Diversity in Medicine

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.

More women die from pregnancy complications in the United States than in any other developed country. The United States is the only industrialized nation with a rising maternal mortality rate.

Those 2 sentences should stop us all in our tracks.

In fact, the United States ranks 47th globally with the worst maternal mortality rate. More than half these deaths are likely preventable, with suicide and drug overdose the leading causes of maternal death in many states. All this occurs despite our advanced medical system, premier medical colleges and universities, embrace of high-tech medical advances, and high percentage of gross domestic product spent on health care.

Need more numbers? According to a 2016 report in Obstetrics and Gynecology, the United States saw a 26% increase in the maternalmortality rate (unadjusted) in only 15 years: from 18.8 deaths per 100,000 live births in 2000 to 23.8 in 2014 (FIGURE 1).¹

Considerable variations by race and by state

The racial disparities in maternal mortality are staggering and have not improved in more than 20 years: African American women are 3.4 times more likely to die than non-Hispanic white women of pregnancy-related complications. In 2011–2013, the maternal mortality ratio for non-Hispanic white women was 12.7 deaths per 100,000 live births compared with 43.5 deaths for non-Hispanic black women (FIGURE 2).² American Indian or Alaska Native women, Asian women, and some Latina women also experience higher rates than non-Hispanic white women. The rate for American Indian or Alaska Native women is 16.9 deaths per 100,000 live births.³

Some states are doing better than others, showing that there is nothing inevitable about the maternal mortality crisis. Texas, for example, has seen the highest rate of maternal mortality increase. Its rate doubled from 2010 to 2012, while California reduced its maternal death rate by 30%, from 21.5 to 15.1, during roughly the same period.¹

This is a challenge of epic proportions, and one that the American College of Obstetricians and Gynecologists (ACOG), under the leadership of President Haywood Brown, MD, and Incoming President Lisa Hollier, MD, is determined to meet, ensuring that a high maternal death rate does not become our nation’s new normal.

Dr. Brown put it this way, “ACOG collaborative initiatives such as Levels of Maternal Care (LOMC) and implementation of OB safety bundles for hemorrhage, hypertension, and thromboembolism through the AIM [Alliance for Innovation on Maternal Health] Program target maternal morbidity and mortality at the community level. Bundles have also been developed to address the disparity in maternal mortality and for the opiate crisis.”

ACOG is making strides in putting in place nationwide meaningful, evidence-driven systems and care approaches that are proven to reduce maternal mortality and morbidity, saving mothers’ lives and keeping families whole.

Read about the AIM Program’s initiatives

ACOG’s AIM Program established to make an impact

The AIM Program (www.safehealthcare foreverywoman.org) is bringing together clinicians, public health officials, hospital administrators, patient safety organizations, and advocates to eliminate preventable maternal mortality throughout the United States. With funding and support from the US Health Resources and Services Administration, AIM is striving to:

• reduce maternal mortality by 1,000 deaths by 2018
• reduce severe maternal morbidity
• assist states and hospitals to improve outcomes
• create and encourage use of maternal safety bundles (evidence-based tool kits to guide the best care).

AIM offers participating physicians and hospitals online learning modules, checklists, work plans, and links to tool kits and published resources. Implementation data is shared with hospitals and states to further improve care. Physicians participating in AIM can receive Part IV maintenance of certification; continuing education units will soon be offered for nurses. In the future, AIM-participating hospitals may be able to receive reduced liability protection costs, too.

To date, 17 states are participating in the AIM initiative (FIGURE 3), with more states ready to enroll.⁴ States must demonstrate a commitment to lasting change to participate. Each AIM state must have an active maternal mortality review committee (MMRC); committed leadership from public health, hospital associations, and provider associations; and a commitment to report AIM data.

• reducing disparities in maternity care
• severe hypertension in pregnancy
• safe reduction of primary cesarean birth
• prevention of venous thromboembolism
• obstetric hemorrhage
• maternal mental health
• patient, family, and staff support following a severe maternal event
• postpartum care basics
• obstetric care of women with opioid use disorder (in use by Illinois, Massachusetts, Maryland, New Jersey, Maine, New Hampshire, Vermont, New York, Ohio, Oklahoma, Tennessee, Texas, and Virginia).

Read about how active MMRCS are critical to success

Review committees are critical to success

In use in many states, MMRCs are groups of local ObGyns, nurses, social workers, and other health care professionals who review specific cases of maternal deaths from their local area and recommend local solutions to prevent future deaths. MMRCs can be a critically important source of data to help us understand the underlying causes of maternal mortality.

Remember California’s success in reducing its maternal mortality rate, previously mentioned? That state was an early adopter of an active MMRC and has worked to bring best practices to maternity care throughout the state.

While every state should have an active MMRC, not every state does. ACOG is working with states, local leaders, and state and federal legislatures to help develop MMRCs in every state.

Dr. Brown pointed out that, “For several decades, Indiana had a legislatively authorized multidisciplinary maternal mortality review committee that I actively participated in and led in the late 1990s. The authorization for the program lapsed in the early 2000s, and the Indiana MMRC had to shut down. Bolstering the federal government’s capacity to help states like Indiana rebuild MMRCs, or start them from scratch, will help state public health officials, hospitals, and physicians take better care of moms and babies.”

Dr. Hollier explained, “In Texas, I chair our Maternal Mortality and Morbidity Task Force, which was legislatively authorized in 2013 in response to the rising rate of maternal death. The detailed state-based maternal mortality reviews provide critical information: verification of vital statistics data, assessment of the causes and contributing factors, and determination of pregnancy relatedness. These reviews identify opportunities for prevention and implementation of the most appropriate interventions to reduce maternal mortality on a local level. Support of essential review functions at the federal level would also enable data to be combined across jurisdictions for national learning that was previously not possible.”

Pending legislation will strengthen efforts

ACOG is working to enact into law the Preventing Maternal Deaths Act, HR 1318 and S1112. This is bipartisan legislation under which the Centers for Disease Control and Prevention would help states create or expand MMRCs and will require the Department of Health and Human Services to research ways to reduce disparities in maternal health outcomes.

Acknowledgement
The author thanks Jean Mahoney, ACOG’s Senior Director, AIM, for her generous assistance.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

More women die from pregnancy complications in the United States than in any other developed country. The United States is the only industrialized nation with a rising maternal mortality rate.

Those 2 sentences should stop us all in our tracks.

In fact, the United States ranks 47th globally with the worst maternal mortality rate. More than half these deaths are likely preventable, with suicide and drug overdose the leading causes of maternal death in many states. All this occurs despite our advanced medical system, premier medical colleges and universities, embrace of high-tech medical advances, and high percentage of gross domestic product spent on health care.

Need more numbers? According to a 2016 report in Obstetrics and Gynecology, the United States saw a 26% increase in the maternalmortality rate (unadjusted) in only 15 years: from 18.8 deaths per 100,000 live births in 2000 to 23.8 in 2014 (FIGURE 1).¹

Considerable variations by race and by state

The racial disparities in maternal mortality are staggering and have not improved in more than 20 years: African American women are 3.4 times more likely to die than non-Hispanic white women of pregnancy-related complications. In 2011–2013, the maternal mortality ratio for non-Hispanic white women was 12.7 deaths per 100,000 live births compared with 43.5 deaths for non-Hispanic black women (FIGURE 2).² American Indian or Alaska Native women, Asian women, and some Latina women also experience higher rates than non-Hispanic white women. The rate for American Indian or Alaska Native women is 16.9 deaths per 100,000 live births.³

Some states are doing better than others, showing that there is nothing inevitable about the maternal mortality crisis. Texas, for example, has seen the highest rate of maternal mortality increase. Its rate doubled from 2010 to 2012, while California reduced its maternal death rate by 30%, from 21.5 to 15.1, during roughly the same period.¹

This is a challenge of epic proportions, and one that the American College of Obstetricians and Gynecologists (ACOG), under the leadership of President Haywood Brown, MD, and Incoming President Lisa Hollier, MD, is determined to meet, ensuring that a high maternal death rate does not become our nation’s new normal.

Dr. Brown put it this way, “ACOG collaborative initiatives such as Levels of Maternal Care (LOMC) and implementation of OB safety bundles for hemorrhage, hypertension, and thromboembolism through the AIM [Alliance for Innovation on Maternal Health] Program target maternal morbidity and mortality at the community level. Bundles have also been developed to address the disparity in maternal mortality and for the opiate crisis.”

ACOG is making strides in putting in place nationwide meaningful, evidence-driven systems and care approaches that are proven to reduce maternal mortality and morbidity, saving mothers’ lives and keeping families whole.

Read about the AIM Program’s initiatives

ACOG’s AIM Program established to make an impact

The AIM Program (www.safehealthcare foreverywoman.org) is bringing together clinicians, public health officials, hospital administrators, patient safety organizations, and advocates to eliminate preventable maternal mortality throughout the United States. With funding and support from the US Health Resources and Services Administration, AIM is striving to:

• reduce maternal mortality by 1,000 deaths by 2018
• reduce severe maternal morbidity
• assist states and hospitals to improve outcomes
• create and encourage use of maternal safety bundles (evidence-based tool kits to guide the best care).

AIM offers participating physicians and hospitals online learning modules, checklists, work plans, and links to tool kits and published resources. Implementation data is shared with hospitals and states to further improve care. Physicians participating in AIM can receive Part IV maintenance of certification; continuing education units will soon be offered for nurses. In the future, AIM-participating hospitals may be able to receive reduced liability protection costs, too.

To date, 17 states are participating in the AIM initiative (FIGURE 3), with more states ready to enroll.⁴ States must demonstrate a commitment to lasting change to participate. Each AIM state must have an active maternal mortality review committee (MMRC); committed leadership from public health, hospital associations, and provider associations; and a commitment to report AIM data.

• reducing disparities in maternity care
• severe hypertension in pregnancy
• safe reduction of primary cesarean birth
• prevention of venous thromboembolism
• obstetric hemorrhage
• maternal mental health
• patient, family, and staff support following a severe maternal event
• postpartum care basics
• obstetric care of women with opioid use disorder (in use by Illinois, Massachusetts, Maryland, New Jersey, Maine, New Hampshire, Vermont, New York, Ohio, Oklahoma, Tennessee, Texas, and Virginia).

Read about how active MMRCS are critical to success

Review committees are critical to success

In use in many states, MMRCs are groups of local ObGyns, nurses, social workers, and other health care professionals who review specific cases of maternal deaths from their local area and recommend local solutions to prevent future deaths. MMRCs can be a critically important source of data to help us understand the underlying causes of maternal mortality.

Remember California’s success in reducing its maternal mortality rate, previously mentioned? That state was an early adopter of an active MMRC and has worked to bring best practices to maternity care throughout the state.

While every state should have an active MMRC, not every state does. ACOG is working with states, local leaders, and state and federal legislatures to help develop MMRCs in every state.

Dr. Brown pointed out that, “For several decades, Indiana had a legislatively authorized multidisciplinary maternal mortality review committee that I actively participated in and led in the late 1990s. The authorization for the program lapsed in the early 2000s, and the Indiana MMRC had to shut down. Bolstering the federal government’s capacity to help states like Indiana rebuild MMRCs, or start them from scratch, will help state public health officials, hospitals, and physicians take better care of moms and babies.”

Dr. Hollier explained, “In Texas, I chair our Maternal Mortality and Morbidity Task Force, which was legislatively authorized in 2013 in response to the rising rate of maternal death. The detailed state-based maternal mortality reviews provide critical information: verification of vital statistics data, assessment of the causes and contributing factors, and determination of pregnancy relatedness. These reviews identify opportunities for prevention and implementation of the most appropriate interventions to reduce maternal mortality on a local level. Support of essential review functions at the federal level would also enable data to be combined across jurisdictions for national learning that was previously not possible.”

Pending legislation will strengthen efforts

ACOG is working to enact into law the Preventing Maternal Deaths Act, HR 1318 and S1112. This is bipartisan legislation under which the Centers for Disease Control and Prevention would help states create or expand MMRCs and will require the Department of Health and Human Services to research ways to reduce disparities in maternal health outcomes.

Acknowledgement
The author thanks Jean Mahoney, ACOG’s Senior Director, AIM, for her generous assistance.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

More women die from pregnancy complications in the United States than in any other developed country. The United States is the only industrialized nation with a rising maternal mortality rate.

Those 2 sentences should stop us all in our tracks.

In fact, the United States ranks 47th globally with the worst maternal mortality rate. More than half these deaths are likely preventable, with suicide and drug overdose the leading causes of maternal death in many states. All this occurs despite our advanced medical system, premier medical colleges and universities, embrace of high-tech medical advances, and high percentage of gross domestic product spent on health care.

Need more numbers? According to a 2016 report in Obstetrics and Gynecology, the United States saw a 26% increase in the maternalmortality rate (unadjusted) in only 15 years: from 18.8 deaths per 100,000 live births in 2000 to 23.8 in 2014 (FIGURE 1).¹

Considerable variations by race and by state

The racial disparities in maternal mortality are staggering and have not improved in more than 20 years: African American women are 3.4 times more likely to die than non-Hispanic white women of pregnancy-related complications. In 2011–2013, the maternal mortality ratio for non-Hispanic white women was 12.7 deaths per 100,000 live births compared with 43.5 deaths for non-Hispanic black women (FIGURE 2).² American Indian or Alaska Native women, Asian women, and some Latina women also experience higher rates than non-Hispanic white women. The rate for American Indian or Alaska Native women is 16.9 deaths per 100,000 live births.³

Some states are doing better than others, showing that there is nothing inevitable about the maternal mortality crisis. Texas, for example, has seen the highest rate of maternal mortality increase. Its rate doubled from 2010 to 2012, while California reduced its maternal death rate by 30%, from 21.5 to 15.1, during roughly the same period.¹

This is a challenge of epic proportions, and one that the American College of Obstetricians and Gynecologists (ACOG), under the leadership of President Haywood Brown, MD, and Incoming President Lisa Hollier, MD, is determined to meet, ensuring that a high maternal death rate does not become our nation’s new normal.

Dr. Brown put it this way, “ACOG collaborative initiatives such as Levels of Maternal Care (LOMC) and implementation of OB safety bundles for hemorrhage, hypertension, and thromboembolism through the AIM [Alliance for Innovation on Maternal Health] Program target maternal morbidity and mortality at the community level. Bundles have also been developed to address the disparity in maternal mortality and for the opiate crisis.”

ACOG is making strides in putting in place nationwide meaningful, evidence-driven systems and care approaches that are proven to reduce maternal mortality and morbidity, saving mothers’ lives and keeping families whole.

Read about the AIM Program’s initiatives

ACOG’s AIM Program established to make an impact

The AIM Program (www.safehealthcare foreverywoman.org) is bringing together clinicians, public health officials, hospital administrators, patient safety organizations, and advocates to eliminate preventable maternal mortality throughout the United States. With funding and support from the US Health Resources and Services Administration, AIM is striving to:

• reduce maternal mortality by 1,000 deaths by 2018
• reduce severe maternal morbidity
• assist states and hospitals to improve outcomes
• create and encourage use of maternal safety bundles (evidence-based tool kits to guide the best care).

AIM offers participating physicians and hospitals online learning modules, checklists, work plans, and links to tool kits and published resources. Implementation data is shared with hospitals and states to further improve care. Physicians participating in AIM can receive Part IV maintenance of certification; continuing education units will soon be offered for nurses. In the future, AIM-participating hospitals may be able to receive reduced liability protection costs, too.

To date, 17 states are participating in the AIM initiative (FIGURE 3), with more states ready to enroll.⁴ States must demonstrate a commitment to lasting change to participate. Each AIM state must have an active maternal mortality review committee (MMRC); committed leadership from public health, hospital associations, and provider associations; and a commitment to report AIM data.

• reducing disparities in maternity care
• severe hypertension in pregnancy
• safe reduction of primary cesarean birth
• prevention of venous thromboembolism
• obstetric hemorrhage
• maternal mental health
• patient, family, and staff support following a severe maternal event
• postpartum care basics
• obstetric care of women with opioid use disorder (in use by Illinois, Massachusetts, Maryland, New Jersey, Maine, New Hampshire, Vermont, New York, Ohio, Oklahoma, Tennessee, Texas, and Virginia).

Read about how active MMRCS are critical to success

Review committees are critical to success

In use in many states, MMRCs are groups of local ObGyns, nurses, social workers, and other health care professionals who review specific cases of maternal deaths from their local area and recommend local solutions to prevent future deaths. MMRCs can be a critically important source of data to help us understand the underlying causes of maternal mortality.

Remember California’s success in reducing its maternal mortality rate, previously mentioned? That state was an early adopter of an active MMRC and has worked to bring best practices to maternity care throughout the state.

While every state should have an active MMRC, not every state does. ACOG is working with states, local leaders, and state and federal legislatures to help develop MMRCs in every state.

Dr. Brown pointed out that, “For several decades, Indiana had a legislatively authorized multidisciplinary maternal mortality review committee that I actively participated in and led in the late 1990s. The authorization for the program lapsed in the early 2000s, and the Indiana MMRC had to shut down. Bolstering the federal government’s capacity to help states like Indiana rebuild MMRCs, or start them from scratch, will help state public health officials, hospitals, and physicians take better care of moms and babies.”

Dr. Hollier explained, “In Texas, I chair our Maternal Mortality and Morbidity Task Force, which was legislatively authorized in 2013 in response to the rising rate of maternal death. The detailed state-based maternal mortality reviews provide critical information: verification of vital statistics data, assessment of the causes and contributing factors, and determination of pregnancy relatedness. These reviews identify opportunities for prevention and implementation of the most appropriate interventions to reduce maternal mortality on a local level. Support of essential review functions at the federal level would also enable data to be combined across jurisdictions for national learning that was previously not possible.”

Pending legislation will strengthen efforts

ACOG is working to enact into law the Preventing Maternal Deaths Act, HR 1318 and S1112. This is bipartisan legislation under which the Centers for Disease Control and Prevention would help states create or expand MMRCs and will require the Department of Health and Human Services to research ways to reduce disparities in maternal health outcomes.

Acknowledgement
The author thanks Jean Mahoney, ACOG’s Senior Director, AIM, for her generous assistance.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.¹ Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.^1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.^2,3

It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,⁴ which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.⁴

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.⁵ Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.^4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.⁶ The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al⁷ showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.⁸ A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.⁹ However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.⁹ Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.¹⁰ Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.¹¹ Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.^6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,¹³ but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.⁵ Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.^5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P₀), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.⁶ Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).⁶ Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.⁵ Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.¹⁴ Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.^5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.^4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.¹⁵ A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.⁴ A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.^4,5

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.¹⁶ Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.^16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.¹⁸ They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.¹⁸ 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.¹⁹ Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer¹⁶; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”²⁰ They extended this statement to include isopropylparaben and isobutylparaben in a later review.²¹ In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.²² This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.^16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”²³ However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,¹⁶ and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.²⁴

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.²⁵ Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.¹⁷

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.¹⁶ Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.¹⁶

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.⁵ Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).¹⁶ However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.¹⁶

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.^2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.²⁸ It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.^2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.^26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.³¹ Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.³⁰ Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.^32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.²⁸ The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.³⁰ The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.³³ Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents^2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.²⁸ However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.^2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.³³ Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.³⁴ Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.³⁴

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.^5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.^36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.^36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.³⁸ Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.³⁸

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.¹ Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.^1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.^2,3

It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,⁴ which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.⁴

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.⁵ Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.^4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.⁶ The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al⁷ showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.⁸ A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.⁹ However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.⁹ Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.¹⁰ Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.¹¹ Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.^6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,¹³ but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.⁵ Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.^5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P₀), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.⁶ Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).⁶ Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.⁵ Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.¹⁴ Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.^5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.^4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.¹⁵ A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.⁴ A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.^4,5

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.¹⁶ Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.^16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.¹⁸ They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.¹⁸ 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.¹⁹ Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer¹⁶; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”²⁰ They extended this statement to include isopropylparaben and isobutylparaben in a later review.²¹ In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.²² This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.^16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”²³ However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,¹⁶ and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.²⁴

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.²⁵ Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.¹⁷

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.¹⁶ Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.¹⁶

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.⁵ Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).¹⁶ However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.¹⁶

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.^2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.²⁸ It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.^2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.^26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.³¹ Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.³⁰ Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.^32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.²⁸ The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.³⁰ The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.³³ Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents^2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.²⁸ However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.^2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.³³ Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.³⁴ Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.³⁴

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.^5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.^36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.^36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.³⁸ Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.³⁸

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

Shampoo is a staple in hair grooming that is ever-evolving along with cultural trends. The global shampoo market is expected to reach an estimated value of $25.73 billion by 2019. A major driver of this upward trend in market growth is the increasing demand for natural and organic hair shampoos.¹ Society today has a growing fixation on healthy living practices, and as of late, the ingredients in shampoos and other cosmetic products have become one of the latest targets in the health-consciousness craze. In the age of the Internet where information—and misinformation—is widely accessible and dispersed, the general public often strives to self-educate on specialized matters that are out of their expertise. As a result, individuals have developed an aversion to using certain shampoos out of fear that the ingredients, often referred to as “chemicals” by patients due to their complex names, are unnatural and therefore unhealthy.^1,2 Product developers are working to meet the demand by reformulating shampoos with labels that indicate sulfate free or paraben free, despite the lack of proof that these formulations are an improvement over traditional approaches to hair health. Additionally, alternative methods of cleansing the hair and scalp, also known as the no-shampoo or “no-poo” method, have begun to gain popularity.^2,3

It is essential that dermatologists acknowledge the concerns that their patients have about common shampoo ingredients to dispel the myths that may misinform patient decision-making. This article reviews the controversy surrounding the use of sulfates and parabens in shampoos as well as commonly used shampoo alternatives. Due to the increased prevalence of dry hair shafts in the skin of color population, especially black women, this group is particularly interested in products that will minimize breakage and dryness of the hair. To that end, this population has great interest in the removal of chemical ingredients that may cause damage to the hair shafts, despite the lack of data to support sulfates and paraben damage to hair shafts or scalp skin. Blogs and uninformed hairstylists may propagate these beliefs in a group of consumers who are desperate for new approaches to hair fragility and breakage.

Surfactants and Sulfates

The cleansing ability of a shampoo depends on the surface activity of its detergents. Surface-active ingredients, or surfactants, reduce the surface tension between water and dirt, thus facilitating the removal of environmental dirt from the hair and scalp,⁴ which is achieved by a molecular structure containing both a hydrophilic and a lipophilic group. Sebum and dirt are bound by the lipophilic ends of the surfactant, becoming the center of a micelle structure with the hydrophilic molecule ends pointing outward. Dirt particles become water soluble and are removed from the scalp and hair shaft upon rinsing with water.⁴

Surfactants are classified according to the electric charge of the hydrophilic polar group as either anionic, cationic, amphoteric (zwitterionic), or nonionic.⁵ Each possesses different hair conditioning and cleansing qualities, and multiple surfactants are used in shampoos in differing ratios to accommodate different hair types. In most shampoos, the base consists of anionic and amphoteric surfactants. Depending on individual product requirements, nonionic and cationic surfactants are used to either modify the effects of the surfactants or as conditioning agents.^4,5

One subcategory of surfactants that receives much attention is the group of anionic surfactants known as sulfates. Sulfates, particularly sodium lauryl sulfate (SLS), recently have developed a negative reputation as cosmetic ingredients, as reports from various unscientific sources have labeled them as hazardous to one’s health; SLS has been described as a skin and scalp irritant, has been linked to cataract formation, and has even been wrongly labeled as carcinogenic.⁶ The origins of some of these claims are not clear, though they likely arose from the misinterpretation of complex scientific studies that are easily accessible to laypeople. The link between SLS and ocular irritation or cataract formation is a good illustration of this unsubstantiated fear. A study by Green et al⁷ showed that corneal exposure to extremely high concentrations of SLS following physical or chemical damage to the eye can result in a slowed healing process. The results of this study have since been wrongly quoted to state that SLS-containing products lead to blindness or severe corneal damage.⁸ A different study tested for possible ocular irritation in vivo by submerging the lens of an eye into a 20% SLS solution, which accurately approximates the concentration of SLS in rinse-off consumer products.⁹ However, to achieve ocular irritation, the eyes of laboratory animals were exposed to SLS constantly for 14 days, which would not occur in practical use.⁹ Similarly, a third study achieved cataract formation in a laboratory only by immersing the lens of an eye into a highly concentrated solution of SLS.¹⁰ Such studies are not appropriate representations of how SLS-containing products are used by consumers and have unfortunately been vulnerable to misinterpretation by the general public.

There is no known study that has shown SLS to be carcinogenic. One possible origin of this idea may be from the wrongful interpretation of studies that used SLS as a vehicle substance to test agents that were deemed to be carcinogenic.¹¹ Another possible source of the idea that SLS is carcinogenic comes from its association with 1,4-dioxane, a by-product of the synthesis of certain sulfates such as sodium laureth sulfate due to a process known as ethoxylation.^6,12 Although SLS does not undergo this process in its formation and is not linked to 1,4-dioxane, there is potential for cross-contamination of SLS with 1,4-dioxane, which cannot be overlooked. 1,4-Dioxane is classified as “possibly carcinogenic to humans (Group 2B)” by the International Agency for Research on Cancer,¹³ but screening of SLS for this substance prior to its use in commercial products is standard.

Sulfates are inexpensive detergents that are responsible for lather formation in shampoos as well as in many household cleaning agents.⁵ Sulfates, similar to all anionic surfactants, are characterized by a negatively charged hydrophilic polar group. The best-known and most commonly used anionic surfactants are sulfated fatty alcohols, alkyl sulfates, and their polyethoxylated analogues alkyl ether sulfates.^5,6 Sodium lauryl sulfate (also known as sodium laurilsulfate or sodium dodecyl sulfate) is the most common of them all, found in shampoo and conditioner formulations. Ammonium lauryl sulfate and sodium laureth sulfate are other sulfates commonly used in shampoos and household cleansing products. Sodium lauryl sulfate is a nonvolatile, water-soluble compound. Its partition coefficient (P₀), a measure of a substance’s hydrophilic or lipophilic nature, is low at 1.6, making it a rather hydrophilic substance.⁶ Hydrophilic substances tend to have low bioaccumulation profiles in the body. Additionally, SLS is readily biodegradable. It can be derived from both synthetic and naturally occurring sources; for example, palm kernel oil, petrolatum, and coconut oil are all sources of lauric acid, the starting ingredient used to synthesize SLS. Sodium lauryl sulfate is created by reacting lauryl alcohol with sulfur trioxide gas, followed by neutralization with sodium carbonate (also a naturally occurring compound).⁶ Sodium lauryl sulfate and other sulfate-containing shampoos widely replaced the usage of traditional soaps formulated from animal or vegetable fats, as these latter formations created a film of insoluble calcium salts on the hair strands upon contact with water, resulting in tangled, dull-appearing hair.⁵ Additionally, sulfates were preferred to the alkaline pH of traditional soap, which can be harsh on hair strands and cause irritation of the skin and mucous membranes.¹⁴ Because they are highly water soluble, sulfates enable the formulation of clear shampoos. They exhibit remarkable cleaning properties and lather formation.^5,14

Because sulfates are potent surfactants, they can remove dirt and debris as well as naturally produced healthy oils from the hair and scalp. As a result, sulfates can leave the hair feeling dry and stripped of moisture.^4,5 Sulfates are used as the primary detergents in the formulation of deep-cleaning shampoos, which are designed for people who accumulate a heavy buildup of dirt, sebum, and debris from frequent use of styling products. Due to their potent detergency, these shampoos typically are not used on a daily basis but rather at longer intervals.¹⁵ A downside to sulfates is that they can have cosmetically unpleasant properties, which can be compensated for by including appropriate softening additives in shampoo formulations.⁴ A number of anionic surfactants such as olefin sulfonate, alkyl sulfosuccinate, acyl peptides, and alkyl ether carboxylates are well tolerated by the skin and are used together with other anionic and amphoteric surfactants to optimize shampoo properties. Alternatively, sulfate-free shampoos are cleansers compounded by the removal of the anionic group and switched for surfactants with less detergency.^4,5

Preservatives and Parabens

Parabens refer to a group of esters of 4-hydroxybenzoic acid commonly used as preservatives in foods, pharmaceuticals, and cosmetics whose widespread use dates back to 1923.¹⁶ Concerns over the presence of parabens in shampoos and other cosmetics have been raised by patients for their reputed estrogenic and antiandrogenic effects and suspected involvement in carcinogenesis via endocrine modulation.^16,17 In in vitro studies done on yeast assays, parabens have shown weak estrogenic activity that increases in proportion to both the length and increased branching of the alkyl side chains in the paraben’s molecular structure.¹⁸ They are 10,000-fold less potent than 17β-estradiol. In in vivo animal studies, parabens show weak estrogenic activity and are 100,000-fold less potent than 17β-estradiol.¹⁸ 4-Hydroxybenzoic acid, a common metabolite, showed no estrogenic activity when tested both in vitro and in vivo.¹⁹ Some concerning research has implicated a link between parabens used in underarm cosmetics, such as deodorants and antiperspirants, and breast cancer¹⁶; however, the studies have been conflicting, and there is simply not enough data to assert that parabens cause breast cancer.

The Cosmetic Ingredient Review expert panel first reviewed parabens in 1984 and concluded that “methylparaben, ethylparaben, propylparaben, and butylparaben are safe as cosmetic ingredients in the present practices of use.”²⁰ They extended this statement to include isopropylparaben and isobutylparaben in a later review.²¹ In 2005, the Scientific Committee on Consumer Products (now known as the Scientific Committee for Consumer Safety) in Europe stated that methylparaben and ethylparaben can be used at levels up to 0.4% in products.²² This decision was reached due to reports of decreased sperm counts and testosterone levels in male juvenile rats exposed to these parabens; however, these reults were not successfully replicated in larger studies.^16,22 In 2010, the Scientific Committee for Consumer Safety revisited its stance on parabens, and they then revised their recommendations to say that concentrations of propylparaben and butylparaben should not exceed concentrations of 0.19%, based on “the conservative choice for the calculation of the [Margin-of-Safety] of butyl- and propylparaben.”²³ However, in 2011 the use of propylparaben and butylparaben was banned in Denmark for cosmetic products used in children 3 years or younger,¹⁶ and the European Commission subsequently amended their directive in 2014, banning isopropylparaben, isobutylparaben, phenylparaben, benzylparaben, and pentylparaben due to lack of data available to evaluate the human risk of these products.²⁴

Contrary to the trends in Europe, there currently are no regulations against the use of parabens in shampoos or other cosmetics in the United States. The American Cancer Society found that there is no evidence to suggest that the current levels of parabens in cosmetic products (eg, antiperspirants) increase one’s risk of breast cancer.²⁵ Parabens are readily absorbed into the body both transdermally and through ingestion but also are believed to be rapidly transformed into harmless and nonspecific metabolites; they are readily metabolized by the liver and excreted in urine, and there is no measured accumulation in tissues.¹⁷

Parabens continue to be the most widely used preservatives in personal care products, usually in conjunction with other preservatives. Parabens are good biocides; short-chain esters (eg, methylparabens, ethylparabens) are effective against gram-positive bacteria and are weakly effective against gram-negative bacteria. Long-chain paraben esters (eg, propylparabens, butylparabens) are effective against mold and yeast. The addition of other preservatives creates a broad spectrum of antimicrobial defense in consumer products. Other preservatives include formaldehyde releasers or phenoxyethanol, as well as chelating agents such as EDTA, which improve the stability of these cosmetic products when exposed to air.¹⁶ Parabens are naturally occurring substances found in foods such as blueberries, barley, strawberries, yeast, olives, and grapes. As a colorless, odorless, and inexpensive substance, their use has been heavily favored in cosmetic and food products.¹⁶

Shampoo Alternatives and the No-Poo Method

Although research has not demonstrated any long-term danger to using shampoo, certain chemicals found in shampoos have the potential to irritate the scalp. Commonly cited allergens in shampoos include cocamidopropyl betaine, propylene glycol, vitamin E (tocopherol), parabens, and benzophenones.⁵ Additionally, the rising use of formaldehyde-releasing preservatives and isothiazolinones due to mounting pressures to move away from parabens has led to an increase in cases of allergic contact dermatitis (ACD).¹⁶ However, the irritability (rather than allergenicity) of these substances often is established during patch testing, a method of detecting delayed-type allergic reactions, which is important to note because patch testing requires a substance to be exposed to the skin for 24 to 48 hours, whereas exposure to shampoo ingredients may last a matter of minutes at most and occur in lesser concentrations because the ingredients are diluted by water in the rinsing process. Given these differences, it is unlikely that a patient would develop a true allergic response from regular shampoo use. Nevertheless, in patients who are already sensitized, exposure could conceivably trigger ACD, and patients must be cognizant of the composition of their shampoos.¹⁶

The no-poo method refers to the avoidance of commercial shampoo products when cleansing the hair and scalp and encompasses different methods of cleansing the hair, such as the use of household items (eg, baking soda, apple cider vinegar [ACV]), the use of conditioners to wash the hair (also known as conditioner-only washing or co-washing), treating the scalp with tea tree oil, or simply rinsing the hair with water. Proponents of the no-poo method believe that abstaining from shampoo use leads to healthier hair, retained natural oils, and less exposure to supposedly dangerous chemicals such as parabens or sulfates.^2,3,26-28 However, there are no known studies in the literature that assess or support the hypotheses of the no-poo method.

Baking Soda and ACV
Baking soda (sodium bicarbonate) is a substance commonly found in the average household. It has been used in toothpaste formulas and cosmetic products and is known for its acid-neutralizing properties. Baking soda has been shown to have some antifungal and viricidal properties through an unknown mechanism of action.²⁸ It has gained popularity for its use as a means of reducing the appearance of excessive greasiness of the hair shafts. Users also have reported that when washing their hair with baking soda, they are able to achieve a clean scalp and hair that feels soft to the touch.^2,3,26,27,29 Despite these reports, users must beware of using baking soda without adequately diluting it with water. Baking soda is a known alkaline irritant.^26,30 With a pH of 9, baking soda causes the cuticle layer of the hair fiber to open, increasing the capacity for water absorption. Water penetrates the scales that open, breaking the hydrogen bonds of the keratin molecule.³¹ Keratin is a spiral helical molecule that keeps its shape due to hydrogen, disulfide, and ionic bonds, as well as Van der Waals force.³⁰ Hydrolysis of these bonds due to exposure to baking soda lowers the elasticity of the hair and increases the negative electrical net charge of the hair fiber surface, which leads to increased friction between fibers, cuticle damage, hair fragility, and fiber breakage.^32,33

Apple cider vinegar is an apple-derived acetic acid solution with a pH ranging from 3.1 to 5.²⁸ The pH range of ACV is considered to be ideal for hair by no-poo proponents, as it is similar to the natural pH of the scalp. Its acidic properties are responsible for its antimicrobial abilities, particularly its effectiveness against gram-negative bacteria.³⁰ The acetic acid of ACV can partially interrupt oil interfaces, which contributes to its mild ability to remove product residue and scalp buildup from the hair shaft; the acetic acid also tightens the cuticles on hair fibers.³³ Apple cider vinegar is used as a means of cleansing the hair and scalp by no-poo proponents^2,3,26; other uses for ACV include using it as a rinse following washing and/or conditioning of the hair or as a means of preserving color in color-treated hair. There also is evidence that ACV may have antifungal properties.²⁸ However, consumers must be aware that if it is not diluted in water, ACV may be too caustic for direct application to the hair and may lead to damage; it can be irritating to eyes, mucus membranes, and acutely inflamed skin. Also, vinegar rinses used on processed or chemically damaged hair may lead to increased hair fragility.^2,3

Hair fibers have a pH of 3.67, while the scalp has a pH between 4.5 and 6.2. This slightly acidic film acts as a barrier to viruses, bacteria, and other potential contaminants.³³ Studies have shown that the pH of skin increases in proportion to the pH of the cleanser used.³⁴ Therefore, due to the naturally acidic pH of the scalp, acid-balanced shampoos generally are recommended. Shampoos should not have a pH higher than 5.5, as hair shafts can swell due to alkalinization, which can be prevented by pH balancing the shampoo through the addition of an acidic substance (eg, glycolic acid, citric acid) to lower the pH down to approximately 5.5. Apple cider vinegar often is used for this purpose. However, one study revealed that 82% of shampoos already have an acidic pH.³⁴

Conditioner-Only Washing (Co-washing)
Conditioner-only washing, or co-washing, is a widely practiced method of hair grooming. It is popular among individuals who find that commercial shampoos strip too much of the natural hair oils away, leaving the hair rough or unmanageable. Co-washing is not harmful to the hair; however, the molecular structure and function of a conditioner and that of a shampoo are very different.^5,35,36 Conditioners are not formulated to remove dirt and buildup in the hair but rather to add substances to the hair, and thus cannot provide extensive cleansing of the hair and scalp; therefore, it is inappropriate to use co-washing as a replacement for shampooing. Quaternary conditioning agents are an exception because they contain amphoteric detergents comprised of both anionic and cationic groups, which allow them both the ability to remove dirt and sebum with its anionic group, typically found in shampoos, as well as the ability to coat and condition the hair due to the high affinity of the cationic group for the negatively charged hair fibers.^36,37 Amphoteric detergents are commonly found in 2-in-1 conditioning cleansers, among other ingredients, such as hydrolyzed animal proteins that temporarily plug surface defects on the hair fiber, and dimethicone, a synthetic oil that creates a thin film over the hair shaft, increasing shine and manageability. Of note, these conditioning shampoos are ideal for individuals with minimal product buildup on the hair and scalp and are not adequate scalp cleansers for individuals who either wash their hair infrequently or who regularly use hairstyling products.^36,37

Tea Tree Oil
Tea tree oil is an essential oil extracted from the Melaleuca alternifolia plant of the Myrtaceae family. It is native to the coast of northeastern Australia. A holy grail of natural cosmetics, tea tree oil is widely known for its antiviral, antifungal, and antiseptic properties.³⁸ Although not used as a stand-alone cleanser, it is often added to a number of cosmetic products, including shampoos and co-washes. Although deemed safe for topical use, it has been shown to be quite toxic when ingested. Symptoms of ingestion include nausea, vomiting, hallucinations, and coma. The common concern with tea tree oil is its ability to cause ACD. In particular, it is believed that the oxidation products of tea tree oil are allergenic rather than the tea tree oil itself. The evaluation of tea tree oil as a potential contact allergen has been quite difficult; it consists of more than 100 distinct compounds and is often mislabeled, or does not meet the guidelines of the International Organization for Standardization. Nonetheless, the prevalence of ACD due to tea tree oil is low (approximately 1.4%). Despite its low prevalence, tea tree oil should remain in the differential as an ACD-inducing agent. Patch testing with the patient’s supply of tea tree oil is advised when possible.³⁸

Conclusion

It is customary that the ingredients used in shampoos undergo periodic testing and monitoring to assure the safety of their use. Although it is encouraging that patients are proactive in their efforts to stay abreast of the literature, it is still important that cosmetic scientists, dermatologists, and other experts remain at the forefront of educating the public about these substances. Not doing so can result in the propagation of misinformation and unnecessary fears, which can lead to the adaptation of unhygienic or even unsafe hair care practices. As dermatologists, we must ensure that patients are educated about the benefits and hazards of off-label use of household ingredients to the extent that evidence-based medicine permits. Patients must be informed that not all synthetic substances are harmful, and likewise not all naturally occurring substances are safe.

The approach to the treatment of common skin disorders and cosmetic concerns in patients with skin of color (SOC) requires the clinician to understand the biological differences, nuances, and special considerations that are unique to patients with darker skin types.^1-3 This article addresses 4 common facial concerns in SOC patients—acne, rosacea, facial hyperpigmentation, and cosmetic enhancement—and provides treatment recommendations and management pearls to assist the clinician with optimal outcomes for SOC patients.

Acne in SOC Patients

Acne vulgaris is one of the most common conditions that dermatologists treat and is estimated to affect 40 to 50 million individuals in the United States.¹ Many of these acne patients are individuals with SOC.^2-4 A study of 2835 females (aged 10–70 years) conducted in 4 different cities—Los Angeles, California; London, United Kingdom; Akita, Japan; and Rome, Italy—demonstrated acne prevalence of 37% in blacks, 32% in Hispanics, 30% in Asians, 24% in whites, and 23% in Continental Indians.⁵ Blacks, Hispanics, and Continental Indians demonstrated equal prevalence with comedonal and inflammatory acne. Asians displayed more inflammatory acne lesions than comedones. In contrast, whites demonstrated more comedones than inflammatory acne. Dyspigmentation, postinflammatory hyperpigmentation (PIH), and atrophic scars were more common in black and Hispanic females than other ethnicities.⁵ This study illustrated that acne-induced PIH is a common sequela in SOC patients and is the main reason they seek treatment.^6,7

The pathogenesis of acne is the same in all racial and ethnic groups: (1) follicular hyperkeratinization and the formation of a microcomedone caused by abnormal desquamation of the keratinocytes within the sebaceous follicle, (2) production of sebum by circulating androgens, (3) proliferation of Propionibacterium acnes, and (4) inflammation. Subclinical inflammation is present throughout all stages of acne, including normal-appearing skin, inflammatory lesions, comedones, and scarring, and may contribute to PIH in acne patients with SOC (Figure 1).⁸ A thorough history should be obtained from acne patients, including answers to the following questions⁷:

• What skin and hair care products do you use?
• Do you use sunscreen daily?
• What cosmetic products or makeup do you use?
• Do you use any ethnic skin care products, including skin lightening creams?
• Do you have a history of keloids?

It is important to ask these questions to assess if the SOC patient has developed pomade acne,⁹ acne cosmetica,¹⁰ or a potential risk of skin irritation from the use of skin care practices. It is best to take total control of the patient’s skin care regimen and discontinue use of toners, astringents, witch hazel, exfoliants, and rubbing alcohol, which may lead to skin dryness and irritation, particularly when combined with topical acne medications.

Treatment
Treatment of acne in SOC patients is similar to generally recommended treatments, with special considerations. Consider the following key points when treating acne in SOC patients:

• Treat acne early and aggressively to prevent or minimize subsequent PIH and acne scarring.
• Balance aggressive treatment with nonirritating topical skin care.
• Most importantly, target PIH in addition to acne and choose a regimen that limits skin irritation that might exacerbate existing PIH.⁷

Develop a maintenance program to control future breakouts. Topical agents can be used as monotherapy or in fixed combinations and may include benzoyl peroxide, antibiotics, dapsone, azelaic acid (AZA), and retinoids. Similar to white patients, topical retinoids remain a first-line treatment for acne in patients with SOC.^11,12

Tolerability must be managed in SOC acne patients. Therapeutic maneuvers that can be instituted should include a discussion on using gentle skin care, initiating therapy with a retinoid applied every other night starting with a low concentration and gradually titrating up, and applying a moisturizer before or after applying acne medication. Oral therapies consist of antibiotics (doxycycline, minocycline), retinoids (isotretinoin), and hormonal modulators (oral contraceptives, spironolactone). Isotretinoin, recommended for patients with nodulocystic acne, may play a possible role in treating acne-induced PIH.¹³

Two common procedural therapies for acne include comedone extraction and intralesional corticosteroid injection. A 6- to 8-week course of a topical retinoid prior to comedonal extraction may facilitate the procedure and is recommended in SOC patients to help reduce cutaneous trauma and PIH.¹¹ Inflammatory acne lesions can be treated with intralesional injection of triamcinolone acetonide 2.5 or 5.0 mg/mL, which usually reduces inflammation within 2 to 5 days.¹¹

Treatment of acne-induced PIH includes sun protection, topical and oral medications, chemical peels, lasers, and energy devices. Treatment of hypertrophic scarring and keloids involves intralesional injection of triamcinolone acetonide 20, 30, or 40 mg/mL every 4 weeks until the lesion is flat.¹¹

Superficial chemical peels can be used to treat acne and PIH in SOC patients,¹⁴ such as salicylic acid (20%–30%), glycolic acid (20%–70%), trichloroacetic acid (15%–30%), and Jessner peels.

Acne Scarring
Surgical approaches to acne scarring in patients with SOC include elliptical excision, punch excision, punch elevation, punch autografting, dermal grafting, dermal planning, subcutaneous incision (subcision), dermabrasion, microneedling, fillers, and laser skin resurfacing. The treatment of choice depends on the size, type, and depth of the scar and the clinician’s preference.

Lasers
Fractional photothermolysis has emerged as a treatment option for acne scars in SOC patients. This procedure produces microscopic columns of thermal injury in the epidermis and dermis, sparing the surrounding tissue and minimizing downtime and adverse events. Because fractional photothermolysis does not target melanin and produces limited epidermal injury, darker Fitzpatrick skin types (IV–VI) can be safely and effectively treated with this procedure.¹⁵

Rosacea in SOC Patients

Rosacea is a chronic inflammatory disorder that affects the vasculature and pilosebaceous units of the face. It commonly is seen in Fitzpatrick skin types I and II; however, rosacea can occur in all skin types (Figure 2). Triggers include emotional stress, extreme environmental temperatures, hot and spicy foods, red wine or alcohol, and topical irritants or allergens found in common cosmetic products.¹⁶

Data suggest that 4% of rosacea patients in the United States are of African, Latino, or Asian descent.¹¹ National Ambulatory Medical Care Survey data revealed that of 31.5 million rosacea visits, 2% of patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino. In a 5-year longitudinal study of 2587 rosacea patients enrolled in Medicaid in North Carolina who were prescribed at least 1 topical treatment for rosacea, 16.27% were black and 10% were of a race other than white.¹⁷

Although the pathogenesis of rosacea is unclear, hypotheses include immune system abnormalities, neurogenic dysregulation, presence of microorganisms (eg, Demodex folliculorum), UV damage, and skin barrier dysfunction.¹⁸

The 4 major subtypes of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea.¹⁶ Interestingly, rosacea in SOC patients may present with hypopigmentation surrounding the borders of the facial erythema. For phymatous rosacea, isotretinoin may reduce incipient rhinophyma but must be carefully monitored and pregnancy must be excluded. Surgical or laser therapy may be indicated to recontour the nose if severe.

There are several skin conditions that can present with facial erythema in patients with SOC, including seborrheic dermatitis, systemic lupus erythematosus, and contact dermatitis. It is important to note that the detection of facial erythema in darker skin types may be difficult; therefore, laboratory evaluation (antinuclear antibodies), patch testing, and skin biopsy should be considered if the clinical diagnosis is unclear.

Treatment
Treatment of rosacea in SOC patients does not differ from other racial groups. Common strategies include gentle skin care, sun protection (sun protection factor 30+), and barrier repair creams. Topical agents include metronidazole, AZA, sodium sulfacetamide/sulfur, ivermectin, and retinoids.¹⁶ Oral treatments include antibiotics in the tetracycline family (eg, subantimicrobial dose doxycycline) and isotretinoin.¹⁶ Persistent erythema associated with rosacea can be treated with brimonidine¹⁹ and oxymetazoline.²⁰ Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea²¹; however, the latter is not recommended in Fitzpatrick skin types IV through VI.

Facial Hyperpigmentation in SOC Patients

Hyperpigmentation disorders can be divided into conditions that affect Fitzpatrick skin types I through III and IV though VI. Mottled hyperpigmentation (photodamage) and solar lentigines occur in patients with lighter skin types as compared to melasma, PIH, and age-related (UV-induced) hyperpigmentation, which occur more commonly in patients with darker skin types. Facial hyperpigmentation is a common concern in SOC patients. In a survey of cosmetic concerns of 100 women with SOC, hyperpigmentation or dark spots (86%) and blotchy uneven skin (80%) were the top concerns.²² In addition, facial hyperpigmentation has been shown to negatively impact quality of life.²³

Postinflammatory hyperpigmentation occurs from a pathophysiological response to inflammation, cutaneous irritation or injury, and subsequent melanocyte lability. Postinflammatory hyperpigmentation is a common presenting concern in patients with SOC and is seen as a result of many inflammatory skin disorders (eg, acne, eczema) and dermatologic procedures (eg, adverse reaction to electrodesiccation, microdermabrasion, chemical peels, laser surgery).²⁴

Melasma is an acquired idiopathic disorder of hyperpigmentation and often referred to as the mask of pregnancy (Figure 3). It occurs on sun-exposed areas of skin, mainly in women with Fitzpatrick skin types III through V. Associated factors or triggers include pregnancy, hormonal treatments, exposure to UV radiation, and medications.²⁵ Hereditary factors play a role in more than 40% of cases.²⁶

Other not-so-common facial dyschromias include contact dermatitis, acanthosis nigricans, exogenous ochronosis, lichen planus pigmentosus (associated with frontal fibrosing alopecia),²⁷ drug-induced hyperpigmentation (associated with minocycline or diltiazem),^28,29 and UV-induced (age-related) hyperpigmentation.

Treatment
The treatment of hyperpigmentation should provide the following: (1) protection from sun exposure; (2) inhibition of tyrosinase, the enzyme responsible for the conversion of tyrosine to melanin; (3) inhibition of melanosome transfer from the melanocyte to the keratinocyte; (4) removal of melanin from the epidermis through exfoliation; and (5) destruction or disruption of melanin in the dermis.³⁰ Therapies for facial hyperpigmentation are listed in Table 1.

Topical therapies include prescription medications and nonprescription cosmeceuticals. Prescription medications include hydroquinone (HQ), topical retinoids, and AZA. Hydroquinone, a tyrosinase inhibitor, is the gold standard for skin lightening and often is used as a first-line therapy. It is used as a monotherapy (HQ 4%) or as a fixed combination with tretinoin 0.05% and fluocinolone 0.01%.³¹ Use caution with HQ in high concentrations (6% and higher) and low concentrations (2% [over-the-counter strength]) used long-term due to the potential risk of exogenous ochronosis.

Topical retinoids have been shown to be effective therapeutic agents for melasma and PIH. Tretinoin,³² tazarotene,³³ and adapalene³⁴ all have demonstrated efficacy for acne and acne-induced PIH in SOC patients. Patients must be monitored for the development of retinoid dermatitis and worsening of hyperpigmentation.

Azelaic acid is a naturally occurring dicarboxylic acid obtained from cultures of Malassezia furfur. Azelaic acid inhibits tyrosinase activity, DNA synthesis, and mitochondrial enzymes, thus blocking direct cytotoxic effects toward melanocytes. Azelaic acid is approved by the US Food and Drug Administration for acne in a 20% cream formulation and rosacea in 15% gel and foam formulations, and it is used off label for melasma and PIH.³⁵

Oral tranexamic acid is currently used as a hemostatic agent due to its ability to inhibit the plasminogen-plasmin pathway. In melasma, it blocks the interaction between melanocytes and keratinocytes in the epidermis and modulates the vascular component of melasma in the dermis. In an open-label study, 561 Asian melasma patients were treated with oral tranexamic acid 250 mg twice daily for 4 months. Results demonstrated improvement in 90% of patients, and 7.1% reported adverse effects (eg, abdominal bloating and pain, nausea, vomiting, headache, tinnitus, numbness, menstrual irregularities).³⁶ Coagulation screening should be monitored monthly, and any patient with a history of clotting abnormalities should be excluded from off-label treatment with oral tranexamic acid.

Nonprescription cosmeceuticals are available over-the-counter or are office dispensed.³⁷ For optimal results, cosmeceutical agents for skin lightening are used in combination. Most of these combinations are HQ free and have additive benefits such as a multimodal skin lightening agent containing key ingredients that correct and prevent skin pigmentation via several pathways affecting melanogenesis.³⁸ It is an excellent alternative to HQ for mottled and diffuse UV-induced hyperpigmentation and can be used for maintenance therapy in patients with melasma.

Photoprotection is an essential component of therapy for melasma and PIH, but there is a paucity of data on the benefits for SOC patients. Halder et al³⁹ performed a randomized prospective study of 89 black and Hispanic patients who applied sunscreen with a sun protection factor of 30 or 60 daily for 8 weeks. Clinical grading, triplicate L*A*B chromameter, and clinical photography were taken at baseline and weeks 4 and 8. The results demonstrated skin lightening in both black and Hispanic patients and support the use of sunscreen in the prevention and management of dyschromia in SOC patients.³⁹ Visible light also may play a role in melasma development, and thus use of sunscreens or makeup containing iron oxides are recommended.⁴⁰

Procedural treatments for facial hyperpigmentation include microdermabrasion, chemical peels, lasers, energy-based devices, and microneedling. There are many types and formulations of chemical peeling agents available; however, superficial and medium-depth chemical peels are recommended for SOC patients (Table 2). Deep chemical peels are not recommended for SOC patients due to the potential increased risk for PIH and scarring.

Cosmetic Enhancement in SOC Patients

Cosmetic procedures are gaining popularity in the SOC population and account for more than 20% of cosmetic procedures in the United States.⁴¹ Facial cosmetic concerns in SOC include dyschromia, benign growths (dermatosis papulosa nigra), hyperkinetic facial lines, volume loss, and skin laxity.⁴² Key principles to consider when treating SOC patients are the impact of ethnicity on aging and facial structure, the patient’s desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient’s expectations for recommended therapies.

Aging in SOC Patients
Skin aging can be classified as intrinsic aging or extrinsic aging. Intrinsic aging is genetic and involves subsurface changes such as volume loss, muscle atrophy, and resorption of bony structure. Extrinsic aging (or photoaging) involves surface changes of the epidermis/dermis and manifests as mottled pigmentation, textural changes, and fine wrinkling. Due to the photoprotection of melanin (black skin=SPF 13.4), skin aging in SOC patients is delayed by 10 to 20 years.⁴³ In addition, SOC patients have more reactive collagen and can benefit from noninvasive cosmetic procedures such as fillers and skin-tightening procedures.⁴²

Cosmetic Treatments and Procedures
Dermatosis papulosa nigra (benign growths of skin that have a genetic predisposition)⁴⁴ occur mainly on the face but can involve the entire body. Treatment modalities include electrodesiccation, cryotherapy, scissor excision, and laser surgery.⁴⁵

Treatment of hyperkinetic facial lines with botulinum toxin type A is a safe and effective procedure in patients with SOC. Grimes and Shabazz⁴⁶ performed a 4-month, randomized, double-blind study that evaluated the treatment of glabellar lines in women with Fitzpatrick skin types V and VI. The results demonstrated that the duration of effects was the same in the patients who received either 20 or 30 U of botulinum toxin type A.⁴⁶ Dynamic rhytides (furrows and frown/scowl lines arising from laughing, frowning, or smiling) can be treated safely in patients with SOC using botulinum toxin type A off label for relaxation of the upper and lower hyperkinetic muscles that result in these unwanted signs of aging. Botulinum toxin type A often is used for etched-in crow’s-feet, which rarely are evident in SOC patients.⁴⁷ Facial shaping also can be accomplished by injecting botulinum toxin type A in combination with soft-tissue dermal fillers.⁴⁷

Although black individuals do not experience perioral rhytides at the frequency of white individuals, they experience a variety of other cosmetic issues related to skin sagging and sinking. Currently available hyaluronic acid (HA) fillers have been shown to be safe in patients with Fitzpatrick skin types IV through VI.⁴⁸ Two studies evaluated fillers in patients with SOC, specifically HA⁴⁹ and calcium hydroxylapatite,⁵⁰ focused on treatment of the nasolabial folds and the potential risk for dyspigmentation and keloidal scarring. Taylor et al⁴⁹ noted that the risk of hyperpigmentation was 6% to 9% for large- and small-particle HA, respectively, and was associated with the serial or multiple puncture injection technique. No hypertrophic or keloidal scarring occurred in both studies.^49,50

Facial contouring applications with fillers include glabellar lines, temples, nasal bridge, tear troughs, malar and submalar areas, nasolabial folds, radial lines, lips, marionette lines, mental crease, and chin. Hyaluronic acid fillers also can be used for lip enhancement.⁴⁷ Although white women are looking to increase the size of their lips, black women are seeking augmentation to restore their lip size to that of their youth. Black individuals do not experience the same frequency of perioral rhytides as white patients, but they experience a variety of other issues related to skin sagging and sinking. Unlike white women, enhancement of the vermilion border rarely is performed in black women due to development of rhytides, predominantly in the body of the lip below the vermilion border in response to volume loss in the upper lip while the lower lip usually maintains its same appearance.⁴⁷

Facial enhancement utilizing poly-L-lactic acid can be used safely in SOC patients.⁵¹ Poly-L-lactic acid microparticles induce collagen formation, leading to dermal thickening over 3 to 6 months; however, multiple sessions are required to achieve optimal aesthetic results.

Patients with more reactive collagen can benefit from noninvasive cosmetic procedures such as skin-tightening procedures.⁵² Radiofrequency and microfocused ultrasound are cosmetic procedures used to provide skin tightening and facial lifting. They are safe and effective treatments for patients with Fitzpatrick skin types IV to VI.⁵³ Histologically, there is less thinning of collagen bundles and elastic tissue in ethnic skin. Due to stimulation of collagen by these procedures, most SOC patients will experience a more enhanced response, requiring fewer treatment sessions than white individuals.

Conclusion

Medical and aesthetic facial concerns in SOC patients vary and can be a source of emotional and psychological distress that can negatively impact quality of life. The approach to the treatment of SOC patients should be a balance between tolerability and efficacy, considering the potential risk for PIH.

The approach to the treatment of common skin disorders and cosmetic concerns in patients with skin of color (SOC) requires the clinician to understand the biological differences, nuances, and special considerations that are unique to patients with darker skin types.^1-3 This article addresses 4 common facial concerns in SOC patients—acne, rosacea, facial hyperpigmentation, and cosmetic enhancement—and provides treatment recommendations and management pearls to assist the clinician with optimal outcomes for SOC patients.

Acne in SOC Patients

Acne vulgaris is one of the most common conditions that dermatologists treat and is estimated to affect 40 to 50 million individuals in the United States.¹ Many of these acne patients are individuals with SOC.^2-4 A study of 2835 females (aged 10–70 years) conducted in 4 different cities—Los Angeles, California; London, United Kingdom; Akita, Japan; and Rome, Italy—demonstrated acne prevalence of 37% in blacks, 32% in Hispanics, 30% in Asians, 24% in whites, and 23% in Continental Indians.⁵ Blacks, Hispanics, and Continental Indians demonstrated equal prevalence with comedonal and inflammatory acne. Asians displayed more inflammatory acne lesions than comedones. In contrast, whites demonstrated more comedones than inflammatory acne. Dyspigmentation, postinflammatory hyperpigmentation (PIH), and atrophic scars were more common in black and Hispanic females than other ethnicities.⁵ This study illustrated that acne-induced PIH is a common sequela in SOC patients and is the main reason they seek treatment.^6,7

The pathogenesis of acne is the same in all racial and ethnic groups: (1) follicular hyperkeratinization and the formation of a microcomedone caused by abnormal desquamation of the keratinocytes within the sebaceous follicle, (2) production of sebum by circulating androgens, (3) proliferation of Propionibacterium acnes, and (4) inflammation. Subclinical inflammation is present throughout all stages of acne, including normal-appearing skin, inflammatory lesions, comedones, and scarring, and may contribute to PIH in acne patients with SOC (Figure 1).⁸ A thorough history should be obtained from acne patients, including answers to the following questions⁷:

• What skin and hair care products do you use?
• Do you use sunscreen daily?
• What cosmetic products or makeup do you use?
• Do you use any ethnic skin care products, including skin lightening creams?
• Do you have a history of keloids?

It is important to ask these questions to assess if the SOC patient has developed pomade acne,⁹ acne cosmetica,¹⁰ or a potential risk of skin irritation from the use of skin care practices. It is best to take total control of the patient’s skin care regimen and discontinue use of toners, astringents, witch hazel, exfoliants, and rubbing alcohol, which may lead to skin dryness and irritation, particularly when combined with topical acne medications.

Treatment
Treatment of acne in SOC patients is similar to generally recommended treatments, with special considerations. Consider the following key points when treating acne in SOC patients:

• Treat acne early and aggressively to prevent or minimize subsequent PIH and acne scarring.
• Balance aggressive treatment with nonirritating topical skin care.
• Most importantly, target PIH in addition to acne and choose a regimen that limits skin irritation that might exacerbate existing PIH.⁷

Develop a maintenance program to control future breakouts. Topical agents can be used as monotherapy or in fixed combinations and may include benzoyl peroxide, antibiotics, dapsone, azelaic acid (AZA), and retinoids. Similar to white patients, topical retinoids remain a first-line treatment for acne in patients with SOC.^11,12

Tolerability must be managed in SOC acne patients. Therapeutic maneuvers that can be instituted should include a discussion on using gentle skin care, initiating therapy with a retinoid applied every other night starting with a low concentration and gradually titrating up, and applying a moisturizer before or after applying acne medication. Oral therapies consist of antibiotics (doxycycline, minocycline), retinoids (isotretinoin), and hormonal modulators (oral contraceptives, spironolactone). Isotretinoin, recommended for patients with nodulocystic acne, may play a possible role in treating acne-induced PIH.¹³

Two common procedural therapies for acne include comedone extraction and intralesional corticosteroid injection. A 6- to 8-week course of a topical retinoid prior to comedonal extraction may facilitate the procedure and is recommended in SOC patients to help reduce cutaneous trauma and PIH.¹¹ Inflammatory acne lesions can be treated with intralesional injection of triamcinolone acetonide 2.5 or 5.0 mg/mL, which usually reduces inflammation within 2 to 5 days.¹¹

Treatment of acne-induced PIH includes sun protection, topical and oral medications, chemical peels, lasers, and energy devices. Treatment of hypertrophic scarring and keloids involves intralesional injection of triamcinolone acetonide 20, 30, or 40 mg/mL every 4 weeks until the lesion is flat.¹¹

Superficial chemical peels can be used to treat acne and PIH in SOC patients,¹⁴ such as salicylic acid (20%–30%), glycolic acid (20%–70%), trichloroacetic acid (15%–30%), and Jessner peels.

Acne Scarring
Surgical approaches to acne scarring in patients with SOC include elliptical excision, punch excision, punch elevation, punch autografting, dermal grafting, dermal planning, subcutaneous incision (subcision), dermabrasion, microneedling, fillers, and laser skin resurfacing. The treatment of choice depends on the size, type, and depth of the scar and the clinician’s preference.

Lasers
Fractional photothermolysis has emerged as a treatment option for acne scars in SOC patients. This procedure produces microscopic columns of thermal injury in the epidermis and dermis, sparing the surrounding tissue and minimizing downtime and adverse events. Because fractional photothermolysis does not target melanin and produces limited epidermal injury, darker Fitzpatrick skin types (IV–VI) can be safely and effectively treated with this procedure.¹⁵

Rosacea in SOC Patients

Rosacea is a chronic inflammatory disorder that affects the vasculature and pilosebaceous units of the face. It commonly is seen in Fitzpatrick skin types I and II; however, rosacea can occur in all skin types (Figure 2). Triggers include emotional stress, extreme environmental temperatures, hot and spicy foods, red wine or alcohol, and topical irritants or allergens found in common cosmetic products.¹⁶

Data suggest that 4% of rosacea patients in the United States are of African, Latino, or Asian descent.¹¹ National Ambulatory Medical Care Survey data revealed that of 31.5 million rosacea visits, 2% of patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino. In a 5-year longitudinal study of 2587 rosacea patients enrolled in Medicaid in North Carolina who were prescribed at least 1 topical treatment for rosacea, 16.27% were black and 10% were of a race other than white.¹⁷

Although the pathogenesis of rosacea is unclear, hypotheses include immune system abnormalities, neurogenic dysregulation, presence of microorganisms (eg, Demodex folliculorum), UV damage, and skin barrier dysfunction.¹⁸

The 4 major subtypes of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea.¹⁶ Interestingly, rosacea in SOC patients may present with hypopigmentation surrounding the borders of the facial erythema. For phymatous rosacea, isotretinoin may reduce incipient rhinophyma but must be carefully monitored and pregnancy must be excluded. Surgical or laser therapy may be indicated to recontour the nose if severe.

There are several skin conditions that can present with facial erythema in patients with SOC, including seborrheic dermatitis, systemic lupus erythematosus, and contact dermatitis. It is important to note that the detection of facial erythema in darker skin types may be difficult; therefore, laboratory evaluation (antinuclear antibodies), patch testing, and skin biopsy should be considered if the clinical diagnosis is unclear.

Treatment
Treatment of rosacea in SOC patients does not differ from other racial groups. Common strategies include gentle skin care, sun protection (sun protection factor 30+), and barrier repair creams. Topical agents include metronidazole, AZA, sodium sulfacetamide/sulfur, ivermectin, and retinoids.¹⁶ Oral treatments include antibiotics in the tetracycline family (eg, subantimicrobial dose doxycycline) and isotretinoin.¹⁶ Persistent erythema associated with rosacea can be treated with brimonidine¹⁹ and oxymetazoline.²⁰ Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea²¹; however, the latter is not recommended in Fitzpatrick skin types IV through VI.

Facial Hyperpigmentation in SOC Patients

Hyperpigmentation disorders can be divided into conditions that affect Fitzpatrick skin types I through III and IV though VI. Mottled hyperpigmentation (photodamage) and solar lentigines occur in patients with lighter skin types as compared to melasma, PIH, and age-related (UV-induced) hyperpigmentation, which occur more commonly in patients with darker skin types. Facial hyperpigmentation is a common concern in SOC patients. In a survey of cosmetic concerns of 100 women with SOC, hyperpigmentation or dark spots (86%) and blotchy uneven skin (80%) were the top concerns.²² In addition, facial hyperpigmentation has been shown to negatively impact quality of life.²³

Postinflammatory hyperpigmentation occurs from a pathophysiological response to inflammation, cutaneous irritation or injury, and subsequent melanocyte lability. Postinflammatory hyperpigmentation is a common presenting concern in patients with SOC and is seen as a result of many inflammatory skin disorders (eg, acne, eczema) and dermatologic procedures (eg, adverse reaction to electrodesiccation, microdermabrasion, chemical peels, laser surgery).²⁴

Melasma is an acquired idiopathic disorder of hyperpigmentation and often referred to as the mask of pregnancy (Figure 3). It occurs on sun-exposed areas of skin, mainly in women with Fitzpatrick skin types III through V. Associated factors or triggers include pregnancy, hormonal treatments, exposure to UV radiation, and medications.²⁵ Hereditary factors play a role in more than 40% of cases.²⁶

Other not-so-common facial dyschromias include contact dermatitis, acanthosis nigricans, exogenous ochronosis, lichen planus pigmentosus (associated with frontal fibrosing alopecia),²⁷ drug-induced hyperpigmentation (associated with minocycline or diltiazem),^28,29 and UV-induced (age-related) hyperpigmentation.

Treatment
The treatment of hyperpigmentation should provide the following: (1) protection from sun exposure; (2) inhibition of tyrosinase, the enzyme responsible for the conversion of tyrosine to melanin; (3) inhibition of melanosome transfer from the melanocyte to the keratinocyte; (4) removal of melanin from the epidermis through exfoliation; and (5) destruction or disruption of melanin in the dermis.³⁰ Therapies for facial hyperpigmentation are listed in Table 1.

Topical therapies include prescription medications and nonprescription cosmeceuticals. Prescription medications include hydroquinone (HQ), topical retinoids, and AZA. Hydroquinone, a tyrosinase inhibitor, is the gold standard for skin lightening and often is used as a first-line therapy. It is used as a monotherapy (HQ 4%) or as a fixed combination with tretinoin 0.05% and fluocinolone 0.01%.³¹ Use caution with HQ in high concentrations (6% and higher) and low concentrations (2% [over-the-counter strength]) used long-term due to the potential risk of exogenous ochronosis.

Topical retinoids have been shown to be effective therapeutic agents for melasma and PIH. Tretinoin,³² tazarotene,³³ and adapalene³⁴ all have demonstrated efficacy for acne and acne-induced PIH in SOC patients. Patients must be monitored for the development of retinoid dermatitis and worsening of hyperpigmentation.

Azelaic acid is a naturally occurring dicarboxylic acid obtained from cultures of Malassezia furfur. Azelaic acid inhibits tyrosinase activity, DNA synthesis, and mitochondrial enzymes, thus blocking direct cytotoxic effects toward melanocytes. Azelaic acid is approved by the US Food and Drug Administration for acne in a 20% cream formulation and rosacea in 15% gel and foam formulations, and it is used off label for melasma and PIH.³⁵

Oral tranexamic acid is currently used as a hemostatic agent due to its ability to inhibit the plasminogen-plasmin pathway. In melasma, it blocks the interaction between melanocytes and keratinocytes in the epidermis and modulates the vascular component of melasma in the dermis. In an open-label study, 561 Asian melasma patients were treated with oral tranexamic acid 250 mg twice daily for 4 months. Results demonstrated improvement in 90% of patients, and 7.1% reported adverse effects (eg, abdominal bloating and pain, nausea, vomiting, headache, tinnitus, numbness, menstrual irregularities).³⁶ Coagulation screening should be monitored monthly, and any patient with a history of clotting abnormalities should be excluded from off-label treatment with oral tranexamic acid.

Nonprescription cosmeceuticals are available over-the-counter or are office dispensed.³⁷ For optimal results, cosmeceutical agents for skin lightening are used in combination. Most of these combinations are HQ free and have additive benefits such as a multimodal skin lightening agent containing key ingredients that correct and prevent skin pigmentation via several pathways affecting melanogenesis.³⁸ It is an excellent alternative to HQ for mottled and diffuse UV-induced hyperpigmentation and can be used for maintenance therapy in patients with melasma.

Photoprotection is an essential component of therapy for melasma and PIH, but there is a paucity of data on the benefits for SOC patients. Halder et al³⁹ performed a randomized prospective study of 89 black and Hispanic patients who applied sunscreen with a sun protection factor of 30 or 60 daily for 8 weeks. Clinical grading, triplicate L*A*B chromameter, and clinical photography were taken at baseline and weeks 4 and 8. The results demonstrated skin lightening in both black and Hispanic patients and support the use of sunscreen in the prevention and management of dyschromia in SOC patients.³⁹ Visible light also may play a role in melasma development, and thus use of sunscreens or makeup containing iron oxides are recommended.⁴⁰

Procedural treatments for facial hyperpigmentation include microdermabrasion, chemical peels, lasers, energy-based devices, and microneedling. There are many types and formulations of chemical peeling agents available; however, superficial and medium-depth chemical peels are recommended for SOC patients (Table 2). Deep chemical peels are not recommended for SOC patients due to the potential increased risk for PIH and scarring.

Cosmetic Enhancement in SOC Patients

Cosmetic procedures are gaining popularity in the SOC population and account for more than 20% of cosmetic procedures in the United States.⁴¹ Facial cosmetic concerns in SOC include dyschromia, benign growths (dermatosis papulosa nigra), hyperkinetic facial lines, volume loss, and skin laxity.⁴² Key principles to consider when treating SOC patients are the impact of ethnicity on aging and facial structure, the patient’s desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient’s expectations for recommended therapies.

Aging in SOC Patients
Skin aging can be classified as intrinsic aging or extrinsic aging. Intrinsic aging is genetic and involves subsurface changes such as volume loss, muscle atrophy, and resorption of bony structure. Extrinsic aging (or photoaging) involves surface changes of the epidermis/dermis and manifests as mottled pigmentation, textural changes, and fine wrinkling. Due to the photoprotection of melanin (black skin=SPF 13.4), skin aging in SOC patients is delayed by 10 to 20 years.⁴³ In addition, SOC patients have more reactive collagen and can benefit from noninvasive cosmetic procedures such as fillers and skin-tightening procedures.⁴²

Cosmetic Treatments and Procedures
Dermatosis papulosa nigra (benign growths of skin that have a genetic predisposition)⁴⁴ occur mainly on the face but can involve the entire body. Treatment modalities include electrodesiccation, cryotherapy, scissor excision, and laser surgery.⁴⁵

Treatment of hyperkinetic facial lines with botulinum toxin type A is a safe and effective procedure in patients with SOC. Grimes and Shabazz⁴⁶ performed a 4-month, randomized, double-blind study that evaluated the treatment of glabellar lines in women with Fitzpatrick skin types V and VI. The results demonstrated that the duration of effects was the same in the patients who received either 20 or 30 U of botulinum toxin type A.⁴⁶ Dynamic rhytides (furrows and frown/scowl lines arising from laughing, frowning, or smiling) can be treated safely in patients with SOC using botulinum toxin type A off label for relaxation of the upper and lower hyperkinetic muscles that result in these unwanted signs of aging. Botulinum toxin type A often is used for etched-in crow’s-feet, which rarely are evident in SOC patients.⁴⁷ Facial shaping also can be accomplished by injecting botulinum toxin type A in combination with soft-tissue dermal fillers.⁴⁷

Although black individuals do not experience perioral rhytides at the frequency of white individuals, they experience a variety of other cosmetic issues related to skin sagging and sinking. Currently available hyaluronic acid (HA) fillers have been shown to be safe in patients with Fitzpatrick skin types IV through VI.⁴⁸ Two studies evaluated fillers in patients with SOC, specifically HA⁴⁹ and calcium hydroxylapatite,⁵⁰ focused on treatment of the nasolabial folds and the potential risk for dyspigmentation and keloidal scarring. Taylor et al⁴⁹ noted that the risk of hyperpigmentation was 6% to 9% for large- and small-particle HA, respectively, and was associated with the serial or multiple puncture injection technique. No hypertrophic or keloidal scarring occurred in both studies.^49,50

Facial contouring applications with fillers include glabellar lines, temples, nasal bridge, tear troughs, malar and submalar areas, nasolabial folds, radial lines, lips, marionette lines, mental crease, and chin. Hyaluronic acid fillers also can be used for lip enhancement.⁴⁷ Although white women are looking to increase the size of their lips, black women are seeking augmentation to restore their lip size to that of their youth. Black individuals do not experience the same frequency of perioral rhytides as white patients, but they experience a variety of other issues related to skin sagging and sinking. Unlike white women, enhancement of the vermilion border rarely is performed in black women due to development of rhytides, predominantly in the body of the lip below the vermilion border in response to volume loss in the upper lip while the lower lip usually maintains its same appearance.⁴⁷

Facial enhancement utilizing poly-L-lactic acid can be used safely in SOC patients.⁵¹ Poly-L-lactic acid microparticles induce collagen formation, leading to dermal thickening over 3 to 6 months; however, multiple sessions are required to achieve optimal aesthetic results.

Patients with more reactive collagen can benefit from noninvasive cosmetic procedures such as skin-tightening procedures.⁵² Radiofrequency and microfocused ultrasound are cosmetic procedures used to provide skin tightening and facial lifting. They are safe and effective treatments for patients with Fitzpatrick skin types IV to VI.⁵³ Histologically, there is less thinning of collagen bundles and elastic tissue in ethnic skin. Due to stimulation of collagen by these procedures, most SOC patients will experience a more enhanced response, requiring fewer treatment sessions than white individuals.

Conclusion

Medical and aesthetic facial concerns in SOC patients vary and can be a source of emotional and psychological distress that can negatively impact quality of life. The approach to the treatment of SOC patients should be a balance between tolerability and efficacy, considering the potential risk for PIH.

The approach to the treatment of common skin disorders and cosmetic concerns in patients with skin of color (SOC) requires the clinician to understand the biological differences, nuances, and special considerations that are unique to patients with darker skin types.^1-3 This article addresses 4 common facial concerns in SOC patients—acne, rosacea, facial hyperpigmentation, and cosmetic enhancement—and provides treatment recommendations and management pearls to assist the clinician with optimal outcomes for SOC patients.

Acne in SOC Patients

Acne vulgaris is one of the most common conditions that dermatologists treat and is estimated to affect 40 to 50 million individuals in the United States.¹ Many of these acne patients are individuals with SOC.^2-4 A study of 2835 females (aged 10–70 years) conducted in 4 different cities—Los Angeles, California; London, United Kingdom; Akita, Japan; and Rome, Italy—demonstrated acne prevalence of 37% in blacks, 32% in Hispanics, 30% in Asians, 24% in whites, and 23% in Continental Indians.⁵ Blacks, Hispanics, and Continental Indians demonstrated equal prevalence with comedonal and inflammatory acne. Asians displayed more inflammatory acne lesions than comedones. In contrast, whites demonstrated more comedones than inflammatory acne. Dyspigmentation, postinflammatory hyperpigmentation (PIH), and atrophic scars were more common in black and Hispanic females than other ethnicities.⁵ This study illustrated that acne-induced PIH is a common sequela in SOC patients and is the main reason they seek treatment.^6,7

The pathogenesis of acne is the same in all racial and ethnic groups: (1) follicular hyperkeratinization and the formation of a microcomedone caused by abnormal desquamation of the keratinocytes within the sebaceous follicle, (2) production of sebum by circulating androgens, (3) proliferation of Propionibacterium acnes, and (4) inflammation. Subclinical inflammation is present throughout all stages of acne, including normal-appearing skin, inflammatory lesions, comedones, and scarring, and may contribute to PIH in acne patients with SOC (Figure 1).⁸ A thorough history should be obtained from acne patients, including answers to the following questions⁷:

• What skin and hair care products do you use?
• Do you use sunscreen daily?
• What cosmetic products or makeup do you use?
• Do you use any ethnic skin care products, including skin lightening creams?
• Do you have a history of keloids?

It is important to ask these questions to assess if the SOC patient has developed pomade acne,⁹ acne cosmetica,¹⁰ or a potential risk of skin irritation from the use of skin care practices. It is best to take total control of the patient’s skin care regimen and discontinue use of toners, astringents, witch hazel, exfoliants, and rubbing alcohol, which may lead to skin dryness and irritation, particularly when combined with topical acne medications.

Treatment
Treatment of acne in SOC patients is similar to generally recommended treatments, with special considerations. Consider the following key points when treating acne in SOC patients:

• Treat acne early and aggressively to prevent or minimize subsequent PIH and acne scarring.
• Balance aggressive treatment with nonirritating topical skin care.
• Most importantly, target PIH in addition to acne and choose a regimen that limits skin irritation that might exacerbate existing PIH.⁷

Develop a maintenance program to control future breakouts. Topical agents can be used as monotherapy or in fixed combinations and may include benzoyl peroxide, antibiotics, dapsone, azelaic acid (AZA), and retinoids. Similar to white patients, topical retinoids remain a first-line treatment for acne in patients with SOC.^11,12

Tolerability must be managed in SOC acne patients. Therapeutic maneuvers that can be instituted should include a discussion on using gentle skin care, initiating therapy with a retinoid applied every other night starting with a low concentration and gradually titrating up, and applying a moisturizer before or after applying acne medication. Oral therapies consist of antibiotics (doxycycline, minocycline), retinoids (isotretinoin), and hormonal modulators (oral contraceptives, spironolactone). Isotretinoin, recommended for patients with nodulocystic acne, may play a possible role in treating acne-induced PIH.¹³

Two common procedural therapies for acne include comedone extraction and intralesional corticosteroid injection. A 6- to 8-week course of a topical retinoid prior to comedonal extraction may facilitate the procedure and is recommended in SOC patients to help reduce cutaneous trauma and PIH.¹¹ Inflammatory acne lesions can be treated with intralesional injection of triamcinolone acetonide 2.5 or 5.0 mg/mL, which usually reduces inflammation within 2 to 5 days.¹¹

Treatment of acne-induced PIH includes sun protection, topical and oral medications, chemical peels, lasers, and energy devices. Treatment of hypertrophic scarring and keloids involves intralesional injection of triamcinolone acetonide 20, 30, or 40 mg/mL every 4 weeks until the lesion is flat.¹¹

Superficial chemical peels can be used to treat acne and PIH in SOC patients,¹⁴ such as salicylic acid (20%–30%), glycolic acid (20%–70%), trichloroacetic acid (15%–30%), and Jessner peels.

Acne Scarring
Surgical approaches to acne scarring in patients with SOC include elliptical excision, punch excision, punch elevation, punch autografting, dermal grafting, dermal planning, subcutaneous incision (subcision), dermabrasion, microneedling, fillers, and laser skin resurfacing. The treatment of choice depends on the size, type, and depth of the scar and the clinician’s preference.

Lasers
Fractional photothermolysis has emerged as a treatment option for acne scars in SOC patients. This procedure produces microscopic columns of thermal injury in the epidermis and dermis, sparing the surrounding tissue and minimizing downtime and adverse events. Because fractional photothermolysis does not target melanin and produces limited epidermal injury, darker Fitzpatrick skin types (IV–VI) can be safely and effectively treated with this procedure.¹⁵

Rosacea in SOC Patients

Rosacea is a chronic inflammatory disorder that affects the vasculature and pilosebaceous units of the face. It commonly is seen in Fitzpatrick skin types I and II; however, rosacea can occur in all skin types (Figure 2). Triggers include emotional stress, extreme environmental temperatures, hot and spicy foods, red wine or alcohol, and topical irritants or allergens found in common cosmetic products.¹⁶

Data suggest that 4% of rosacea patients in the United States are of African, Latino, or Asian descent.¹¹ National Ambulatory Medical Care Survey data revealed that of 31.5 million rosacea visits, 2% of patients were black, 2.3% were Asian or Pacific Islander, and 3.9% were Hispanic or Latino. In a 5-year longitudinal study of 2587 rosacea patients enrolled in Medicaid in North Carolina who were prescribed at least 1 topical treatment for rosacea, 16.27% were black and 10% were of a race other than white.¹⁷

Although the pathogenesis of rosacea is unclear, hypotheses include immune system abnormalities, neurogenic dysregulation, presence of microorganisms (eg, Demodex folliculorum), UV damage, and skin barrier dysfunction.¹⁸

The 4 major subtypes of rosacea are erythematotelangiectatic, papulopustular, phymatous, and ocular rosacea.¹⁶ Interestingly, rosacea in SOC patients may present with hypopigmentation surrounding the borders of the facial erythema. For phymatous rosacea, isotretinoin may reduce incipient rhinophyma but must be carefully monitored and pregnancy must be excluded. Surgical or laser therapy may be indicated to recontour the nose if severe.

There are several skin conditions that can present with facial erythema in patients with SOC, including seborrheic dermatitis, systemic lupus erythematosus, and contact dermatitis. It is important to note that the detection of facial erythema in darker skin types may be difficult; therefore, laboratory evaluation (antinuclear antibodies), patch testing, and skin biopsy should be considered if the clinical diagnosis is unclear.

Treatment
Treatment of rosacea in SOC patients does not differ from other racial groups. Common strategies include gentle skin care, sun protection (sun protection factor 30+), and barrier repair creams. Topical agents include metronidazole, AZA, sodium sulfacetamide/sulfur, ivermectin, and retinoids.¹⁶ Oral treatments include antibiotics in the tetracycline family (eg, subantimicrobial dose doxycycline) and isotretinoin.¹⁶ Persistent erythema associated with rosacea can be treated with brimonidine¹⁹ and oxymetazoline.²⁰ Vascular lasers and intense pulsed light may be used to address the vascular components of rosacea²¹; however, the latter is not recommended in Fitzpatrick skin types IV through VI.

Facial Hyperpigmentation in SOC Patients

Hyperpigmentation disorders can be divided into conditions that affect Fitzpatrick skin types I through III and IV though VI. Mottled hyperpigmentation (photodamage) and solar lentigines occur in patients with lighter skin types as compared to melasma, PIH, and age-related (UV-induced) hyperpigmentation, which occur more commonly in patients with darker skin types. Facial hyperpigmentation is a common concern in SOC patients. In a survey of cosmetic concerns of 100 women with SOC, hyperpigmentation or dark spots (86%) and blotchy uneven skin (80%) were the top concerns.²² In addition, facial hyperpigmentation has been shown to negatively impact quality of life.²³

Postinflammatory hyperpigmentation occurs from a pathophysiological response to inflammation, cutaneous irritation or injury, and subsequent melanocyte lability. Postinflammatory hyperpigmentation is a common presenting concern in patients with SOC and is seen as a result of many inflammatory skin disorders (eg, acne, eczema) and dermatologic procedures (eg, adverse reaction to electrodesiccation, microdermabrasion, chemical peels, laser surgery).²⁴

Melasma is an acquired idiopathic disorder of hyperpigmentation and often referred to as the mask of pregnancy (Figure 3). It occurs on sun-exposed areas of skin, mainly in women with Fitzpatrick skin types III through V. Associated factors or triggers include pregnancy, hormonal treatments, exposure to UV radiation, and medications.²⁵ Hereditary factors play a role in more than 40% of cases.²⁶

Other not-so-common facial dyschromias include contact dermatitis, acanthosis nigricans, exogenous ochronosis, lichen planus pigmentosus (associated with frontal fibrosing alopecia),²⁷ drug-induced hyperpigmentation (associated with minocycline or diltiazem),^28,29 and UV-induced (age-related) hyperpigmentation.

Treatment
The treatment of hyperpigmentation should provide the following: (1) protection from sun exposure; (2) inhibition of tyrosinase, the enzyme responsible for the conversion of tyrosine to melanin; (3) inhibition of melanosome transfer from the melanocyte to the keratinocyte; (4) removal of melanin from the epidermis through exfoliation; and (5) destruction or disruption of melanin in the dermis.³⁰ Therapies for facial hyperpigmentation are listed in Table 1.

Topical therapies include prescription medications and nonprescription cosmeceuticals. Prescription medications include hydroquinone (HQ), topical retinoids, and AZA. Hydroquinone, a tyrosinase inhibitor, is the gold standard for skin lightening and often is used as a first-line therapy. It is used as a monotherapy (HQ 4%) or as a fixed combination with tretinoin 0.05% and fluocinolone 0.01%.³¹ Use caution with HQ in high concentrations (6% and higher) and low concentrations (2% [over-the-counter strength]) used long-term due to the potential risk of exogenous ochronosis.

Topical retinoids have been shown to be effective therapeutic agents for melasma and PIH. Tretinoin,³² tazarotene,³³ and adapalene³⁴ all have demonstrated efficacy for acne and acne-induced PIH in SOC patients. Patients must be monitored for the development of retinoid dermatitis and worsening of hyperpigmentation.

Azelaic acid is a naturally occurring dicarboxylic acid obtained from cultures of Malassezia furfur. Azelaic acid inhibits tyrosinase activity, DNA synthesis, and mitochondrial enzymes, thus blocking direct cytotoxic effects toward melanocytes. Azelaic acid is approved by the US Food and Drug Administration for acne in a 20% cream formulation and rosacea in 15% gel and foam formulations, and it is used off label for melasma and PIH.³⁵

Oral tranexamic acid is currently used as a hemostatic agent due to its ability to inhibit the plasminogen-plasmin pathway. In melasma, it blocks the interaction between melanocytes and keratinocytes in the epidermis and modulates the vascular component of melasma in the dermis. In an open-label study, 561 Asian melasma patients were treated with oral tranexamic acid 250 mg twice daily for 4 months. Results demonstrated improvement in 90% of patients, and 7.1% reported adverse effects (eg, abdominal bloating and pain, nausea, vomiting, headache, tinnitus, numbness, menstrual irregularities).³⁶ Coagulation screening should be monitored monthly, and any patient with a history of clotting abnormalities should be excluded from off-label treatment with oral tranexamic acid.

Nonprescription cosmeceuticals are available over-the-counter or are office dispensed.³⁷ For optimal results, cosmeceutical agents for skin lightening are used in combination. Most of these combinations are HQ free and have additive benefits such as a multimodal skin lightening agent containing key ingredients that correct and prevent skin pigmentation via several pathways affecting melanogenesis.³⁸ It is an excellent alternative to HQ for mottled and diffuse UV-induced hyperpigmentation and can be used for maintenance therapy in patients with melasma.

Photoprotection is an essential component of therapy for melasma and PIH, but there is a paucity of data on the benefits for SOC patients. Halder et al³⁹ performed a randomized prospective study of 89 black and Hispanic patients who applied sunscreen with a sun protection factor of 30 or 60 daily for 8 weeks. Clinical grading, triplicate L*A*B chromameter, and clinical photography were taken at baseline and weeks 4 and 8. The results demonstrated skin lightening in both black and Hispanic patients and support the use of sunscreen in the prevention and management of dyschromia in SOC patients.³⁹ Visible light also may play a role in melasma development, and thus use of sunscreens or makeup containing iron oxides are recommended.⁴⁰

Procedural treatments for facial hyperpigmentation include microdermabrasion, chemical peels, lasers, energy-based devices, and microneedling. There are many types and formulations of chemical peeling agents available; however, superficial and medium-depth chemical peels are recommended for SOC patients (Table 2). Deep chemical peels are not recommended for SOC patients due to the potential increased risk for PIH and scarring.

Cosmetic Enhancement in SOC Patients

Cosmetic procedures are gaining popularity in the SOC population and account for more than 20% of cosmetic procedures in the United States.⁴¹ Facial cosmetic concerns in SOC include dyschromia, benign growths (dermatosis papulosa nigra), hyperkinetic facial lines, volume loss, and skin laxity.⁴² Key principles to consider when treating SOC patients are the impact of ethnicity on aging and facial structure, the patient’s desired cosmetic outcome, tissue reaction to anticipated treatments, and the patient’s expectations for recommended therapies.

Aging in SOC Patients
Skin aging can be classified as intrinsic aging or extrinsic aging. Intrinsic aging is genetic and involves subsurface changes such as volume loss, muscle atrophy, and resorption of bony structure. Extrinsic aging (or photoaging) involves surface changes of the epidermis/dermis and manifests as mottled pigmentation, textural changes, and fine wrinkling. Due to the photoprotection of melanin (black skin=SPF 13.4), skin aging in SOC patients is delayed by 10 to 20 years.⁴³ In addition, SOC patients have more reactive collagen and can benefit from noninvasive cosmetic procedures such as fillers and skin-tightening procedures.⁴²

Cosmetic Treatments and Procedures
Dermatosis papulosa nigra (benign growths of skin that have a genetic predisposition)⁴⁴ occur mainly on the face but can involve the entire body. Treatment modalities include electrodesiccation, cryotherapy, scissor excision, and laser surgery.⁴⁵

Treatment of hyperkinetic facial lines with botulinum toxin type A is a safe and effective procedure in patients with SOC. Grimes and Shabazz⁴⁶ performed a 4-month, randomized, double-blind study that evaluated the treatment of glabellar lines in women with Fitzpatrick skin types V and VI. The results demonstrated that the duration of effects was the same in the patients who received either 20 or 30 U of botulinum toxin type A.⁴⁶ Dynamic rhytides (furrows and frown/scowl lines arising from laughing, frowning, or smiling) can be treated safely in patients with SOC using botulinum toxin type A off label for relaxation of the upper and lower hyperkinetic muscles that result in these unwanted signs of aging. Botulinum toxin type A often is used for etched-in crow’s-feet, which rarely are evident in SOC patients.⁴⁷ Facial shaping also can be accomplished by injecting botulinum toxin type A in combination with soft-tissue dermal fillers.⁴⁷

Although black individuals do not experience perioral rhytides at the frequency of white individuals, they experience a variety of other cosmetic issues related to skin sagging and sinking. Currently available hyaluronic acid (HA) fillers have been shown to be safe in patients with Fitzpatrick skin types IV through VI.⁴⁸ Two studies evaluated fillers in patients with SOC, specifically HA⁴⁹ and calcium hydroxylapatite,⁵⁰ focused on treatment of the nasolabial folds and the potential risk for dyspigmentation and keloidal scarring. Taylor et al⁴⁹ noted that the risk of hyperpigmentation was 6% to 9% for large- and small-particle HA, respectively, and was associated with the serial or multiple puncture injection technique. No hypertrophic or keloidal scarring occurred in both studies.^49,50

Facial contouring applications with fillers include glabellar lines, temples, nasal bridge, tear troughs, malar and submalar areas, nasolabial folds, radial lines, lips, marionette lines, mental crease, and chin. Hyaluronic acid fillers also can be used for lip enhancement.⁴⁷ Although white women are looking to increase the size of their lips, black women are seeking augmentation to restore their lip size to that of their youth. Black individuals do not experience the same frequency of perioral rhytides as white patients, but they experience a variety of other issues related to skin sagging and sinking. Unlike white women, enhancement of the vermilion border rarely is performed in black women due to development of rhytides, predominantly in the body of the lip below the vermilion border in response to volume loss in the upper lip while the lower lip usually maintains its same appearance.⁴⁷

Facial enhancement utilizing poly-L-lactic acid can be used safely in SOC patients.⁵¹ Poly-L-lactic acid microparticles induce collagen formation, leading to dermal thickening over 3 to 6 months; however, multiple sessions are required to achieve optimal aesthetic results.

Patients with more reactive collagen can benefit from noninvasive cosmetic procedures such as skin-tightening procedures.⁵² Radiofrequency and microfocused ultrasound are cosmetic procedures used to provide skin tightening and facial lifting. They are safe and effective treatments for patients with Fitzpatrick skin types IV to VI.⁵³ Histologically, there is less thinning of collagen bundles and elastic tissue in ethnic skin. Due to stimulation of collagen by these procedures, most SOC patients will experience a more enhanced response, requiring fewer treatment sessions than white individuals.

Conclusion

Medical and aesthetic facial concerns in SOC patients vary and can be a source of emotional and psychological distress that can negatively impact quality of life. The approach to the treatment of SOC patients should be a balance between tolerability and efficacy, considering the potential risk for PIH.

Physician diversity benefits patient care: Patients are more satisfied during race-concordant visits, report their physicians as more engaged and responsive to their needs, and experience notably longer visits.^1,2 Nonwhite physicians (ie, races and ethnicities that are underrepresented in medicine [URM] with respect to the general population) are more likely to care for underserved communities. Furthermore, increased diversity in the learning environment supports preparedness of all trainees to serve diverse patients.³ For these reasons, a more diverse physician workforce can contribute to better access to care in all communities, thus addressing health disparities.^1,4

Increasing diversity in the dermatology workforce has been identified as an emerging priority.⁵ Dermatology is one of the least diverse specialties,⁵ and the representation of URM dermatologists is lower compared to other medical specialties and the general US population. The proportion of specialty leaders from underrepresented backgrounds may be even smaller. The lack of diversity in academic dermatology has negative consequences for patients and communities. Increasing the diversity of resident trainees is the only way to improve the diversity gap within the dermatology workforce.⁶

Recent commentary on this topic has highlighted several priorities for addressing the dermatology diversity gap,^6-11 including the following: (1) making diversity an explicit goal in dermatology; (2) ensuring early exposure to dermatology in medical school; (3) supporting mentorship programs for minority medical students; (4) increasing medical student diversity; (5) encouraging that all dermatology program directors and leaders train in implicit bias; and (6) reviewing residency admission criteria to ensure they are objective and equitable, not biased against any applicants.

The process of reviewing residency selection criteria has begun. In 2017, Chen and Shinkai⁷ called for our specialty to rethink the selection process. The authors argued that emphasis on test scores, grades, and publications systematically disadvantages underrepresented minorities and students from lower socioeconomic statuses. The authors proposed several solutions: (1) make diversity an explicit goal of the selection process, (2) shift away from test scores for all applicants, (3) change the interview format, (4) prioritize other competencies such as observation skills, and (5) recruit and retain faculty who support URM trainees.⁷

Several dermatology leadership groups have taken action to promote programs that aim to improve diversity within dermatology. The Dermatology Diversity Champions initiative includes 6 US dermatology residency programs that are committed to increasing diversity and collaborate to evaluate pilot approaches. The American Academy of Dermatology President’s Conference on Diversity in Dermatology in Chicago, Illinois, in August 2017, as well as the focus on diversity in residency training programs at the Annual Meeting of the Association of Professors of Dermatology in Chicago, Illinois, in October 2017, are strong indicators that our specialty as a whole is aware and eager to embrace diversity as a priority. The American Academy of Dermatology President’s Conference, which was comprised of representatives from many leadership organizations and interest groups within dermatology, identified 3 action items: (1) increase the pipeline of URM students into medical school, (2) increase interest in dermatology among URM medical students, and (3) increase URM representation in residency training programs.

There are many strengths, weaknesses, opportunities, and threats/barriers (SWOT) to attaining this goal. Current strengths include strong support from dermatology leaders and activities that build on existing mentorship and diversity efforts by leaders within our specialty. SWOT analysis highlights several key opportunities of this mission, including connecting with the House of Medicine in shared efforts to improve diversity, as well as increased understanding of skin of color, health disparities, and implicit bias among physicians. Although faculty development will require time and financial investment, it will lead to tremendous benefits and opportunities for all dermatologists, including URM physicians. Other weaknesses and threats/barriers are outlined in the Figure.

Final Thoughts

We are far from reaching our goal of a diverse dermatology workforce, and the road ahead is long. We have a start and we have momentum. We can move forward by spreading the word that all types of diversity are a priority for our specialty. Making a true difference will require commitment and sustained efforts. Dermatology can lead the way as all of American medicine strives to attain workforce diversity.

Physician diversity benefits patient care: Patients are more satisfied during race-concordant visits, report their physicians as more engaged and responsive to their needs, and experience notably longer visits.^1,2 Nonwhite physicians (ie, races and ethnicities that are underrepresented in medicine [URM] with respect to the general population) are more likely to care for underserved communities. Furthermore, increased diversity in the learning environment supports preparedness of all trainees to serve diverse patients.³ For these reasons, a more diverse physician workforce can contribute to better access to care in all communities, thus addressing health disparities.^1,4

Increasing diversity in the dermatology workforce has been identified as an emerging priority.⁵ Dermatology is one of the least diverse specialties,⁵ and the representation of URM dermatologists is lower compared to other medical specialties and the general US population. The proportion of specialty leaders from underrepresented backgrounds may be even smaller. The lack of diversity in academic dermatology has negative consequences for patients and communities. Increasing the diversity of resident trainees is the only way to improve the diversity gap within the dermatology workforce.⁶

Recent commentary on this topic has highlighted several priorities for addressing the dermatology diversity gap,^6-11 including the following: (1) making diversity an explicit goal in dermatology; (2) ensuring early exposure to dermatology in medical school; (3) supporting mentorship programs for minority medical students; (4) increasing medical student diversity; (5) encouraging that all dermatology program directors and leaders train in implicit bias; and (6) reviewing residency admission criteria to ensure they are objective and equitable, not biased against any applicants.

The process of reviewing residency selection criteria has begun. In 2017, Chen and Shinkai⁷ called for our specialty to rethink the selection process. The authors argued that emphasis on test scores, grades, and publications systematically disadvantages underrepresented minorities and students from lower socioeconomic statuses. The authors proposed several solutions: (1) make diversity an explicit goal of the selection process, (2) shift away from test scores for all applicants, (3) change the interview format, (4) prioritize other competencies such as observation skills, and (5) recruit and retain faculty who support URM trainees.⁷

Several dermatology leadership groups have taken action to promote programs that aim to improve diversity within dermatology. The Dermatology Diversity Champions initiative includes 6 US dermatology residency programs that are committed to increasing diversity and collaborate to evaluate pilot approaches. The American Academy of Dermatology President’s Conference on Diversity in Dermatology in Chicago, Illinois, in August 2017, as well as the focus on diversity in residency training programs at the Annual Meeting of the Association of Professors of Dermatology in Chicago, Illinois, in October 2017, are strong indicators that our specialty as a whole is aware and eager to embrace diversity as a priority. The American Academy of Dermatology President’s Conference, which was comprised of representatives from many leadership organizations and interest groups within dermatology, identified 3 action items: (1) increase the pipeline of URM students into medical school, (2) increase interest in dermatology among URM medical students, and (3) increase URM representation in residency training programs.

There are many strengths, weaknesses, opportunities, and threats/barriers (SWOT) to attaining this goal. Current strengths include strong support from dermatology leaders and activities that build on existing mentorship and diversity efforts by leaders within our specialty. SWOT analysis highlights several key opportunities of this mission, including connecting with the House of Medicine in shared efforts to improve diversity, as well as increased understanding of skin of color, health disparities, and implicit bias among physicians. Although faculty development will require time and financial investment, it will lead to tremendous benefits and opportunities for all dermatologists, including URM physicians. Other weaknesses and threats/barriers are outlined in the Figure.

Final Thoughts

We are far from reaching our goal of a diverse dermatology workforce, and the road ahead is long. We have a start and we have momentum. We can move forward by spreading the word that all types of diversity are a priority for our specialty. Making a true difference will require commitment and sustained efforts. Dermatology can lead the way as all of American medicine strives to attain workforce diversity.

Physician diversity benefits patient care: Patients are more satisfied during race-concordant visits, report their physicians as more engaged and responsive to their needs, and experience notably longer visits.^1,2 Nonwhite physicians (ie, races and ethnicities that are underrepresented in medicine [URM] with respect to the general population) are more likely to care for underserved communities. Furthermore, increased diversity in the learning environment supports preparedness of all trainees to serve diverse patients.³ For these reasons, a more diverse physician workforce can contribute to better access to care in all communities, thus addressing health disparities.^1,4

Increasing diversity in the dermatology workforce has been identified as an emerging priority.⁵ Dermatology is one of the least diverse specialties,⁵ and the representation of URM dermatologists is lower compared to other medical specialties and the general US population. The proportion of specialty leaders from underrepresented backgrounds may be even smaller. The lack of diversity in academic dermatology has negative consequences for patients and communities. Increasing the diversity of resident trainees is the only way to improve the diversity gap within the dermatology workforce.⁶

Recent commentary on this topic has highlighted several priorities for addressing the dermatology diversity gap,^6-11 including the following: (1) making diversity an explicit goal in dermatology; (2) ensuring early exposure to dermatology in medical school; (3) supporting mentorship programs for minority medical students; (4) increasing medical student diversity; (5) encouraging that all dermatology program directors and leaders train in implicit bias; and (6) reviewing residency admission criteria to ensure they are objective and equitable, not biased against any applicants.

The process of reviewing residency selection criteria has begun. In 2017, Chen and Shinkai⁷ called for our specialty to rethink the selection process. The authors argued that emphasis on test scores, grades, and publications systematically disadvantages underrepresented minorities and students from lower socioeconomic statuses. The authors proposed several solutions: (1) make diversity an explicit goal of the selection process, (2) shift away from test scores for all applicants, (3) change the interview format, (4) prioritize other competencies such as observation skills, and (5) recruit and retain faculty who support URM trainees.⁷

Several dermatology leadership groups have taken action to promote programs that aim to improve diversity within dermatology. The Dermatology Diversity Champions initiative includes 6 US dermatology residency programs that are committed to increasing diversity and collaborate to evaluate pilot approaches. The American Academy of Dermatology President’s Conference on Diversity in Dermatology in Chicago, Illinois, in August 2017, as well as the focus on diversity in residency training programs at the Annual Meeting of the Association of Professors of Dermatology in Chicago, Illinois, in October 2017, are strong indicators that our specialty as a whole is aware and eager to embrace diversity as a priority. The American Academy of Dermatology President’s Conference, which was comprised of representatives from many leadership organizations and interest groups within dermatology, identified 3 action items: (1) increase the pipeline of URM students into medical school, (2) increase interest in dermatology among URM medical students, and (3) increase URM representation in residency training programs.

There are many strengths, weaknesses, opportunities, and threats/barriers (SWOT) to attaining this goal. Current strengths include strong support from dermatology leaders and activities that build on existing mentorship and diversity efforts by leaders within our specialty. SWOT analysis highlights several key opportunities of this mission, including connecting with the House of Medicine in shared efforts to improve diversity, as well as increased understanding of skin of color, health disparities, and implicit bias among physicians. Although faculty development will require time and financial investment, it will lead to tremendous benefits and opportunities for all dermatologists, including URM physicians. Other weaknesses and threats/barriers are outlined in the Figure.

Final Thoughts

We are far from reaching our goal of a diverse dermatology workforce, and the road ahead is long. We have a start and we have momentum. We can move forward by spreading the word that all types of diversity are a priority for our specialty. Making a true difference will require commitment and sustained efforts. Dermatology can lead the way as all of American medicine strives to attain workforce diversity.

Patients who are Muslim—followers of the religion of Islam—struggle with a political climate that has demonized them and the continued fallout of terrorist attacks perpetrated by individuals who identify themselves as Muslim. These patients may experience low self-esteem, bullying, depression, anxiety, or posttraumatic stress disorder.¹ Some have expressed feeling judged, labeled, attacked, and subjected to discrimination. Islamophobia and a spike in hate crimes have further marginalized this already vulnerable population.² Thus, understanding your Muslim patients is the first step to treating their mental illness.

How Muslim culture might affect care

Muslims are not a monolithic group; they vary widely in their religious adherence, cultural background, and acculturation. Some are American-born, including a significant African American Muslim population. Others are children of immigrants or have recently immigrated, including many who came to the United States because of the ongoing war in Syria. Many can trace their heritage to >50 predominantly Muslim countries. Many Muslim patients want to find a balance between their religious and American identities.

As clinicians, we should not make assumptions based on outward appearances or our preconceived notions of our patients, especially when it comes to gender roles. Our job is to ask how highly personal, individualized decisions, such as a woman’s choice to wear a hijab as an expression of her faith and a symbol of modesty, factor into our patients’ day-to-day lives. Doing so can help build the therapeutic alliance and improve the accuracy of the diagnosis and the appropriateness of treatment.

Mental health clinicians are well aware of the dangers of the social stigma that their patients may experience.³ These dangers are no different when it comes to Muslim patients, who often may face “double discrimination” for their religion and for having a mental illness. They may seek support from religious leaders, family, and friends before seeing a mental health provider. Some may view their mental illness as a weakness of faith, a punishment by God, or an affliction caused by a supernatural spirit, and therefore may feel that following religious doctrine will resolve their psychological distress.⁴ They may need additional encouragement to see a therapist or take psycho­tropics, and they may prefer specific treatments that reflect their cultural values, such as supplements.

Because some Muslim patients may be more comfortable presenting their psycho­logical concerns as somatic symptoms, they may first seek care from a primary care physician. Some patients may not be open or comfortable enough to address sensitive issues, such as substance use. Providing psychoeducation, comparing mental illness with medical illness, and emphasizing doctor–patient confidentiality may help these patients overcome the stigma that can act as a barrier to care.

Provide culturally competent care

Resources are available to help us provide the best possible care to our patients from various cultures and religions, including Muslim patients. A good starting point is the DSM-5’s Cultural Formulation Interview, which is a set of 16 questions psychiatrists can use to determine the impact of culture on a patient’s clinical presentation and care.⁵ Other resources include the American Psychiatric Association’s Assessment of Cultural Factors and the American Academy of Child and Adolescent Psychiatry’s Practice Parameter for Cultural Competence.⁶

When treating Muslim patients, remember to:

• Ask about what roles their culture and religion play
• Understand their explanation of their symptoms
• Work to overcome any stigma patients may perceive related to having a psychiatric disorder
• Engage your team to identify cultural and religious factors
• Connect to community resources, such as the patient’s family and friends.

Patients who are Muslim—followers of the religion of Islam—struggle with a political climate that has demonized them and the continued fallout of terrorist attacks perpetrated by individuals who identify themselves as Muslim. These patients may experience low self-esteem, bullying, depression, anxiety, or posttraumatic stress disorder.¹ Some have expressed feeling judged, labeled, attacked, and subjected to discrimination. Islamophobia and a spike in hate crimes have further marginalized this already vulnerable population.² Thus, understanding your Muslim patients is the first step to treating their mental illness.

How Muslim culture might affect care

Muslims are not a monolithic group; they vary widely in their religious adherence, cultural background, and acculturation. Some are American-born, including a significant African American Muslim population. Others are children of immigrants or have recently immigrated, including many who came to the United States because of the ongoing war in Syria. Many can trace their heritage to >50 predominantly Muslim countries. Many Muslim patients want to find a balance between their religious and American identities.

As clinicians, we should not make assumptions based on outward appearances or our preconceived notions of our patients, especially when it comes to gender roles. Our job is to ask how highly personal, individualized decisions, such as a woman’s choice to wear a hijab as an expression of her faith and a symbol of modesty, factor into our patients’ day-to-day lives. Doing so can help build the therapeutic alliance and improve the accuracy of the diagnosis and the appropriateness of treatment.

Mental health clinicians are well aware of the dangers of the social stigma that their patients may experience.³ These dangers are no different when it comes to Muslim patients, who often may face “double discrimination” for their religion and for having a mental illness. They may seek support from religious leaders, family, and friends before seeing a mental health provider. Some may view their mental illness as a weakness of faith, a punishment by God, or an affliction caused by a supernatural spirit, and therefore may feel that following religious doctrine will resolve their psychological distress.⁴ They may need additional encouragement to see a therapist or take psycho­tropics, and they may prefer specific treatments that reflect their cultural values, such as supplements.

Because some Muslim patients may be more comfortable presenting their psycho­logical concerns as somatic symptoms, they may first seek care from a primary care physician. Some patients may not be open or comfortable enough to address sensitive issues, such as substance use. Providing psychoeducation, comparing mental illness with medical illness, and emphasizing doctor–patient confidentiality may help these patients overcome the stigma that can act as a barrier to care.

Provide culturally competent care

Resources are available to help us provide the best possible care to our patients from various cultures and religions, including Muslim patients. A good starting point is the DSM-5’s Cultural Formulation Interview, which is a set of 16 questions psychiatrists can use to determine the impact of culture on a patient’s clinical presentation and care.⁵ Other resources include the American Psychiatric Association’s Assessment of Cultural Factors and the American Academy of Child and Adolescent Psychiatry’s Practice Parameter for Cultural Competence.⁶

When treating Muslim patients, remember to:

• Ask about what roles their culture and religion play
• Understand their explanation of their symptoms
• Work to overcome any stigma patients may perceive related to having a psychiatric disorder
• Engage your team to identify cultural and religious factors
• Connect to community resources, such as the patient’s family and friends.

Patients who are Muslim—followers of the religion of Islam—struggle with a political climate that has demonized them and the continued fallout of terrorist attacks perpetrated by individuals who identify themselves as Muslim. These patients may experience low self-esteem, bullying, depression, anxiety, or posttraumatic stress disorder.¹ Some have expressed feeling judged, labeled, attacked, and subjected to discrimination. Islamophobia and a spike in hate crimes have further marginalized this already vulnerable population.² Thus, understanding your Muslim patients is the first step to treating their mental illness.

How Muslim culture might affect care

Muslims are not a monolithic group; they vary widely in their religious adherence, cultural background, and acculturation. Some are American-born, including a significant African American Muslim population. Others are children of immigrants or have recently immigrated, including many who came to the United States because of the ongoing war in Syria. Many can trace their heritage to >50 predominantly Muslim countries. Many Muslim patients want to find a balance between their religious and American identities.

As clinicians, we should not make assumptions based on outward appearances or our preconceived notions of our patients, especially when it comes to gender roles. Our job is to ask how highly personal, individualized decisions, such as a woman’s choice to wear a hijab as an expression of her faith and a symbol of modesty, factor into our patients’ day-to-day lives. Doing so can help build the therapeutic alliance and improve the accuracy of the diagnosis and the appropriateness of treatment.

Mental health clinicians are well aware of the dangers of the social stigma that their patients may experience.³ These dangers are no different when it comes to Muslim patients, who often may face “double discrimination” for their religion and for having a mental illness. They may seek support from religious leaders, family, and friends before seeing a mental health provider. Some may view their mental illness as a weakness of faith, a punishment by God, or an affliction caused by a supernatural spirit, and therefore may feel that following religious doctrine will resolve their psychological distress.⁴ They may need additional encouragement to see a therapist or take psycho­tropics, and they may prefer specific treatments that reflect their cultural values, such as supplements.

Because some Muslim patients may be more comfortable presenting their psycho­logical concerns as somatic symptoms, they may first seek care from a primary care physician. Some patients may not be open or comfortable enough to address sensitive issues, such as substance use. Providing psychoeducation, comparing mental illness with medical illness, and emphasizing doctor–patient confidentiality may help these patients overcome the stigma that can act as a barrier to care.

Provide culturally competent care

Resources are available to help us provide the best possible care to our patients from various cultures and religions, including Muslim patients. A good starting point is the DSM-5’s Cultural Formulation Interview, which is a set of 16 questions psychiatrists can use to determine the impact of culture on a patient’s clinical presentation and care.⁵ Other resources include the American Psychiatric Association’s Assessment of Cultural Factors and the American Academy of Child and Adolescent Psychiatry’s Practice Parameter for Cultural Competence.⁶

When treating Muslim patients, remember to:

• Ask about what roles their culture and religion play
• Understand their explanation of their symptoms
• Work to overcome any stigma patients may perceive related to having a psychiatric disorder
• Engage your team to identify cultural and religious factors
• Connect to community resources, such as the patient’s family and friends.