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Common Skin Disorders in Pediatric Skin of Color

      Abstract

      Children with skin of color represent a large proportion of the pediatric population. There are numerous skin conditions that commonly occur in this population, including but not limited to acne, atopic dermatitis, pityriasis alba, tinea versicolor, progressive macular hypomelanosis, traction alopecia, and confluent and reticulated papillomatosis. This article highlights the clinical presentations of these conditions in skin of color and briefly addresses pathophysiology and treatment modalities.

      KEY WORDS

      INTRODUCTION

      Pediatric patients with skin of color, which refers to individuals with Fitzpatrick skin types III through VI (Table 1), comprise many racial and ethnic groups, including but not limited to Africans, African Americans, Asians, Native Americans, Hispanics, and Latinos (
      ). According to the U.S. Census Bureau, by 2044, people with skin of color will represent 50.3% of the U.S. population (
      • Colby S.L.
      • Ortman J.M.
      Projections of the size and composition of the U.S. population: 2014 to 2060.
      ). It is critical to recognize the vast and unique clinical presentations and treatment challenges of this growing population. This article will discuss common dermatologic diagnoses in children with skin of color including acne, atopic dermatitis (AD), pityriasis alba (PA), tinea versicolor (TV), progressive macular hypomelanosis (PMH), traction alopecia, confluent and reticulated papillomatosis (CARP), and keloids, with an emphasis on clinical presentation and diagnostic pearls. Although these conditions can appear in both children and adults with varying skin types, children with ethnic skin may have different patterns of clinical presentation and response to therapy (
      • Shen L.Y.
      • Kenner-Bell B.M.
      • Ricketts J.
      • Kundu R.V.
      Ethnic skin: Kids are not just little people.
      ). This article will also briefly address differences in pathophysiology and treatment modalities in those with richly pigmented skin (Table 2).

      Instructions

      To obtain continuing education credit:
      • 1.
        Read the article carefully.
      • 2.
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      Objectives

      • 1.
        Discuss common skin conditions in pediatric patients with darker skin types.
      • 2.
        Explain early clinical signs of inflammation in skin of color.
      • 3.
        Understand the subtle differences in clinical presentation, pathophysiology, and treatment options, including pharmacologic management, for common dermatologic conditions in pediatric skin of color.
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      TABLE 1Fitzpatrick skin scale
      Type IAlways burns, never tans
      Type IIUsually burns, tans minimally
      Type IIISometimes mildly burns, tans uniformly
      Type IVBurns minimally, always tans well
      Type VVery rarely burns, tans very easily
      Type VINever burns
      TABLE 2Common pediatric skin disorders in skin of color
      DiagnosisAge of onsetClinical featuresTreatment
      AcneAdolescenceInflammatory papules and pustules, comedones ± cystic lesions

      Typically located on face ± chest and back
      Topical antibiotics (clindamycin, erythromycin), topical benzoyl peroxide, topical retinoids, oral tetracyclines

      Oral contraceptives and spironolactone (females only)

      Isotretinoin for severe cases
      Atopic dermatitisVaries (infantile atopic dermatitis has onset < 2 years of age)Infantile atopic dermatitis: eczematous dermatitis on cheeks and extensor surfaces

      Childhood atopic dermatitis: subacute and chronic dermatitis predominantly on flexural areas
      Topical steroids, topical calcineurin inhibitors, phosphodiaterase-4 inhibitors, systemic medication or phototherapy for severe disease
      Pityriasis alba3–16 years of agePoorly defined, hypopigmented macules and patches with minimal scale, typically on faceEmollients, low-potency topical steroids, topical calcineurin inhibitors, sun protection
      Tinea versicolorAdolescenceHypopigmented, hyperpigmented, or erythematous round to oval macules or thin papules that coalesce into patches or thin plaques

      Typically seen on trunk, but can be seen on face/neck in darker-skinned patients
      Topical antifungals (ketoconazole), selenium sulfide shampoo

      Systemic antifungals for severe disease

      Photoprotective measures
      Progressive macular hypomelanosisAdolescenceNonscaly, hypopigmented macules, typically on the trunkBenzoyl peroxide, topical antibiotics, oral antibiotics, phototherapy
      Traction alopeciaAdolescence/adulthoodEarly stage: mild hair loss (typically on frontal and temporal scalp), no loss of orifices ± perifollicular erythema and scale, ± fringe sign.

      Late stage: alopecia (typically on frontal and temporal scalp) with partial or total loss of orifices ± fringe sign
      Discontinuation of tight hairstyles, avoidance of chemical relaxers and heat styling, topical steroids, intralesional steroids, sub-antimicrobial doses of oral antibiotics
      Confluent and reticulated papillomatosisAdolescenceScaly, brown, thin papules that coalesce into reticulated plaques, often on central chest and backOral minocycline (first line)

      Isotretinoin
      KeloidsAdolescenceSkin-colored to hyperpigmented firm plaques that extend beyond wound marginsTopical and intralesional steroids, intralesional injection of interferon or 5-fluorouracil, cryotherapy, surgical excision, laser therapy, silicone gel sheets, pressure application, or combination treatment

      ACNE

      Regardless of race or ethnicity, acne is one of the most common skin disorders observed in children and adolescents. A retrospective cohort study showed that acne was among the top three most common dermatologic diagnoses in African American and Asian adolescents (
      • Perkins A.C.
      • Cheng C.E.
      • Hillebrand G.G.
      • Miyamoto K.
      • Kimball A.B.
      Comparison of the epidemiology of acne vulgaris among Caucasian, Asian, Continental Indian and African American women: The spectrum of acne: prevalence of subtypes across races.
      ).
      Regardless of race or ethnicity, acne is one of the most common skin disorders observed in children and adolescents.

      Clinical Presentation

      The clinical picture of adolescent acne can include open and closed comedones, inflammatory papules, pustules, nodules, and cysts (Figure 1). The presence of erythema may be harder to appreciate in darker skin types, and additional tools, such as palpation and presence of pain, may be helpful to distinguish active from resolving acne lesions (
      ). Patients with skin of color are more likely to suffer from acne scars, keloid scars, and postinflammatory hyperpigmentation (PIH) than patients with lighter skin (
      • Perkins A.C.
      • Cheng C.E.
      • Hillebrand G.G.
      • Miyamoto K.
      • Kimball A.B.
      Comparison of the epidemiology of acne vulgaris among Caucasian, Asian, Continental Indian and African American women: The spectrum of acne: prevalence of subtypes across races.
      ,
      • Robles D.T.
      • Berg D.
      Abnormal wound healing: Keloids.
      ).
      FIGURE 1
      FIGURE 1Acne vulgaris.
      (This figure appears in color online at www.jpedhc.org)

      Pathogenesis

      The general pathogenesis of acne, including hyperkeratinization, inflammation, increased sebum production, and proliferation of Cutibacterium acnes (formally known as Propionibacterium acne), is similar between different races and ethnic groups (
      • Bolognia J.L.
      • Schaffer J.V.
      • Cerroni L.
      Dermatology.
      ). One notable difference is that females with darker skin types show a higher level of inflammation histologically without correspondent clinical inflammation, a finding that may explain increased risk of postinflammatory hyperpigmentation in patients with darker skin types (
      • Halder R.M.
      • Brooks H.L.
      • Callender V.D.
      Acne in ethnic skin.
      ,
      • Halder R.M.
      • Nootheti P.K.
      Ethnic skin disorders overview.
      ).

      Treatment

      Treatment of acne in adolescents with skin of color is similar to treatment of acne in patients with lighter skin types, but unique challenges exist. The use of topical retinoids is the first-line therapy because of their effectiveness in controlling follicular hyperkeratinization, inflammation, and dyspigmentation (
      • Davis E.C.
      • Callender V.D.
      A review of acne in ethnic skin: Pathogenesis, clinical manifestations, and management strategies.
      ,
      • Yin N.C.
      • McMichael A.J.
      Acne in patients with skin of color: Practical management.
      ). However, caution must be exercised in using topical retinoids in patients with skin of color to prevent retinoid dermatitis, which is characterized by xerosis and erythema. This can be avoided by starting with every-other-day application of a low-concentration (0.025%) topical retinoid in a cream-based vehicle. Additionally, certain retinoid formulations, such as adapalene and micronized forms, have been shown to be well tolerated in skin of color (
      ). Topical antimicrobials, such as erythromycin and clindamycin, are well tolerated and effective in controlling C. acnes. A combination of topical antimicrobials and/or retinoids with benzoyl peroxide can also be helpful (
      • Spann C.T.
      Ten tips for treating acne vulgaris in Fitzpatrick skin types IV-VI.
      ).
      • Alexis A.F.
      • Johnson L.A.
      • Kerrouche N.
      • Callender V.D.
      A subgroup analysis to evaluate the efficacy and safety of adapalene-benzoyl peroxide topical gel in African American subjects with moderate acne.
      evaluated the efficacy and safety of adapalene 0.1%/benzoyl peroxide 2.5% gel in 238 African American individuals and found that this combination was well tolerated, and no cases of treatment-related PIH were observed (
      • Alexis A.F.
      • Johnson L.A.
      • Kerrouche N.
      • Callender V.D.
      A subgroup analysis to evaluate the efficacy and safety of adapalene-benzoyl peroxide topical gel in African American subjects with moderate acne.
      ). A similar study found no differences in cutaneous irritation in Fitzpatrick skin types I to II versus IV to VI when clindamycin phosphate 1.2%/benzoyl peroxide gel was used (
      • Callender V.D.
      Fitzpatrick skin types and clindamycin phosphate 1.2%/benzoylperoxide gel: Efficacy and tolerability of treatment in moderate to severe acne.
      ).
      If topical acne medications are insufficient, the addition of oral medication and a referral to a dermatologist are often necessary. Providers should have a low threshold for dermatology referral and oral medication use in patients with skin of color given the greater risk of acne complications (
      • Alexis A.F.
      Acne vulgaris in skin of color: Understanding nuances and optimizing treatment outcomes.
      ). Antibiotics such as tetracycline derivatives are used in moderate to severe acne because of their antimicrobial and antiinflammatory properties (
      • Spann C.T.
      Ten tips for treating acne vulgaris in Fitzpatrick skin types IV-VI.
      ). Oral isotretinoin is usually reserved for severe nodulocystic, scarring, or treatment-resistant acne. In patients with skin of color, it has been recommended to start with a lower dose of isotretinoin (such as 20 mg daily) to avoid initial acne flaring and sequelae (
      ).
      Another important aspect of treating acne in skin of color is taking a thorough history, inquiring about all skin and hair products. Some products such as cocoa butter and hair oils, often used by African Americans, are comedogenic and can cause a monomorphic type of acne called pomade acne. This subtype of acne is typically confined to the frontal hairline, forehead, and temples (
      • Davis E.C.
      • Callender V.D.
      A review of acne in ethnic skin: Pathogenesis, clinical manifestations, and management strategies.
      ). In addition, it is crucial to emphasize the importance of avoiding harsh skin products and using gentle cleansers and noncomedogenic facial moisturizers and sunscreens.
      Acne in children with skin of color should be treated aggressively to help avoid postinflammatory pigmentary changes and scarring that can be both cosmetically and psychologically burdensome to patients. Early acknowledgment and treatment of PIH changes is of extreme importance. In many instances, PIH is of greater concern to the patient than the acne itself and is often the force driving patients with skin of color to seek dermatologic care (
      • Alexis A.F.
      Acne vulgaris in skin of color: Understanding nuances and optimizing treatment outcomes.
      ). Products such as azelaic acid, retinoid derivatives, and hydroquinone can help lighten PIH, but these products can occasionally irritate the skin paradoxically, worsening the PIH (
      • Callender V.D.
      Fitzpatrick skin types and clindamycin phosphate 1.2%/benzoylperoxide gel: Efficacy and tolerability of treatment in moderate to severe acne.
      ,
      • Grimes P.
      • Callender V.
      Tazarotene cream for postinflammatory hyperpigmentation and acne vulgaris in darker skin: A double-blind, randomized, vehicle-controlled study.
      ). Strict sun protection is essential to help prevent PIH from darkening. With time and strict sun protection, PIH will slowly fade.
      Microneedling, a cosmetic procedure in which very fine needles puncture the skin to induce collagen formation, is an effective treatment for both acne scars and associated pigmentation in patients with dark skin color; however, additional treatments may be needed relative to patients with lighter skin (
      • Al Qarqaz F.
      • Al-Yousef A.
      Skin microneedling for acne scars associated with pigmentation in patients with dark skin.
      ). Although superficial chemical peels are generally well tolerated in patients with skin of color, a recent study showed that patients with skin type VI had higher odds of experiencing an adverse event, including prolonged crust and PIH (
      • Vemula S.
      • Maymomne M.B.C.
      • Secemsky E.A.
      • Widjajahakim R.
      • Patzelt N.M.
      • Saade D.
      • Vashi N.A.
      Assessing the safety of superficial chemical peels in darker skin: A retrospective study.
      ).

      ATOPIC DERMATITIS

      AD is the most common chronic inflammatory disease that affects children worldwide. General prevalence of AD in the United States is estimated at 9% to 25% (
      • Siegfried E.C.
      • Jaworski J.C.
      • Mina-Osorio P.
      A systematic scoping literature review of publications supporting treatment guidelines for pediatric atopic dermatitis in contrast to clinical practice patterns.
      ). A study that sought to assess heath care use for AD found that Asian and African American individuals were, respectively, seven and three times more likely to seek dermatologic care for AD than White individuals (
      • Janumpally S.R.
      • Feldman S.R.
      • Gupta A.K.
      • Fleischer A.B.
      In the United States, blacks and Asian/Pacific Islanders are more likely than whites to seek medical care for atopic dermatitis.
      ).

      Clinical Presentation

      The clinical presentation of AD varies according with age of onset. Infantile AD, which occurs before 2 years of age, typically presents as an acute and/or subacute eczematous dermatitis. Common sites of involvement include the cheeks, neck, scalp, and extensor surfaces (Figure 2). Childhood AD is characterized by subacute and chronic, lichenified skin lesions involving the neck, flexural areas, wrists, and ankles (
      • Bolognia J.L.
      • Schaffer J.V.
      • Cerroni L.
      Dermatology.
      ) . Although the general clinical presentation is similar among all races and ethnicities, darker-skinned individuals have a few distinct clinical features. African American patients typically present with a more papular variant on the arms, legs, and periumbilical area (
      • Julián-Gónzalez R.E.
      • Orozco-Covarrubias L.
      • Durán-McKinster C.
      • Palacios-Lopez C.
      • Ruiz-Maldonado R.
      • Sáez-de-Ocariz M.
      Less common clinical manifestations of atopic dermatitis: prevalence by age.
      ). In patients with skin of color, lesions of AD are more likely to resolve with hypo- or hyperpigmentation. A small study done in Mexican children evaluating the prevalence of clinical variants of AD found that 76% of children studied had at least one infrequent clinical sign of AD, including but not limited to nipple dermatitis, follicular dermatitis, prurigo-type dermatitis, and genital dermatitis (
      • Julián-Gónzalez R.E.
      • Orozco-Covarrubias L.
      • Durán-McKinster C.
      • Palacios-Lopez C.
      • Ruiz-Maldonado R.
      • Sáez-de-Ocariz M.
      Less common clinical manifestations of atopic dermatitis: prevalence by age.
      ). Providers should be cognizant that cutaneous diseases, such as AD, that rely on the detection of erythema to determine diagnosis and severity may be underdiagnosed and undertreated in patients with skin of color (
      • Ben-Gashir M.A.
      • Hay R.J.
      Reliance on erythema scores may mask severe atopic dermatitis in black children compared with their white counterparts.
      ). Moreover, dark-skinned patients may deem their atopic symptoms as less severe than those with lighter skin types (
      • Zhao C.Y.
      • Hao E.Y.
      • Oh D.D.
      • Daniel B.S.
      • Martin L.K.
      • Su J.C.
      • Murrell D.F.
      A comparison study of clinician-rated atopic dermatitis outcome measures for intermediate- to dark-skinned patients.
      ).
      FIGURE 2
      FIGURE 2Atopic dermatitis.
      (This figure appears in color online at www.jpedhc.org)

      Pathogenesis

      The pathogenesis of AD is complex and involves genetic and environmental factors. Metabolites of filaggrin, a protein present on the cornified envelope, are responsible for skin moisturizing, and it has been found that a reduction in the filaggrin metabolites and uncommon filaggrin variants contribute to AD in African American children (
      • Margolis D.J.
      • Mitra N.
      • Gochnauer H.
      • Wubbenhorst B.
      • D'Andrea K.
      • Kraya A.
      • Nathanson K.L.
      Uncommon filaggrin variants are associated with persistent atopic dermatitis in african americans.
      ,
      • Quiggle A.M.
      • Goodwin Z.A.
      • Marfatia T.R.
      • Kumar M.G.
      • Ciliberto H.
      • Bayliss S.J.
      • de Guzman Strong C.
      Low filaggrin monomer repeats in African American pediatric patients with moderate to severe atopic dermatitis.
      ). In addition, African Americans have reduced ceramide levels and increased transepidermal water loss, which contributes to xerosis (
      • Vachiramon V.
      • Tey H.L.
      • Thompson A.E.
      • Yosipovitch G.
      Atopic dermatitis in African American children: addressing unmet needs of a common disease.
      ). Children born outside the United States have lower risk of AD than U.S.-born children; however, children born outside the United States who have lived in the United States for longer than 10 years have significantly higher odds of developing eczema than children who have lived in the United States for shorter periods of time (
      • Silverberg J.I.
      • Simpson E.L.
      • Durkin H.G.
      • Joks R.
      Prevalence of allergic disease in foreign-born American children.
      ).

      Treatment

      AD has a significant impact on patients’ and families’ quality of life, and appropriate and prompt treatment to minimize skin burden is imperative (
      • Marciniak J.
      • Reich A.
      • Szepietowski J.C.
      Quality of life of parents of children with atopic dermatitis.
      ,
      • Pustisek N.
      • Vurnek Zivkovic M.
      • Situm M.
      Quality of life in families with children with atopic dermatitis.
      ). Asking patients about their sleep, presence and intensity of pruritus, and impact on daily life are good estimates of disease impact on quality of life (
      • Eichenfield L.F.
      • Tom W.L.
      • Chamlin S.L.
      • Feldman S.R.
      • Hanifin J.M.
      • Simpson E.L.
      • Sidbury R.
      Guidelines of care for the management of atopic dermatitis: Section 1. Diagnosis and assessment of atopic dermatitis.
      ). It is essential to counsel patients and their caretakers on the initial signs of AD to avoid postinflammatory pigment alterations that are commonly seen in chronically inflamed areas of skin. Treatment is based on repair and protection of the epidermal barrier, management of skin inflammation (with topical steroids or topical steroid–sparing agents), control of pruritus, and appropriate treatment of secondary skin infection (with topical or oral antibiotics and bleach baths;
      • Bolognia J.L.
      • Schaffer J.V.
      • Cerroni L.
      Dermatology.
      ). Recalcitrant AD may require systemic treatment or phototherapy (
      • Ortiz-Salvador J.M.
      • Pérez-Ferriols A.
      Phototherapy in atopic dermatitis.
      ). Crisaborole, a phosphodiaesterase-4 inhibitor, is a promising nonsteroid alternative for treatment of mild to moderate AD in children older than 2 years (
      • Paller A.S.
      • Tom W.L.
      • Lebwohl M.G.
      • Blumenthal R.L.
      • Boguniewicz M.
      • Call R.S.
      • Hebert A.A.
      Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults.
      ). Limited studies are available evaluating treatment efficacy of AD in different races and ethnicities.

      PITYRIASIS ALBA

      PA is a benign, hypopigmented dermatosis that most commonly occurs in children with darker skin types and is less commonly seen in postpubertal adolescents and adults because of the proposed protective effect of sebum (
      • Miazek N.
      • Michalek I.
      • Pawlowska-Kisiel M.
      • Olszewska M.
      • Rudnicka L.
      Pityriasis alba—Common disease, enigmatic entity: Up-to-date review of the literature.
      ).

      Clinical Presentation

      PA is characterized clinically by poorly defined, hypopigmented macules and patches with minimal scale (Figure 3). Early lesions present as subclinical dermatitis, and erythema may be less evident in children with skin of color. Typically, lesions are located on the face, but other body sites, such as the chest and back, can be affected. There is no clear sex predilection. The onset of disease is typically around 3 to 16 years of age (
      • Miazek N.
      • Michalek I.
      • Pawlowska-Kisiel M.
      • Olszewska M.
      • Rudnicka L.
      Pityriasis alba—Common disease, enigmatic entity: Up-to-date review of the literature.
      ).
      FIGURE 3
      FIGURE 3Pityriasis alba.
      (This figure appears in color online at www.jpedhc.org)
      Diagnosis of PA is established by clinical presentation and history, and therefore it is important to inquire about a personal or family history of atopy. Histologic findings are nonspecific, but biopsy may occasionally be helpful in ruling out other hypo- and depigmenting conditions when the presentation is not typical (
      • Givler D.N.
      • Givler A.
      Pityriasis alba.
      ).

      Pathogenesis

      Environmental factors such as sun exposure, long and frequent baths, and mechanical exfoliation appear to be predisposing factors in susceptible skin. African American children, as mentioned, may be genetically predisposed to xerosis, which can lead to PA. PA is one of the minor criteria for AD and may precede the clinical findings of AD (
      • Givler D.N.
      • Givler A.
      Pityriasis alba.
      ).

      Treatment

      Even though PA is benign and may undergo spontaneous remission, it can be particularly bothersome for those with darker phototypes. Patient counseling and use of sunscreen, protective hats, sun-protective clothing, and skin emollients may be of help. Emphasis should be placed on sun-protective clothing, given the fact that mineral-based sunscreens (zinc oxide, titanium dioxide) that are typically recommended for atopic patients may be cosmetically difficult to tolerate for patients with darker skin types. Low-potency topical corticosteroids and calcineurin inhibitors have also shown good response (
      • Miazek N.
      • Michalek I.
      • Pawlowska-Kisiel M.
      • Olszewska M.
      • Rudnicka L.
      Pityriasis alba—Common disease, enigmatic entity: Up-to-date review of the literature.
      ).
      Even though PA is benign and may undergo spontaneous remission, it can be particularly bothersome for those with darker phototypes.

      TINEA VERSICOLOR

      TV, also known as pityriasis versicolor, is a common superficial nondermatophyte mycosis. Some studies report a predilection for darker-skinned individuals. Alterations of skin pigmentation are often the presenting complaint, especially in patients with skin of color (
      • Kallini J.R.
      • Riaz F.
      • Khachemoune A.
      Tinea versicolor in dark-skinned individuals.
      ).

      Clinical Presentation

      Contrary to TV in lighter-skinned patients, which can present as either hypopigmented, hyperpigmented, or erythematous round to oval macules or thin papules, many dark-skinned patients present solely with hypopigmented lesions (Figure 4;
      • Aljabre S.H.
      • Alzayir A.A.
      • Abdulghani M.
      • Osman O.O.
      Pigmentary changes of tinea versicolor in dark-skinned patients.
      ,
      • Kallini J.R.
      • Riaz F.
      • Khachemoune A.
      Tinea versicolor in dark-skinned individuals.
      ). When active, there is usually an associated subtle scale and occasionally associated pruritus. TV is typically symmetrically distributed on the upper trunk, shoulders, or flexural areas, but there is more common facial and neck involvement in those with darker skin. Diagnosis can be easily confirmed by potassium hydroxide skin-scraping showing a mixture of yeast and hyphae. Wood's lamp evaluation shows a yellow-green fluorescence in one third of cases (
      • Kallini J.R.
      • Riaz F.
      • Khachemoune A.
      Tinea versicolor in dark-skinned individuals.
      ). TV commonly affects adolescents and young adults but may also occur in children. It is especially prevalent in tropical climates and during summer months.
      FIGURE 4
      FIGURE 4Tinea versicolor.
      (This figure appears in color online at www.jpedhc.org)

      Pathogenesis

      TV is caused by lipid-dependent Malassezia yeasts (formerly known as Pityrosporum). Some propose that the hypopigmented forms more commonly seen in darker-skinned patients are due to damage to melanocytes, inhibition of tyrosinase by the dicarboxylic acid produced by Malassezia species, or blockage of ultraviolet light by lipid-like material accumulating in the stratum corneum (
      • Nazzaro-Porro M.
      • Passi S.
      Identification of tyrosinase inhibitors in cultures of Pityrosporum.
      ). In addition, under light microscopy, lesions on dark skin involved with TV tend to have a thicker stratum corneum, more tonofilaments in the granulosum, and more sequestered melanosomes (
      • Kallini J.R.
      • Riaz F.
      • Khachemoune A.
      Tinea versicolor in dark-skinned individuals.
      ).

      Treatment

      Currently, the treatment guidelines of TV do not differ based on skin phototype. Treatment of TV involves use of topical antifungals or shampoo or selenium sulfide lotion/shampoo. Severe or refractory cases may require oral antifungal therapy and/or monthly prophylactic treatment (
      • Aljabre S.H.
      • Alzayir A.A.
      • Abdulghani M.
      • Osman O.O.
      Pigmentary changes of tinea versicolor in dark-skinned patients.
      ). Pigmentary changes in the absence of scale may persist for months even after successful treatment, which is an important point to emphasize to patients.

      PROGRESSIVE MACULAR HYPOMELANOSIS

      PMH is a relatively common but underrecognized skin disorder that involves alteration of pigment and usually affects patient with skin types IV to VI (
      • Martínez-Martínez M.L.
      • Azaña-Defez J.M.
      • Rodríguez-Vázquez M.
      • Faura-Berruga C.
      • Escario-Travesedo E.
      Progressive macular hypomelanosis.
      ).

      Clinical Presentation

      PMH is characterized by spreading nonscaly, asymptomatic, hypopigmented macules on the trunk (Figure 5). Wood's lamp evaluation shows red perifollicular fluorescence attributed to the porphyrin produced by C. acnes (
      • Pflederer R.T.
      • Wuennenberg J.P.
      • Foote C.
      • Aires D.
      • Rajpara A.
      Use of Wood's lamp to diagnose progressive macular hypomelanosis.
      ). Potassium hydroxide scraping results will be negative. A skin biopsy may be helpful to rule out other clinically similar skin diseases, because PMH is a diagnosis of exclusion. This condition poses cosmetic concerns for patients with skin of color because the condition may be more noticeable in darker-skinned individuals.
      FIGURE 5
      FIGURE 5Progressive macular hypomelanosis.
      (This figure appears in color online at www.jpedhc.org)

      Pathogenesis

      No differences have been found in the pathogenesis of PMH in different skin phototypes. C. acnes is thought to play a role in the pathogenesis of this condition (
      • Westerhof W.
      • Relyveld G.N.
      • Kingswijk M.M.
      • de Man P.
      • Menke H.E.
      Propionibacterium acnes and the pathogenesis of progressive macular hypomelanosis.
      ).

      Treatment

      Treatment options include topical and oral antibiotics, topical benzoyl peroxide, and ultraviolet light irradiation (
      • Thng S.T.G.
      • Long V.S.H.
      • Chuah S.Y.
      • Tan V.W.D.
      Efficacy and relapse rates of different treatment modalities for progressive macular hypomelanosis.
      ). Both the response to treatment and clinical course are variable. PMH may gradually progress with time or may resolve spontaneously within a few years (
      • Bolognia J.L.
      • Schaffer J.V.
      • Cerroni L.
      Dermatology.
      ).

      TRACTION ALOPECIA

      Traction alopecia is a form of hair loss caused by chronic tension on the hair follicles and is primarily seen in African American adolescents and women. Early disease is nonscarring and reversible, but chronic disease is scarring and may result in permanent hair loss.

      Clinical Presentation

      Clinical findings vary depending on the stage of disease. Early disease will manifest with mild hair loss and pruritus along with perifollicular erythema, pustules, and scale. Later stages will result in irreversible, scarring alopecia with partial or total loss of orifices (
      • Billero V.
      • Miteva M.
      Traction alopecia: The root of the problem.
      ,
      • Pulickal J.K.
      • Kaliyadan F.
      Alopecia, traction.
      ). The most common sites for traction alopecia are the frontal and temporal hairline above the ears (Figure 6). A clinical clue is the fringe sign, which refers to locks of short residual hair observed at the margin of the anterior and temporal hairlines, anterior to the patches of alopecia (
      • Samrao A.
      • Price V.H.
      • Zedek D.
      • Mirmirani P.
      The “Fringe Sign”—A useful clinical finding in traction alopecia of the marginal hair line.
      ). The diagnosis is usually clinical, but difficult cases may require a skin biopsy. Differential diagnoses include tinea capitis, alopecia areata, trichotillomania, frontal fibrosing alopecia, infectious folliculitis, and syphilis (
      • Castelo-Soccio L.
      Diagnosis and management of alopecia in children.
      ).
      FIGURE 6
      FIGURE 6Traction alopecia.
      (This figure appears in color online at www.jpedhc.org)

      Pathogenesis

      Traction alopecia is seen primarily in African American adolescents and women due to their unique hair styling practices (braids, cornrows, dreadlocks, and tight ponytails) along with lesser tensile strength and lower moisture content of their hair follicles (
      • Ji J.H.
      • Park T.-S.
      • Lee H.-J.
      • Kim Y.-D.
      • Pi L.-Q.
      • Jin X.-H.
      • Lee W.-S.
      The ethnic differences of the damage of hair and integral hair lipid after ultra violet radiation.
      ,
      • Lawson C.N.
      • Hollinger J.
      • Sethi S.
      • Rodney I.
      • Sarkar R.
      • Dlova N.
      • Callender V.D.
      Updates in the understanding and treatments of skin & hair disorders in women of color.
      ).

      Treatment

      Management includes discontinuation of tight hairstyles, avoidance of practices that may cause hair breakage (such as use of chemical relaxers or heat styling), and use of topical or intralesional corticosteroids or sub-antimicrobial doses of oral antibiotics. Behavioral changes may be particularly challenging for patients with traction alopecia. Prognosis of this preventable condition will depend largely on the stage of the disease (
      • Bolognia J.L.
      • Schaffer J.V.
      • Cerroni L.
      Dermatology.
      ).
      Behavioral changes may be particularly challenging for patients with traction alopecia.

      CONFLUENT AND RETICULATED PAPILLOMATOSIS

      CARP of Gougerot and Carteaud is an uncommon skin disease that typically affects adolescents and young adults, especially women. African American individuals are twice as likely as White individuals to have CARP (
      • Bolognia J.L.
      • Schaffer J.V.
      • Cerroni L.
      Dermatology.
      ).

      Clinical Presentation

      CARP is characterized by scaly, brown, thin papules that coalesce into reticulated, often hyperkeratotic and verrucous plaques on the midchest and back (Figure 7). Early in the disease process, the eruption may be erythematous and later transition to gray or brown. This condition is either asymptomatic or mildly pruritic. It has been hypothesized that CARP is a variant of acanthosis nigricans, given its similar clinical presentation and association with insulin resistance and obesity. Acanthosis nigricans, however, is more frequently observed in the axillae, whereas CARP is typically more concentrated on the trunk (
      • Park Y.J.
      • Kang H.Y.
      • Lee E.-S.
      • Kim Y.C.
      Differentiating confluent and reticulated papillomatosis from acanthosis nigricans.
      ).
      FIGURE 7
      FIGURE 7Confluent and reticulated papillomatosis. Image courtesy of Dr. Brandi Kenner-Bell.
      (This figure appears in color online at www.jpedhc.org)

      Pathogenesis

      Some believe that CARP is a disorder of keratinization due to an abnormal host response; however, to date, there is no clear consensus on the etiologic trigger (
      • Lim J.H.-L.
      • Tey H.L.
      • Chong W.-S.
      Confluent and reticulated papillomatosis: Diagnostic and treatment challenges.
      ). The involvement of bacteria in the pathogenesis of CARP is supported by its response to treatment with oral antibiotics including minocycline, azithromycin, and, less often, clarithromycin (
      • Lim J.H.-L.
      • Tey H.L.
      • Chong W.-S.
      Confluent and reticulated papillomatosis: Diagnostic and treatment challenges.
      ). Fungal staining results are usually negative, and this condition typically does not respond to antifungal treatment. Histologically, CARP is often indistinguishable from acanthosis nigricans, because both have hyperkeratosis, acanthosis, and epidermal papillomatosis. Clinicopathologic correlation is required to make the distinction. The clinical course has a relapsing and remitting nature, and therefore, management is often frustrating.

      Treatment

      The first-line treatment for CARP is oral minocycline (
      • Lee S.W.
      • Loo C.H.
      • Tan W.C.
      Confluent and reticulated papillomatosis: Case series of 3 patients from Kedah, Malaysia and literature review.
      ). Both oral and topical retinoids can also be tried for treatment failure with antibiotics (
      • Lim J.H.-L.
      • Tey H.L.
      • Chong W.-S.
      Confluent and reticulated papillomatosis: Diagnostic and treatment challenges.
      ).

      KELOIDS

      Keloids are benign dermal tumors that typically result after skin injury. Keloids are most often seen in patients with skin of color (
      • Velez Edwards D.R.
      • Tsosie K.S.
      • Williams S.M.
      • Edwards T.L.
      • Russell S.B.
      Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans.
      ), with the highest prevalence in those of African descent (
      • Glass 2nd., D.A.
      Current understanding of the genetic causes of keloid formation.
      ).

      Clinical Presentation

      Keloids present as skin-colored to hyperpigmented firm plaques that extend beyond wound margins and are commonly distributed at sites of high skin tension (Figure 8). Hypertrophic scars differ from keloids in that the former do not extend beyond the wound margin. The word keloid originates from a Greek word meaning “crab's claw,” owing to the tendency of this disorder to expand laterally into normal tissue.
      FIGURE 8
      FIGURE 8Keloid.
      (This figure appears in color online at www.jpedhc.org)
      Diagnosis is based on history, scar shape, and growth pattern. Keloids are not only a source of cosmetic concern for patients, but they also are often associated with pruritus, dysesthesia, and, in extreme cases, functional impairment (
      • Troiano M.
      • Simeone A.
      • Scaramuzzi G.
      • Parisi S.
      • Guglielmi G.
      Giant keloid of left buttock treated with post-excisional radiotherapy.
      ).

      Pathogenesis

      Keloids result from overexpression of growth factors and decreased matrix metalloproteases. Patients with skin of color are at higher risk of keloid development, which may be attributed to a common genetic element on chromosome bands 15q21.2 to 22.3 that predisposes this population to keloids (
      • Velez Edwards D.R.
      • Tsosie K.S.
      • Williams S.M.
      • Edwards T.L.
      • Russell S.B.
      Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans.
      ). Keloids and hypertrophic scars are also genetically associated with human leukocyte antigens HLA-B14, HLA-B21, HLA-BW16, HLA-BW35, HLA-DR5, and HLA-DQW3 and blood group A (
      • Laurentaci G.
      • Dioguardi D.
      HLA antigens in keloids and hypertrophic scars.
      ). Moreover, several genetic loci are associated with increased susceptibility to keloid, and four single-nucleotide polymorphisms identified by genome studies were associated with keloid formation; however, it remains to be elucidated if these are ethnicity specific (
      • Glass 2nd., D.A.
      Current understanding of the genetic causes of keloid formation.
      ).
      Young patients are more commonly affected than adults, given that individuals in this age group are more frequently subjected to skin trauma and their higher rate of collagen synthesis. Younger skin also has greater tensile strength compared with older skin, which has less elasticity (
      • English R.S.
      • Shenefelt P.D.
      Keloids and hypertrophic scars.
      ).

      Treatment

      Treatment includes surgical therapies, topical and intralesional steroids, intralesional injection of interferon or 5-fluorouracil, cryotherapy, surgical excision, laser therapy, silicone gel sheeting, or combination treatment (
      • Hsu K.-C.
      • Luan C.-W.
      • &Tsai Y.-W.
      Review of silicone gel sheeting and silicone gel for the prevention of hypertrophic scars and keloids.
      ,
      • Patel P.A.
      • Bailey J.K.
      • Yakuboff K.P.
      Treatment outcomes for keloid scar management in the pediatric burn population.
      ). Results vary from patient to patient. Occlusion, hydration, and pressure application to scars are helpful adjuvant treatment modalities. Prevention is the most important consideration in the management of keloid scar formation. Nonessential surgery should be avoided in patients with a family history of keloids. Ear piercing–associated keloids are more likely to occur in patients older than 11 years; thus, piercing at a younger age may be a helpful preventative measure (
      • Lane J.E.
      • Waller J.L.
      • Davis L.S.
      Relationship between age of ear piercing and keloid formation.
      ). For patients requiring surgical intervention, preoperative radiation therapy has been used as a preventative measure, but benefits must outweigh the risks.

      CONCLUSION

      It is important to recognize common skin conditions that frequently affect children with ethnic skin. Clinical presentation of these skin conditions may vary based on skin type. Care should be taken to offer therapies that are safe and effective and improve quality of life.
      The authors would like to thank Dr. Brandi Kenner-Bell for providing the image of confluent and reticulated papillomatosis (Figure 7).

      Appendix B. Supplementary materials

      References

        • Al Qarqaz F.
        • Al-Yousef A.
        Skin microneedling for acne scars associated with pigmentation in patients with dark skin.
        Journal of Cosmetic Dermatology. 2018; 17: 390-395
        • Alexis A.F.
        Acne vulgaris in skin of color: Understanding nuances and optimizing treatment outcomes.
        Journal of Drugs in Dermatology. 2014; 13: s61-s65
        • Alexis A.F.
        • Johnson L.A.
        • Kerrouche N.
        • Callender V.D.
        A subgroup analysis to evaluate the efficacy and safety of adapalene-benzoyl peroxide topical gel in African American subjects with moderate acne.
        Journal of Drugs in Dermatology. 2014; 13: 170-174
        • Aljabre S.H.
        • Alzayir A.A.
        • Abdulghani M.
        • Osman O.O.
        Pigmentary changes of tinea versicolor in dark-skinned patients.
        International Journal of Dermatology. 2001; 40: 273-275
        • Ben-Gashir M.A.
        • Hay R.J.
        Reliance on erythema scores may mask severe atopic dermatitis in black children compared with their white counterparts.
        British Journal of Dermatology. 2002; 147: 920-925
        • Billero V.
        • Miteva M.
        Traction alopecia: The root of the problem.
        Clinical, Cosmetic and Investigational Dermatology. 2018; 11: 149-159
        • Bolognia J.L.
        • Schaffer J.V.
        • Cerroni L.
        Dermatology.
        4th ed. Elsevier, Edinburgh2018
        • Callender V.D.
        Fitzpatrick skin types and clindamycin phosphate 1.2%/benzoylperoxide gel: Efficacy and tolerability of treatment in moderate to severe acne.
        Journal of Drugs in Dermatology. 2012; 11: 643-648
        • Castelo-Soccio L.
        Diagnosis and management of alopecia in children.
        Pediatric Clinics of North America. 2014; 61: 427-442
        • Colby S.L.
        • Ortman J.M.
        Projections of the size and composition of the U.S. population: 2014 to 2060.
        U.S. Census Bureau, Washington, DC2015 (Retrieved from)
        • Davis E.C.
        • Callender V.D.
        A review of acne in ethnic skin: Pathogenesis, clinical manifestations, and management strategies.
        Journal of Clinic and Aesthetic Dermatology. 2010; 3: 24-38
        • Eichenfield L.F.
        • Tom W.L.
        • Chamlin S.L.
        • Feldman S.R.
        • Hanifin J.M.
        • Simpson E.L.
        • Sidbury R.
        Guidelines of care for the management of atopic dermatitis: Section 1. Diagnosis and assessment of atopic dermatitis.
        Journal of the American Academy of Dermatology. 2014; 70: 338-351
        • English R.S.
        • Shenefelt P.D.
        Keloids and hypertrophic scars.
        Dermatologic Surgery. 1999; 25: 631-638
        • Givler D.N.
        • Givler A.
        Pityriasis alba.
        StatPearls Publishing, Treasure Island, FL2018
        • Glass 2nd., D.A.
        Current understanding of the genetic causes of keloid formation.
        Journal of Investigative Dermatology Symposium Proceedings. 2017; 18: S50-S53
        • Grimes P.
        • Callender V.
        Tazarotene cream for postinflammatory hyperpigmentation and acne vulgaris in darker skin: A double-blind, randomized, vehicle-controlled study.
        Cutis. 2006; 77: 45-50
        • Halder R.M.
        • Brooks H.L.
        • Callender V.D.
        Acne in ethnic skin.
        Dermatologic Clinics. 2003; 21: 609-615
        • Halder R.M.
        • Nootheti P.K.
        Ethnic skin disorders overview.
        Journal of the American Academy of Dermatology. 2003; 48: S143-S148
        • Hsu K.-C.
        • Luan C.-W.
        • &Tsai Y.-W.
        Review of silicone gel sheeting and silicone gel for the prevention of hypertrophic scars and keloids.
        Wounds. 2017; 29: 154-158
        • Janumpally S.R.
        • Feldman S.R.
        • Gupta A.K.
        • Fleischer A.B.
        In the United States, blacks and Asian/Pacific Islanders are more likely than whites to seek medical care for atopic dermatitis.
        Archives of Dermatology. 2002; 138: 634-637
        • Ji J.H.
        • Park T.-S.
        • Lee H.-J.
        • Kim Y.-D.
        • Pi L.-Q.
        • Jin X.-H.
        • Lee W.-S.
        The ethnic differences of the damage of hair and integral hair lipid after ultra violet radiation.
        Annals of Dermatology. 2013; 25: 54-60
        • Julián-Gónzalez R.E.
        • Orozco-Covarrubias L.
        • Durán-McKinster C.
        • Palacios-Lopez C.
        • Ruiz-Maldonado R.
        • Sáez-de-Ocariz M.
        Less common clinical manifestations of atopic dermatitis: prevalence by age.
        Pediatric Dermatology. 2012; 29: 580-583
        • Kallini J.R.
        • Riaz F.
        • Khachemoune A.
        Tinea versicolor in dark-skinned individuals.
        International Journal of Dermatology. 2014; 53: 137-141
        • Lane J.E.
        • Waller J.L.
        • Davis L.S.
        Relationship between age of ear piercing and keloid formation.
        Pediatrics. 2005; 115: 1312-1314
        • Laurentaci G.
        • Dioguardi D.
        HLA antigens in keloids and hypertrophic scars.
        Archives of Dermatology. 1977; 113: 1726
        • Lawson C.N.
        • Hollinger J.
        • Sethi S.
        • Rodney I.
        • Sarkar R.
        • Dlova N.
        • Callender V.D.
        Updates in the understanding and treatments of skin & hair disorders in women of color.
        International Journal of Women's Dermatology. 2017; 3: S21-S37
        • Lee S.W.
        • Loo C.H.
        • Tan W.C.
        Confluent and reticulated papillomatosis: Case series of 3 patients from Kedah, Malaysia and literature review.
        Medical Journal of Malaysia. 2018; 73: 338-339
        • Lim J.H.-L.
        • Tey H.L.
        • Chong W.-S.
        Confluent and reticulated papillomatosis: Diagnostic and treatment challenges.
        Clinical, Cosmetic and Investigational Dermatology. 2016; 9: 217-223
        • Marciniak J.
        • Reich A.
        • Szepietowski J.C.
        Quality of life of parents of children with atopic dermatitis.
        Acta Dermato Venereologica. 2017; 97: 711-714
        • Margolis D.J.
        • Mitra N.
        • Gochnauer H.
        • Wubbenhorst B.
        • D'Andrea K.
        • Kraya A.
        • Nathanson K.L.
        Uncommon filaggrin variants are associated with persistent atopic dermatitis in african americans.
        Journal of Investigative Dermatology. 2018; 138: 1501-1506
        • Martínez-Martínez M.L.
        • Azaña-Defez J.M.
        • Rodríguez-Vázquez M.
        • Faura-Berruga C.
        • Escario-Travesedo E.
        Progressive macular hypomelanosis.
        Pediatric Dermatology. 2012; 29: 460-462
        • Miazek N.
        • Michalek I.
        • Pawlowska-Kisiel M.
        • Olszewska M.
        • Rudnicka L.
        Pityriasis alba—Common disease, enigmatic entity: Up-to-date review of the literature.
        Pediatric Dermatology. 2015; 32: 786-791
        • Nazzaro-Porro M.
        • Passi S.
        Identification of tyrosinase inhibitors in cultures of Pityrosporum.
        Journal of Investigative Dermatology. 1978; 71: 205-208
        • Ortiz-Salvador J.M.
        • Pérez-Ferriols A.
        Phototherapy in atopic dermatitis.
        Advances in Experimental Medicine and Biology. 2017; 996: 279-286
        • Paller A.S.
        • Tom W.L.
        • Lebwohl M.G.
        • Blumenthal R.L.
        • Boguniewicz M.
        • Call R.S.
        • Hebert A.A.
        Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults.
        Journal of the American Academy of Dermatology. 2016; 75: 494-503
        • Park Y.J.
        • Kang H.Y.
        • Lee E.-S.
        • Kim Y.C.
        Differentiating confluent and reticulated papillomatosis from acanthosis nigricans.
        Journal of Cutaneous Pathology. 2015; 42: 944-952
        • Patel P.A.
        • Bailey J.K.
        • Yakuboff K.P.
        Treatment outcomes for keloid scar management in the pediatric burn population.
        Burns. 2012; 38: 767-771
        • Perkins A.C.
        • Cheng C.E.
        • Hillebrand G.G.
        • Miyamoto K.
        • Kimball A.B.
        Comparison of the epidemiology of acne vulgaris among Caucasian, Asian, Continental Indian and African American women: The spectrum of acne: prevalence of subtypes across races.
        Journal of the European Academy of Dermatology and Venereology. 2011; 25: 1054-1060
        • Pflederer R.T.
        • Wuennenberg J.P.
        • Foote C.
        • Aires D.
        • Rajpara A.
        Use of Wood's lamp to diagnose progressive macular hypomelanosis.
        Journal of the American Academy of Dermatology. 2017; 77: e99-e100
        • Pulickal J.K.
        • Kaliyadan F.
        Alopecia, traction.
        StatPearls Publishing, Treasure Island, FL2018
        • Pustisek N.
        • Vurnek Zivkovic M.
        • Situm M.
        Quality of life in families with children with atopic dermatitis.
        Pediatric Dermatology. 2016; 33: 28-32
        • Quiggle A.M.
        • Goodwin Z.A.
        • Marfatia T.R.
        • Kumar M.G.
        • Ciliberto H.
        • Bayliss S.J.
        • de Guzman Strong C.
        Low filaggrin monomer repeats in African American pediatric patients with moderate to severe atopic dermatitis.
        JAMA Dermatology. 2015; 151: 557-559
        • Robles D.T.
        • Berg D.
        Abnormal wound healing: Keloids.
        Clinics in Dermatology. 2007; 25: 26-32
        • Samrao A.
        • Price V.H.
        • Zedek D.
        • Mirmirani P.
        The “Fringe Sign”—A useful clinical finding in traction alopecia of the marginal hair line.
        Dermatology Online Journal. 2011; 17: 1
        • Shen L.Y.
        • Kenner-Bell B.M.
        • Ricketts J.
        • Kundu R.V.
        Ethnic skin: Kids are not just little people.
        Clinics in Dermatology. 2016; 34: 690-697
        • Siegfried E.C.
        • Jaworski J.C.
        • Mina-Osorio P.
        A systematic scoping literature review of publications supporting treatment guidelines for pediatric atopic dermatitis in contrast to clinical practice patterns.
        Dermatologic Therapy (Heidelb). 2018; 8: 349-377
        • Silverberg J.I.
        • Simpson E.L.
        • Durkin H.G.
        • Joks R.
        Prevalence of allergic disease in foreign-born American children.
        JAMA Pediatrics. 2013; 167: 554-560
      1. Silverberg N.B. Duran-McKinster C. Tay Y.-K. Pediatric skin of color. Springer, New York, NY2015
        • Spann C.T.
        Ten tips for treating acne vulgaris in Fitzpatrick skin types IV-VI.
        Journal of Drugs in Dermatology. 2011; 10: 654-657
        • Thng S.T.G.
        • Long V.S.H.
        • Chuah S.Y.
        • Tan V.W.D.
        Efficacy and relapse rates of different treatment modalities for progressive macular hypomelanosis.
        Indian Journal of Dermatology, Venereology and Leprology. 2016; 82: 673-676
        • Troiano M.
        • Simeone A.
        • Scaramuzzi G.
        • Parisi S.
        • Guglielmi G.
        Giant keloid of left buttock treated with post-excisional radiotherapy.
        Journal of Radiology Case Report. 2011; 5: 8-15
        • Vachiramon V.
        • Tey H.L.
        • Thompson A.E.
        • Yosipovitch G.
        Atopic dermatitis in African American children: addressing unmet needs of a common disease.
        Pediatric Dermatology. 2012; 29: 395-402
        • Velez Edwards D.R.
        • Tsosie K.S.
        • Williams S.M.
        • Edwards T.L.
        • Russell S.B.
        Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans.
        Human Genetics. 2014; 133: 1513-1523
        • Vemula S.
        • Maymomne M.B.C.
        • Secemsky E.A.
        • Widjajahakim R.
        • Patzelt N.M.
        • Saade D.
        • Vashi N.A.
        Assessing the safety of superficial chemical peels in darker skin: A retrospective study.
        Journal of the American Academy of Dermatology. 2018; 79: 508-513
        • Westerhof W.
        • Relyveld G.N.
        • Kingswijk M.M.
        • de Man P.
        • Menke H.E.
        Propionibacterium acnes and the pathogenesis of progressive macular hypomelanosis.
        Archives of Dermatology. 2004; 140: 210-214
        • Yin N.C.
        • McMichael A.J.
        Acne in patients with skin of color: Practical management.
        American Journal of Clinical Dermatology. 2014; 15: 7-16
        • Zhao C.Y.
        • Hao E.Y.
        • Oh D.D.
        • Daniel B.S.
        • Martin L.K.
        • Su J.C.
        • Murrell D.F.
        A comparison study of clinician-rated atopic dermatitis outcome measures for intermediate- to dark-skinned patients.
        Britsh Journal of Dermatology. 2017; 176: 985-992

      Biography

      Mayra B.C. Maymone, Trainee, Department of Dermatology, Boston University School of Medicine, Boston, MA.
      Jacqueline D. Watchmaker, Trainee, Department of Dermatology, Boston University School of Medicine, Boston, MA.
      Michelle Dubiel, Trainee, Department of Dermatology, Boston University School of Medicine, Boston, MA.
      Stephen A. Wirya, Trainee, Department of Dermatology, Boston University School of Medicine, Boston, MA.
      Lisa Y. Shen, Associate Professor of Dermatology, Department of Dermatology, Boston University School of Medicine, Boston, MA.
      Neelam A. Vashi, Associate Professor of Dermatology, Department of Dermatology, Boston University School of Medicine; US Department of Veteran Affairs, Boston Health Care System, Boston, MA.