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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.
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 (
). 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 (
). This article will also briefly address differences in pathophysiology and treatment modalities in those with richly pigmented skin (Table 2).
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Objectives
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Discuss common skin conditions in pediatric patients with darker skin types.
2.
Explain early clinical signs of inflammation in skin of color.
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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 2Common pediatric skin disorders in skin of color
Diagnosis
Age of onset
Clinical features
Treatment
Acne
Adolescence
Inflammatory 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 dermatitis
Varies (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 alba
3–16 years of age
Poorly defined, hypopigmented macules and patches with minimal scale, typically on face
Emollients, low-potency topical steroids, topical calcineurin inhibitors, sun protection
Tinea versicolor
Adolescence
Hypopigmented, 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 hypomelanosis
Adolescence
Nonscaly, hypopigmented macules, typically on the trunk
Early 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 papillomatosis
Adolescence
Scaly, brown, thin papules that coalesce into reticulated plaques, often on central chest and back
Oral minocycline (first line) Isotretinoin
Keloids
Adolescence
Skin-colored to hyperpigmented firm plaques that extend beyond wound margins
Topical and intralesional steroids, intralesional injection of interferon or 5-fluorouracil, cryotherapy, surgical excision, laser therapy, silicone gel sheets, pressure application, or combination treatment
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 (
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
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 (
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
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 (
). 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 (
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 (
). 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 (
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 (
). 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 (
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 (
). 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 (
). 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 (
). 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 (
). 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 (
). 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 (
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% (
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 (
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 (
) . 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 (
). 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 (
). 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 (
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 (
). 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 (
). 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 (
). 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;
). Crisaborole, a phosphodiaesterase-4 inhibitor, is a promising nonsteroid alternative for treatment of mild to moderate AD in children older than 2 years (
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
). 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 (
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 (
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 (
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 (
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 (
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 (
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;
). 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 (
). TV commonly affects adolescents and young adults but may also occur in children. It is especially prevalent in tropical climates and during summer months.
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 (
). 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 (
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 (
). 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 (
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 (
). 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.
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 (
). Both the response to treatment and clinical course are variable. PMH may gradually progress with time or may resolve spontaneously within a few years (
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 (
). 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 (
). 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 (
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 (
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 (
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 (
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 (
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 (
). 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 (
). 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 (
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.
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 (
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 (
). 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 (
). 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 (
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 (
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 (
). 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 (
). 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).
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
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
A systematic scoping literature review of publications supporting treatment guidelines for pediatric atopic dermatitis in contrast to clinical practice patterns.
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.
Article info
Footnotes
Conflicts of interest: None to report.
Dr. Maymone and Dr. Watchmaker should be considered as co-lead authors.
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