations of FFA include eyebrow loss, glabellar red dots, and prominent frontal veins. Eyebrow loss occurs secondary to fibrosis of eyebrow hair follicles and has been found in 40% to 80% of patients with FFA; it is thought to be associated with milder forms of FFA.⁸ Glabellar red dots correlate with histopathologic lymphocytic inflammation of vellus hair follicles.¹² Additionally, frontal vein prominence has been described in FFA and is thought to be secondary to atrophy in this scarring process, perhaps worsened by local steroid treatments.¹³ Mucocutaneous lichen planus, rosacea, thyroid disease, vitiligo, and other autoimmune disorders also have been reported in patients with FFA.¹⁴

Conclusion

Concomitant FFA, LPP, and facial papules have been rarely reported and exemplify the spectrum of cutaneous associations with FFA, particularly in individuals with skin of color. Clinical variants and associations of FFA are broad, including predictors of poorer prognosis such as eyelash loss and vellus hair involvement seen as facial papules. Lichen planus pigmentosus is well described in association with FFA and may serve as a herald sign that frontal hair loss should not be mistaken for traction alopecia in early stages. Eyebrow loss is thought to represent milder disease. It is important for dermatologists to be aware of these findings to understand the breadth of this disease and for appropriate evaluation and management of patients with FFA.

I recently had the privilege of treating a family who spoke my first language, Hindi. My patient, Ms. M, was 16 years old and struggling to adjust to her new life in the United States, having recently come from India. America’s schooling, culture, and “open society” was a contrast to her life in a semi-rural town, especially her close-knit family structure in which her parents and siblings are everything. Due to their cultural beliefs and religious faith in Islam, both Ms. M and her father were initially resistant to begin treatment for her depression and anxiety. “Let’s give it a trial” was the attitude I finally got from the father. But to me, there was a clear discordance in the communication among the family members in addition to the primary mental illness that led them to come for treatment. I was attracted to work with this family because I had a reasonable understanding of their faith, their culture, and their family system, and I have an inclination toward spirituality. Even though I recognized this family’s social isolation, I wondered why they were still in a state of unrest, given their deep commitment to their faith.

Ms. M was isolating herself at home, in an environment that wasn’t supportive of talking about her concerns. These included being bullied for being “different,” for how she dressed, and for having home-cooked traditional meals for lunch, and being unable to socialize with most of her male peers, except for those from her same community. This led her to dream of returning to India.

The family did not have a social life. Ms. M told me, “I wanted to socialize, but I cannot because of my faith and religion.” So she chose to wear attire to identify with her mother and her culture of origin. She also did this to hide her emotional pain from enduring trauma related to bullying at her school. It was a challenge to understand how faith, resilience, and trauma were intermingled in Ms. M and her family.

I saw Ms. M and her family for 12 one-hour family psychotherapy sessions. The initial session unfolded uneasily. It was a challenge to build rapport and help them understand how family therapy works. Circular inquiries to each family member, specifically to get the mother’s point of view, brought mourning, shame, and guilt to this family. The importance of marriage, education, and immigration were processed in reference to their culture and their incomplete acculturation to life in the United States.

I wondered if there were other families with different cultural backgrounds who struggled with similar conflicts. I also wondered if those families understood the value of family therapy or had ever experienced this therapeutic process.

The 3 key signs that made me believe that this family was making progress through our work together included:

• They complied with treatment; the family never missed a session.
• The parents acknowledged that their daughter was doing better.
• The mother brought me a dinner as a gesture of gratitude in our last session. This is a particularly meaningful gesture on the part of people with their cultural background.

I clearly remember our first meeting, when Ms. M asked me disapprovingly about family therapy, “Why do we need to come here? Can’t we do it at home?” The question itself gave me the answer, for our goal for family therapy was to get her to function better at home and school. Although we ended our work together after 12 sessions, I hope this family continues to participate in therapy, to resolve the difficulties they are now aware of as a result of our family work.

I recently had the privilege of treating a family who spoke my first language, Hindi. My patient, Ms. M, was 16 years old and struggling to adjust to her new life in the United States, having recently come from India. America’s schooling, culture, and “open society” was a contrast to her life in a semi-rural town, especially her close-knit family structure in which her parents and siblings are everything. Due to their cultural beliefs and religious faith in Islam, both Ms. M and her father were initially resistant to begin treatment for her depression and anxiety. “Let’s give it a trial” was the attitude I finally got from the father. But to me, there was a clear discordance in the communication among the family members in addition to the primary mental illness that led them to come for treatment. I was attracted to work with this family because I had a reasonable understanding of their faith, their culture, and their family system, and I have an inclination toward spirituality. Even though I recognized this family’s social isolation, I wondered why they were still in a state of unrest, given their deep commitment to their faith.

Ms. M was isolating herself at home, in an environment that wasn’t supportive of talking about her concerns. These included being bullied for being “different,” for how she dressed, and for having home-cooked traditional meals for lunch, and being unable to socialize with most of her male peers, except for those from her same community. This led her to dream of returning to India.

The family did not have a social life. Ms. M told me, “I wanted to socialize, but I cannot because of my faith and religion.” So she chose to wear attire to identify with her mother and her culture of origin. She also did this to hide her emotional pain from enduring trauma related to bullying at her school. It was a challenge to understand how faith, resilience, and trauma were intermingled in Ms. M and her family.

I saw Ms. M and her family for 12 one-hour family psychotherapy sessions. The initial session unfolded uneasily. It was a challenge to build rapport and help them understand how family therapy works. Circular inquiries to each family member, specifically to get the mother’s point of view, brought mourning, shame, and guilt to this family. The importance of marriage, education, and immigration were processed in reference to their culture and their incomplete acculturation to life in the United States.

I wondered if there were other families with different cultural backgrounds who struggled with similar conflicts. I also wondered if those families understood the value of family therapy or had ever experienced this therapeutic process.

The 3 key signs that made me believe that this family was making progress through our work together included:

• They complied with treatment; the family never missed a session.
• The parents acknowledged that their daughter was doing better.
• The mother brought me a dinner as a gesture of gratitude in our last session. This is a particularly meaningful gesture on the part of people with their cultural background.

I clearly remember our first meeting, when Ms. M asked me disapprovingly about family therapy, “Why do we need to come here? Can’t we do it at home?” The question itself gave me the answer, for our goal for family therapy was to get her to function better at home and school. Although we ended our work together after 12 sessions, I hope this family continues to participate in therapy, to resolve the difficulties they are now aware of as a result of our family work.

I recently had the privilege of treating a family who spoke my first language, Hindi. My patient, Ms. M, was 16 years old and struggling to adjust to her new life in the United States, having recently come from India. America’s schooling, culture, and “open society” was a contrast to her life in a semi-rural town, especially her close-knit family structure in which her parents and siblings are everything. Due to their cultural beliefs and religious faith in Islam, both Ms. M and her father were initially resistant to begin treatment for her depression and anxiety. “Let’s give it a trial” was the attitude I finally got from the father. But to me, there was a clear discordance in the communication among the family members in addition to the primary mental illness that led them to come for treatment. I was attracted to work with this family because I had a reasonable understanding of their faith, their culture, and their family system, and I have an inclination toward spirituality. Even though I recognized this family’s social isolation, I wondered why they were still in a state of unrest, given their deep commitment to their faith.

Ms. M was isolating herself at home, in an environment that wasn’t supportive of talking about her concerns. These included being bullied for being “different,” for how she dressed, and for having home-cooked traditional meals for lunch, and being unable to socialize with most of her male peers, except for those from her same community. This led her to dream of returning to India.

The family did not have a social life. Ms. M told me, “I wanted to socialize, but I cannot because of my faith and religion.” So she chose to wear attire to identify with her mother and her culture of origin. She also did this to hide her emotional pain from enduring trauma related to bullying at her school. It was a challenge to understand how faith, resilience, and trauma were intermingled in Ms. M and her family.

I saw Ms. M and her family for 12 one-hour family psychotherapy sessions. The initial session unfolded uneasily. It was a challenge to build rapport and help them understand how family therapy works. Circular inquiries to each family member, specifically to get the mother’s point of view, brought mourning, shame, and guilt to this family. The importance of marriage, education, and immigration were processed in reference to their culture and their incomplete acculturation to life in the United States.

I wondered if there were other families with different cultural backgrounds who struggled with similar conflicts. I also wondered if those families understood the value of family therapy or had ever experienced this therapeutic process.

The 3 key signs that made me believe that this family was making progress through our work together included:

• They complied with treatment; the family never missed a session.
• The parents acknowledged that their daughter was doing better.
• The mother brought me a dinner as a gesture of gratitude in our last session. This is a particularly meaningful gesture on the part of people with their cultural background.

I clearly remember our first meeting, when Ms. M asked me disapprovingly about family therapy, “Why do we need to come here? Can’t we do it at home?” The question itself gave me the answer, for our goal for family therapy was to get her to function better at home and school. Although we ended our work together after 12 sessions, I hope this family continues to participate in therapy, to resolve the difficulties they are now aware of as a result of our family work.

As do women from a wide range of cultures, South Asian (SA) women frequently report feelings of shame associated with receiving a psychiatric diagnosis during the postpartum period because they fear it may reflect poorly on their ability to be good mothers or negatively impact their family’s reputation. To improve outcomes for these patients, clinicians should strive to provide culturally competent care. Based on our experience caring for SA women, we review several social and cultural barriers these women face when seeking psychiatric treatment, and provide approaches to incorporate into your therapeutic interactions with them.

Be aware of psychosomatic presentations. SA mothers who develop postpartum psychiatric symptoms might not present with complaints of dysphoria, crying, low energy, or suicidal thoughts. They may instead describe psychosomatic symptoms such as headaches and body pains.

Consider their hesitation to use psychiatric terms. SA women may not be comfortable using psychiatric terms such as depression or anxiety. Instead, they might respond more positively when their preferred descriptive terms (ie, sadness, worry, stress) are used by the clinicians who treat them.

Engage the partner and/or family. SA women may emphasize that they are part of a family unit, rather than regarding themselves as individuals. Thus, including family members in the treatment plan may help improve adherence.

Screen for suicide risk. Evidence suggests that young SA women have a higher rate of suicide and suicide attempts than young SA men or non-SA women.^1,2 Further, they may be less willing to speak openly about it.

Ask questions about cultural or traditional forms of treatment. SA mothers, particularly those who are breastfeeding, might be wary of Western medicine and may be familiar with traditional Indian medicine practices such as herbal, homeopathic, or Ayurvedic approaches.³ These interventions may include a specified diet, use of herbal treatments, exercise, and lifestyle recommendations.When taking the patient’s history, find out which treatments she is currently using, and discuss whether she can safely continue to use them.

Do not mistake poor eye contact for lack of engagement. Because SA patients may view a physician as a source of authority, they might regard direct eye contact with a physician as being somewhat disrespectful, and they may avoid eye contact altogether.

Continue to: Maintain an active approach

Maintain an active approach. SA women may prefer to view the physician as an expert, rather than a partner with whom to develop a collaborative relationship. Thus, they may feel more comfortable with direct feedback rather than a passive or reflective approach.

Suggest a postpartum support group. In a U.K. study of 17 SA postpartum women, age 20 to 45, group therapy improved health outcomes and overall satisfaction.⁴ It may be particularly helpful to SA patients if group therapy is facilitated by a culturally sensitive moderator.

Help patients overcome logistical barriers. Lack of transportation, childcare difficulties, and financial limitations are common deterrents to treatment. These barriers may be particularly challenging for SA women of lower socioeconomic status. Postpartum mothers who feel overtasked with caring for their children and undertaking household duties may feel less able to complete therapy.

Screen for adherence. Although SA patients may view clinicians as authority figures, adherence with medications or treatment plans should not be assumed. Many patients may quietly avoid treatments or recommendations instead of discussing their ambivalence with their clinicians.

As do women from a wide range of cultures, South Asian (SA) women frequently report feelings of shame associated with receiving a psychiatric diagnosis during the postpartum period because they fear it may reflect poorly on their ability to be good mothers or negatively impact their family’s reputation. To improve outcomes for these patients, clinicians should strive to provide culturally competent care. Based on our experience caring for SA women, we review several social and cultural barriers these women face when seeking psychiatric treatment, and provide approaches to incorporate into your therapeutic interactions with them.

Be aware of psychosomatic presentations. SA mothers who develop postpartum psychiatric symptoms might not present with complaints of dysphoria, crying, low energy, or suicidal thoughts. They may instead describe psychosomatic symptoms such as headaches and body pains.

Consider their hesitation to use psychiatric terms. SA women may not be comfortable using psychiatric terms such as depression or anxiety. Instead, they might respond more positively when their preferred descriptive terms (ie, sadness, worry, stress) are used by the clinicians who treat them.

Engage the partner and/or family. SA women may emphasize that they are part of a family unit, rather than regarding themselves as individuals. Thus, including family members in the treatment plan may help improve adherence.

Screen for suicide risk. Evidence suggests that young SA women have a higher rate of suicide and suicide attempts than young SA men or non-SA women.^1,2 Further, they may be less willing to speak openly about it.

Ask questions about cultural or traditional forms of treatment. SA mothers, particularly those who are breastfeeding, might be wary of Western medicine and may be familiar with traditional Indian medicine practices such as herbal, homeopathic, or Ayurvedic approaches.³ These interventions may include a specified diet, use of herbal treatments, exercise, and lifestyle recommendations.When taking the patient’s history, find out which treatments she is currently using, and discuss whether she can safely continue to use them.

Do not mistake poor eye contact for lack of engagement. Because SA patients may view a physician as a source of authority, they might regard direct eye contact with a physician as being somewhat disrespectful, and they may avoid eye contact altogether.

Continue to: Maintain an active approach

Maintain an active approach. SA women may prefer to view the physician as an expert, rather than a partner with whom to develop a collaborative relationship. Thus, they may feel more comfortable with direct feedback rather than a passive or reflective approach.

Suggest a postpartum support group. In a U.K. study of 17 SA postpartum women, age 20 to 45, group therapy improved health outcomes and overall satisfaction.⁴ It may be particularly helpful to SA patients if group therapy is facilitated by a culturally sensitive moderator.

Help patients overcome logistical barriers. Lack of transportation, childcare difficulties, and financial limitations are common deterrents to treatment. These barriers may be particularly challenging for SA women of lower socioeconomic status. Postpartum mothers who feel overtasked with caring for their children and undertaking household duties may feel less able to complete therapy.

Screen for adherence. Although SA patients may view clinicians as authority figures, adherence with medications or treatment plans should not be assumed. Many patients may quietly avoid treatments or recommendations instead of discussing their ambivalence with their clinicians.

As do women from a wide range of cultures, South Asian (SA) women frequently report feelings of shame associated with receiving a psychiatric diagnosis during the postpartum period because they fear it may reflect poorly on their ability to be good mothers or negatively impact their family’s reputation. To improve outcomes for these patients, clinicians should strive to provide culturally competent care. Based on our experience caring for SA women, we review several social and cultural barriers these women face when seeking psychiatric treatment, and provide approaches to incorporate into your therapeutic interactions with them.

Be aware of psychosomatic presentations. SA mothers who develop postpartum psychiatric symptoms might not present with complaints of dysphoria, crying, low energy, or suicidal thoughts. They may instead describe psychosomatic symptoms such as headaches and body pains.

Consider their hesitation to use psychiatric terms. SA women may not be comfortable using psychiatric terms such as depression or anxiety. Instead, they might respond more positively when their preferred descriptive terms (ie, sadness, worry, stress) are used by the clinicians who treat them.

Engage the partner and/or family. SA women may emphasize that they are part of a family unit, rather than regarding themselves as individuals. Thus, including family members in the treatment plan may help improve adherence.

Screen for suicide risk. Evidence suggests that young SA women have a higher rate of suicide and suicide attempts than young SA men or non-SA women.^1,2 Further, they may be less willing to speak openly about it.

Ask questions about cultural or traditional forms of treatment. SA mothers, particularly those who are breastfeeding, might be wary of Western medicine and may be familiar with traditional Indian medicine practices such as herbal, homeopathic, or Ayurvedic approaches.³ These interventions may include a specified diet, use of herbal treatments, exercise, and lifestyle recommendations.When taking the patient’s history, find out which treatments she is currently using, and discuss whether she can safely continue to use them.

Do not mistake poor eye contact for lack of engagement. Because SA patients may view a physician as a source of authority, they might regard direct eye contact with a physician as being somewhat disrespectful, and they may avoid eye contact altogether.

Continue to: Maintain an active approach

Maintain an active approach. SA women may prefer to view the physician as an expert, rather than a partner with whom to develop a collaborative relationship. Thus, they may feel more comfortable with direct feedback rather than a passive or reflective approach.

Suggest a postpartum support group. In a U.K. study of 17 SA postpartum women, age 20 to 45, group therapy improved health outcomes and overall satisfaction.⁴ It may be particularly helpful to SA patients if group therapy is facilitated by a culturally sensitive moderator.

Help patients overcome logistical barriers. Lack of transportation, childcare difficulties, and financial limitations are common deterrents to treatment. These barriers may be particularly challenging for SA women of lower socioeconomic status. Postpartum mothers who feel overtasked with caring for their children and undertaking household duties may feel less able to complete therapy.

Screen for adherence. Although SA patients may view clinicians as authority figures, adherence with medications or treatment plans should not be assumed. Many patients may quietly avoid treatments or recommendations instead of discussing their ambivalence with their clinicians.

Cutaneous melanoma is a considerable public health concern. In the United States, an estimated 87,110 cases were diagnosed in 2017, and more than 9000 deaths are expected as result of this disease in 2018.¹ Early diagnosis of melanoma is associated with favorable survival rates (5-year overall survival rates for melanoma in situ and stage IA melanoma, 99% and 97%, respectively).² In contrast, the prognosis for advanced-stage melanoma is poor, with a 5-year survival rate of 16% for patients with stage IV disease. Therefore, early detection is critical to reducing mortality in melanoma patients.³

The term Hispanic refers to a panethnic category primarily encompassing Mexican-Americans, Cubans, and Puerto Ricans, as well as individuals from the Caribbean and Central and South America. These populations are diverse in birth origin, primary language, acculturation, distinct ethnic traditions, education level, and occupation. Hispanics in the United States are heterogeneous in many dimensions related to health risks, health care use, and health outcomes.⁴ Genetic predisposition, lifestyle risks, and access to and use of health care services can shape melanoma diagnosis, treatment, and progression across Hispanic populations differently than in other populations.

In this review, the epidemiology and clinical presentation of melanoma in US Hispanics is summarized, and recommendations for a research agenda to advance understanding of this disease in the most rapidly growing segment of the US population is provided.

Melanoma Incidence, Presentation, and Outcomes in US Hispanics

In the period from 2008 to 2012, the age-adjusted incidence of melanoma in US Hispanics (4.6 per 100,00 men and 4.2 per 100,00 women) was lower than in NHWs.⁵ Garnett et al⁵ reported a decline in melanoma incidence in US Hispanics between 2003 and 2012—an observation that stands in contrast to state-level studies in California and Florida, in which small but substantial increases in melanoma incidence among Hispanics were reported.^6,7 The rising incidence of melanomas thicker than 1.5 mm at presentation among Hispanic men living in California is particularly worrisome.⁶ Discrepancies in incidence trends might reflect changes in incidence over time or differences in state-level registry reporting of melanoma.⁵

Despite a lower overall incidence of melanoma in US Hispanics, those who do develop the disease are 2.4 times more likely (age-adjusted odds ratio) to present with stage III disease (confidence interval, 1.89-3.05)⁸ and are 3.64 times more likely to develop distant metastases (confidence interval, 2.65-5.0) than NHWs.^3,7,9-13 Disparities also exist in the diagnosis of childhood melanoma: Hispanic children and adolescents who have a diagnosis of melanoma are 3 times more likely to present with advanced disease than NHW counterparts.¹⁴ Survival analyses by age and stage show considerably lower survival among Hispanic patients compared to NHW patients with stage I and II disease. In part, worse survival outcomes among Hispanics are the result of the pattern of more advanced disease at presentation.^8,14,15

Late presentation for evaluation of melanomas in Hispanics has been attributed to a number of variables, including a lack of skin cancer awareness and knowledge,^9,16 a lower rate of self- and physician-performed skin examinations,¹⁰ differences in tumor biology,⁹ and socioeconomic forces.^7,17

In a previous study investigating the relationship between neighborhood characteristics and tumor stage at melanoma diagnosis in Hispanic men in California, Texas, and Florida, several key findings emerged.¹⁷ First, residency in a census tract with a high density of immigrants (California, Texas) and a high composition of Hispanics (California, Florida) was an important predictor of a late-stage melanoma diagnosis in fully adjusted models. Additionally, the strength of association between measures of socioeconomic status (ie, poverty and education) and tumor stage at melanoma diagnosis was attenuated in multivariate models when enclaves and availability of primary care resources were taken into account. Hispanic melanoma cases in areas with a low density of primary care physicians had an increased likelihood of late-stage diagnosis in California and Texas. The probability of late-stage diagnosis was concentrated in specific regions along the United States–Mexico border, in south central California, and along the southeastern coast of Florida. Lastly, in Texas, Hispanic men aged 18 to 34 years and 35 to 49 years were at an increased risk of late-stage melanoma diagnosis compared to men 65 years and older.¹⁷

Demographic and Clinical Characteristics of Melanoma in Hispanic Patients

Among Hispanics, white Hispanics comprise the majority of melanoma cases.⁵ Median age at diagnosis is younger in Hispanics compared to whites.^5,6 Hispanic men typically are older (median age, 61 years) than Hispanic women (median age, 52 years) at diagnosis.⁵ Similar to what is seen in NHWs, young Hispanic women experience a higher melanoma incidence than young Hispanic men.⁵ Among older Hispanics, melanoma is more common in men.^5,8

Melanomas located on the lower extremities and hips are more prevalent in Hispanics than in NHWs.^5,8,18 Among Hispanics, there are age- and sex-based variations in the anatomic location of primary tumors: in Hispanic men, truncal tumors predominate, and in Hispanic women, tumors of the lower extremities are most common across all age groups.⁵ The incidence of melanomas located in the head and neck region increases with age for both Hispanic men and women.

For melanomas in which the histologic type is known, superficial spreading melanoma is the most common subtype among Hispanics.^5,17,19 Acral lentiginous melanomas and nodular melanomas are more common among Hispanics than among NHWs.^5,17,19

The observation that Hispanics with melanoma are more prone to lower-extremity tumors and nodular and acral lentiginous melanoma subtypes than NHWs suggests that UV exposure history may be of less importance in this population. Although numerous studies have explored melanoma risk factors in NHWs, there is a striking paucity of such studies in Hispanics. For example, there are conflicting data regarding the role of UV exposure in melanoma risk among Hispanics. Hu et al²⁰ found that UV index and latitude correlated with melanoma risk in this population, whereas Eide et al²¹ found no association between UV exposure and melanoma incidence in Hispanics. A prospective study involving a multiethnic cohort (of whom 40 of the 107 participants were Hispanic) found no clear association between a history of sunburn and melanoma risk in Hispanics.¹⁸

Strategies for Reducing Disparities in Outcomes

Our knowledge of melanoma epidemiology in Hispanics derives mainly from secondary analyses of state-level and national cancer registry data sets.^{5-8,13-15,17,19,20} These administrative data sources often are limited by missing data (eg, tumor thickness, histologic subtype) or lack important patient-level information (eg, self-identified race and ethnicity, health insurance status). Additionally, the manner in which data are collected and integrated into research varies; for example, socioeconomic measures often are reported as either area-based or composite measures. Thus, there is a need to improve the consistency of reporting on demographic and socioeconomic measures across studies. Polite et al²² recommended standardization of reporting criteria and that a standard set of demographic and socioeconomic status measures be included in clinical registries and research protocols.²² Researchers should strive to collect self-reported information on race and ethnicity, as well as the most granular level of detail on health insurance status, ancestry, and immigration status.

The host phenotypic characteristics of melanoma in NHWs are well understood, but the biological and environmental determinants of melanoma risk in Hispanics and other minorities are unknown. For example, fair complexion, red hair, blue eyes, increased freckling density, and the presence of numerous dysplastic and common melanocytic nevi indicate a propensity toward cutaneous melanoma.^23,24 However, the relevance of such risk factors in Hispanics is unknown and has not been widely investigated in this patient population. Park et al¹⁸ found that a person’s sunburn susceptibility phenotype (defined as hair and eye color, ability to tan, and skin reaction to sunlight) was associated with an increased risk of melanoma among nonwhite, multiracial individuals. However, this study was limited by a small number of minority cases, which included only 40 Hispanic participants with melanoma.¹⁸ There is a need for rigorous observational studies to clearly define the phenotypic characteristics, sun-exposure behavior patterns, and genetic contributors to melanoma genesis in Hispanics.

The biologic determinants of postdiagnosis survival in Hispanics with melanoma are not well understood. It is unknown if genetic predisposition modifies melanoma risk in Hispanics. For example, the frequency of BRAF gene mutation or other driver mutations in US Hispanics has been understudied. It is important to know if mutation frequency patterns differ in Hispanics patients compared to NHWs because this knowledge could have considerable implications for treatment. Several recommendations should be considered to address these knowledge gaps. First, there is a need for development or enhancement of melanoma biorepositories, which should include tumor and nontumor specimens from a diverse sample of melanoma patients. Additionally, multi-institutional and multidisciplinary consortiums need to be created in order to amass a number of Hispanic melanoma patients to identify genetic, biologic, and behavioral risk factors specific to this subgroup of patients. The AMBER Consortium, which focuses on breast cancer epidemiology and risk in black women, is a model for the type of consortium needed for the study of melanoma in Hispanics.²⁵ Lastly, community engagement will be central to developing sustainable recruitment and data-collection efforts.²⁶ Involvement of key stakeholders will provide an in-depth assessment of community needs as well as real-time feedback on the process and practicality of research questions. Buy-in from affected communities also may facilitate dissemination of research findings to affected communities.

Conclusion

Hispanics are more likely to present with an advanced stages of disease and have higher melanoma-specific mortality rates than NHWs. Regrettably, a huge knowledge gap exists regarding contributors and solutions to melanoma disparities among this fast-growing, understudied segment of the US population. Accordingly, critical research is needed to address the most pressing questions regarding melanoma risk and poor outcomes among Hispanics to foster implementation of interventional efforts in prevention, early detection, and treatment. A multi-institutional and multidisciplinary approach across multiple levels is needed to eliminate disparate outcomes. Although melanoma is relatively uncommon among Hispanics, studies of melanoma in Hispanics (given their diverse genetic ancestry and migration) provide a unique backdrop against which researchers can explicate melanoma etiology—thus benefiting Hispanics and non-Hispanics alike.

Cutaneous melanoma is a considerable public health concern. In the United States, an estimated 87,110 cases were diagnosed in 2017, and more than 9000 deaths are expected as result of this disease in 2018.¹ Early diagnosis of melanoma is associated with favorable survival rates (5-year overall survival rates for melanoma in situ and stage IA melanoma, 99% and 97%, respectively).² In contrast, the prognosis for advanced-stage melanoma is poor, with a 5-year survival rate of 16% for patients with stage IV disease. Therefore, early detection is critical to reducing mortality in melanoma patients.³

The term Hispanic refers to a panethnic category primarily encompassing Mexican-Americans, Cubans, and Puerto Ricans, as well as individuals from the Caribbean and Central and South America. These populations are diverse in birth origin, primary language, acculturation, distinct ethnic traditions, education level, and occupation. Hispanics in the United States are heterogeneous in many dimensions related to health risks, health care use, and health outcomes.⁴ Genetic predisposition, lifestyle risks, and access to and use of health care services can shape melanoma diagnosis, treatment, and progression across Hispanic populations differently than in other populations.

In this review, the epidemiology and clinical presentation of melanoma in US Hispanics is summarized, and recommendations for a research agenda to advance understanding of this disease in the most rapidly growing segment of the US population is provided.

Melanoma Incidence, Presentation, and Outcomes in US Hispanics

In the period from 2008 to 2012, the age-adjusted incidence of melanoma in US Hispanics (4.6 per 100,00 men and 4.2 per 100,00 women) was lower than in NHWs.⁵ Garnett et al⁵ reported a decline in melanoma incidence in US Hispanics between 2003 and 2012—an observation that stands in contrast to state-level studies in California and Florida, in which small but substantial increases in melanoma incidence among Hispanics were reported.^6,7 The rising incidence of melanomas thicker than 1.5 mm at presentation among Hispanic men living in California is particularly worrisome.⁶ Discrepancies in incidence trends might reflect changes in incidence over time or differences in state-level registry reporting of melanoma.⁵

Despite a lower overall incidence of melanoma in US Hispanics, those who do develop the disease are 2.4 times more likely (age-adjusted odds ratio) to present with stage III disease (confidence interval, 1.89-3.05)⁸ and are 3.64 times more likely to develop distant metastases (confidence interval, 2.65-5.0) than NHWs.^3,7,9-13 Disparities also exist in the diagnosis of childhood melanoma: Hispanic children and adolescents who have a diagnosis of melanoma are 3 times more likely to present with advanced disease than NHW counterparts.¹⁴ Survival analyses by age and stage show considerably lower survival among Hispanic patients compared to NHW patients with stage I and II disease. In part, worse survival outcomes among Hispanics are the result of the pattern of more advanced disease at presentation.^8,14,15

Late presentation for evaluation of melanomas in Hispanics has been attributed to a number of variables, including a lack of skin cancer awareness and knowledge,^9,16 a lower rate of self- and physician-performed skin examinations,¹⁰ differences in tumor biology,⁹ and socioeconomic forces.^7,17

In a previous study investigating the relationship between neighborhood characteristics and tumor stage at melanoma diagnosis in Hispanic men in California, Texas, and Florida, several key findings emerged.¹⁷ First, residency in a census tract with a high density of immigrants (California, Texas) and a high composition of Hispanics (California, Florida) was an important predictor of a late-stage melanoma diagnosis in fully adjusted models. Additionally, the strength of association between measures of socioeconomic status (ie, poverty and education) and tumor stage at melanoma diagnosis was attenuated in multivariate models when enclaves and availability of primary care resources were taken into account. Hispanic melanoma cases in areas with a low density of primary care physicians had an increased likelihood of late-stage diagnosis in California and Texas. The probability of late-stage diagnosis was concentrated in specific regions along the United States–Mexico border, in south central California, and along the southeastern coast of Florida. Lastly, in Texas, Hispanic men aged 18 to 34 years and 35 to 49 years were at an increased risk of late-stage melanoma diagnosis compared to men 65 years and older.¹⁷

Demographic and Clinical Characteristics of Melanoma in Hispanic Patients

Among Hispanics, white Hispanics comprise the majority of melanoma cases.⁵ Median age at diagnosis is younger in Hispanics compared to whites.^5,6 Hispanic men typically are older (median age, 61 years) than Hispanic women (median age, 52 years) at diagnosis.⁵ Similar to what is seen in NHWs, young Hispanic women experience a higher melanoma incidence than young Hispanic men.⁵ Among older Hispanics, melanoma is more common in men.^5,8

Melanomas located on the lower extremities and hips are more prevalent in Hispanics than in NHWs.^5,8,18 Among Hispanics, there are age- and sex-based variations in the anatomic location of primary tumors: in Hispanic men, truncal tumors predominate, and in Hispanic women, tumors of the lower extremities are most common across all age groups.⁵ The incidence of melanomas located in the head and neck region increases with age for both Hispanic men and women.

For melanomas in which the histologic type is known, superficial spreading melanoma is the most common subtype among Hispanics.^5,17,19 Acral lentiginous melanomas and nodular melanomas are more common among Hispanics than among NHWs.^5,17,19

The observation that Hispanics with melanoma are more prone to lower-extremity tumors and nodular and acral lentiginous melanoma subtypes than NHWs suggests that UV exposure history may be of less importance in this population. Although numerous studies have explored melanoma risk factors in NHWs, there is a striking paucity of such studies in Hispanics. For example, there are conflicting data regarding the role of UV exposure in melanoma risk among Hispanics. Hu et al²⁰ found that UV index and latitude correlated with melanoma risk in this population, whereas Eide et al²¹ found no association between UV exposure and melanoma incidence in Hispanics. A prospective study involving a multiethnic cohort (of whom 40 of the 107 participants were Hispanic) found no clear association between a history of sunburn and melanoma risk in Hispanics.¹⁸

Strategies for Reducing Disparities in Outcomes

Our knowledge of melanoma epidemiology in Hispanics derives mainly from secondary analyses of state-level and national cancer registry data sets.^{5-8,13-15,17,19,20} These administrative data sources often are limited by missing data (eg, tumor thickness, histologic subtype) or lack important patient-level information (eg, self-identified race and ethnicity, health insurance status). Additionally, the manner in which data are collected and integrated into research varies; for example, socioeconomic measures often are reported as either area-based or composite measures. Thus, there is a need to improve the consistency of reporting on demographic and socioeconomic measures across studies. Polite et al²² recommended standardization of reporting criteria and that a standard set of demographic and socioeconomic status measures be included in clinical registries and research protocols.²² Researchers should strive to collect self-reported information on race and ethnicity, as well as the most granular level of detail on health insurance status, ancestry, and immigration status.

The host phenotypic characteristics of melanoma in NHWs are well understood, but the biological and environmental determinants of melanoma risk in Hispanics and other minorities are unknown. For example, fair complexion, red hair, blue eyes, increased freckling density, and the presence of numerous dysplastic and common melanocytic nevi indicate a propensity toward cutaneous melanoma.^23,24 However, the relevance of such risk factors in Hispanics is unknown and has not been widely investigated in this patient population. Park et al¹⁸ found that a person’s sunburn susceptibility phenotype (defined as hair and eye color, ability to tan, and skin reaction to sunlight) was associated with an increased risk of melanoma among nonwhite, multiracial individuals. However, this study was limited by a small number of minority cases, which included only 40 Hispanic participants with melanoma.¹⁸ There is a need for rigorous observational studies to clearly define the phenotypic characteristics, sun-exposure behavior patterns, and genetic contributors to melanoma genesis in Hispanics.

The biologic determinants of postdiagnosis survival in Hispanics with melanoma are not well understood. It is unknown if genetic predisposition modifies melanoma risk in Hispanics. For example, the frequency of BRAF gene mutation or other driver mutations in US Hispanics has been understudied. It is important to know if mutation frequency patterns differ in Hispanics patients compared to NHWs because this knowledge could have considerable implications for treatment. Several recommendations should be considered to address these knowledge gaps. First, there is a need for development or enhancement of melanoma biorepositories, which should include tumor and nontumor specimens from a diverse sample of melanoma patients. Additionally, multi-institutional and multidisciplinary consortiums need to be created in order to amass a number of Hispanic melanoma patients to identify genetic, biologic, and behavioral risk factors specific to this subgroup of patients. The AMBER Consortium, which focuses on breast cancer epidemiology and risk in black women, is a model for the type of consortium needed for the study of melanoma in Hispanics.²⁵ Lastly, community engagement will be central to developing sustainable recruitment and data-collection efforts.²⁶ Involvement of key stakeholders will provide an in-depth assessment of community needs as well as real-time feedback on the process and practicality of research questions. Buy-in from affected communities also may facilitate dissemination of research findings to affected communities.

Conclusion

Hispanics are more likely to present with an advanced stages of disease and have higher melanoma-specific mortality rates than NHWs. Regrettably, a huge knowledge gap exists regarding contributors and solutions to melanoma disparities among this fast-growing, understudied segment of the US population. Accordingly, critical research is needed to address the most pressing questions regarding melanoma risk and poor outcomes among Hispanics to foster implementation of interventional efforts in prevention, early detection, and treatment. A multi-institutional and multidisciplinary approach across multiple levels is needed to eliminate disparate outcomes. Although melanoma is relatively uncommon among Hispanics, studies of melanoma in Hispanics (given their diverse genetic ancestry and migration) provide a unique backdrop against which researchers can explicate melanoma etiology—thus benefiting Hispanics and non-Hispanics alike.

Cutaneous melanoma is a considerable public health concern. In the United States, an estimated 87,110 cases were diagnosed in 2017, and more than 9000 deaths are expected as result of this disease in 2018.¹ Early diagnosis of melanoma is associated with favorable survival rates (5-year overall survival rates for melanoma in situ and stage IA melanoma, 99% and 97%, respectively).² In contrast, the prognosis for advanced-stage melanoma is poor, with a 5-year survival rate of 16% for patients with stage IV disease. Therefore, early detection is critical to reducing mortality in melanoma patients.³

The term Hispanic refers to a panethnic category primarily encompassing Mexican-Americans, Cubans, and Puerto Ricans, as well as individuals from the Caribbean and Central and South America. These populations are diverse in birth origin, primary language, acculturation, distinct ethnic traditions, education level, and occupation. Hispanics in the United States are heterogeneous in many dimensions related to health risks, health care use, and health outcomes.⁴ Genetic predisposition, lifestyle risks, and access to and use of health care services can shape melanoma diagnosis, treatment, and progression across Hispanic populations differently than in other populations.

In this review, the epidemiology and clinical presentation of melanoma in US Hispanics is summarized, and recommendations for a research agenda to advance understanding of this disease in the most rapidly growing segment of the US population is provided.

Melanoma Incidence, Presentation, and Outcomes in US Hispanics

In the period from 2008 to 2012, the age-adjusted incidence of melanoma in US Hispanics (4.6 per 100,00 men and 4.2 per 100,00 women) was lower than in NHWs.⁵ Garnett et al⁵ reported a decline in melanoma incidence in US Hispanics between 2003 and 2012—an observation that stands in contrast to state-level studies in California and Florida, in which small but substantial increases in melanoma incidence among Hispanics were reported.^6,7 The rising incidence of melanomas thicker than 1.5 mm at presentation among Hispanic men living in California is particularly worrisome.⁶ Discrepancies in incidence trends might reflect changes in incidence over time or differences in state-level registry reporting of melanoma.⁵

Despite a lower overall incidence of melanoma in US Hispanics, those who do develop the disease are 2.4 times more likely (age-adjusted odds ratio) to present with stage III disease (confidence interval, 1.89-3.05)⁸ and are 3.64 times more likely to develop distant metastases (confidence interval, 2.65-5.0) than NHWs.^3,7,9-13 Disparities also exist in the diagnosis of childhood melanoma: Hispanic children and adolescents who have a diagnosis of melanoma are 3 times more likely to present with advanced disease than NHW counterparts.¹⁴ Survival analyses by age and stage show considerably lower survival among Hispanic patients compared to NHW patients with stage I and II disease. In part, worse survival outcomes among Hispanics are the result of the pattern of more advanced disease at presentation.^8,14,15

Late presentation for evaluation of melanomas in Hispanics has been attributed to a number of variables, including a lack of skin cancer awareness and knowledge,^9,16 a lower rate of self- and physician-performed skin examinations,¹⁰ differences in tumor biology,⁹ and socioeconomic forces.^7,17

In a previous study investigating the relationship between neighborhood characteristics and tumor stage at melanoma diagnosis in Hispanic men in California, Texas, and Florida, several key findings emerged.¹⁷ First, residency in a census tract with a high density of immigrants (California, Texas) and a high composition of Hispanics (California, Florida) was an important predictor of a late-stage melanoma diagnosis in fully adjusted models. Additionally, the strength of association between measures of socioeconomic status (ie, poverty and education) and tumor stage at melanoma diagnosis was attenuated in multivariate models when enclaves and availability of primary care resources were taken into account. Hispanic melanoma cases in areas with a low density of primary care physicians had an increased likelihood of late-stage diagnosis in California and Texas. The probability of late-stage diagnosis was concentrated in specific regions along the United States–Mexico border, in south central California, and along the southeastern coast of Florida. Lastly, in Texas, Hispanic men aged 18 to 34 years and 35 to 49 years were at an increased risk of late-stage melanoma diagnosis compared to men 65 years and older.¹⁷

Demographic and Clinical Characteristics of Melanoma in Hispanic Patients

Among Hispanics, white Hispanics comprise the majority of melanoma cases.⁵ Median age at diagnosis is younger in Hispanics compared to whites.^5,6 Hispanic men typically are older (median age, 61 years) than Hispanic women (median age, 52 years) at diagnosis.⁵ Similar to what is seen in NHWs, young Hispanic women experience a higher melanoma incidence than young Hispanic men.⁵ Among older Hispanics, melanoma is more common in men.^5,8

Melanomas located on the lower extremities and hips are more prevalent in Hispanics than in NHWs.^5,8,18 Among Hispanics, there are age- and sex-based variations in the anatomic location of primary tumors: in Hispanic men, truncal tumors predominate, and in Hispanic women, tumors of the lower extremities are most common across all age groups.⁵ The incidence of melanomas located in the head and neck region increases with age for both Hispanic men and women.

For melanomas in which the histologic type is known, superficial spreading melanoma is the most common subtype among Hispanics.^5,17,19 Acral lentiginous melanomas and nodular melanomas are more common among Hispanics than among NHWs.^5,17,19

The observation that Hispanics with melanoma are more prone to lower-extremity tumors and nodular and acral lentiginous melanoma subtypes than NHWs suggests that UV exposure history may be of less importance in this population. Although numerous studies have explored melanoma risk factors in NHWs, there is a striking paucity of such studies in Hispanics. For example, there are conflicting data regarding the role of UV exposure in melanoma risk among Hispanics. Hu et al²⁰ found that UV index and latitude correlated with melanoma risk in this population, whereas Eide et al²¹ found no association between UV exposure and melanoma incidence in Hispanics. A prospective study involving a multiethnic cohort (of whom 40 of the 107 participants were Hispanic) found no clear association between a history of sunburn and melanoma risk in Hispanics.¹⁸

Strategies for Reducing Disparities in Outcomes

Our knowledge of melanoma epidemiology in Hispanics derives mainly from secondary analyses of state-level and national cancer registry data sets.^{5-8,13-15,17,19,20} These administrative data sources often are limited by missing data (eg, tumor thickness, histologic subtype) or lack important patient-level information (eg, self-identified race and ethnicity, health insurance status). Additionally, the manner in which data are collected and integrated into research varies; for example, socioeconomic measures often are reported as either area-based or composite measures. Thus, there is a need to improve the consistency of reporting on demographic and socioeconomic measures across studies. Polite et al²² recommended standardization of reporting criteria and that a standard set of demographic and socioeconomic status measures be included in clinical registries and research protocols.²² Researchers should strive to collect self-reported information on race and ethnicity, as well as the most granular level of detail on health insurance status, ancestry, and immigration status.

The host phenotypic characteristics of melanoma in NHWs are well understood, but the biological and environmental determinants of melanoma risk in Hispanics and other minorities are unknown. For example, fair complexion, red hair, blue eyes, increased freckling density, and the presence of numerous dysplastic and common melanocytic nevi indicate a propensity toward cutaneous melanoma.^23,24 However, the relevance of such risk factors in Hispanics is unknown and has not been widely investigated in this patient population. Park et al¹⁸ found that a person’s sunburn susceptibility phenotype (defined as hair and eye color, ability to tan, and skin reaction to sunlight) was associated with an increased risk of melanoma among nonwhite, multiracial individuals. However, this study was limited by a small number of minority cases, which included only 40 Hispanic participants with melanoma.¹⁸ There is a need for rigorous observational studies to clearly define the phenotypic characteristics, sun-exposure behavior patterns, and genetic contributors to melanoma genesis in Hispanics.

The biologic determinants of postdiagnosis survival in Hispanics with melanoma are not well understood. It is unknown if genetic predisposition modifies melanoma risk in Hispanics. For example, the frequency of BRAF gene mutation or other driver mutations in US Hispanics has been understudied. It is important to know if mutation frequency patterns differ in Hispanics patients compared to NHWs because this knowledge could have considerable implications for treatment. Several recommendations should be considered to address these knowledge gaps. First, there is a need for development or enhancement of melanoma biorepositories, which should include tumor and nontumor specimens from a diverse sample of melanoma patients. Additionally, multi-institutional and multidisciplinary consortiums need to be created in order to amass a number of Hispanic melanoma patients to identify genetic, biologic, and behavioral risk factors specific to this subgroup of patients. The AMBER Consortium, which focuses on breast cancer epidemiology and risk in black women, is a model for the type of consortium needed for the study of melanoma in Hispanics.²⁵ Lastly, community engagement will be central to developing sustainable recruitment and data-collection efforts.²⁶ Involvement of key stakeholders will provide an in-depth assessment of community needs as well as real-time feedback on the process and practicality of research questions. Buy-in from affected communities also may facilitate dissemination of research findings to affected communities.

Conclusion

Hispanics are more likely to present with an advanced stages of disease and have higher melanoma-specific mortality rates than NHWs. Regrettably, a huge knowledge gap exists regarding contributors and solutions to melanoma disparities among this fast-growing, understudied segment of the US population. Accordingly, critical research is needed to address the most pressing questions regarding melanoma risk and poor outcomes among Hispanics to foster implementation of interventional efforts in prevention, early detection, and treatment. A multi-institutional and multidisciplinary approach across multiple levels is needed to eliminate disparate outcomes. Although melanoma is relatively uncommon among Hispanics, studies of melanoma in Hispanics (given their diverse genetic ancestry and migration) provide a unique backdrop against which researchers can explicate melanoma etiology—thus benefiting Hispanics and non-Hispanics alike.