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Common Skin Disorders in Pediatric Skin of Color
DEPARTMENT
Pharmacology Continuing Education
Common Skin Disorders in Pediatric Skin of Color Mayra B.C. Maymone, DDS, MD, DSc, Jacqueline D. Watchmaker, MD, Michelle Dubiel, MD, Stephen A. Wirya, MD, Lisa Y. Shen, MD, & Neelam A. Vashi, MD INSTRUCTIONS To obtain continuing education credit: 1. Read the article carefully. 2. Read each question and determine the correct answer. 3. Visit PedsCESM, ce.napnap.org, to complete the online Posttest and evaluation. 4. You must receive 70% correct responses to receive the certificate. 5. Tests will be accepted until December 31, 2020.
OBJECTIVES 1. Discuss common skin conditions in pediatric patients with darker skin types.
Mayra B.C. Maymone, Trainee, Department of Dermatology, Boston University School of Medicine, Boston, MA.
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. Posttest Questions Contact hours: 0.75 Passing score: 70% This continuing education activity is administered by the National Association of Pediatric Nurse Practitioners (NAPNAP) as an Agency providing continuing education credit. Individuals who complete this program and earn a 70% or higher score on the Posttest will be awarded 0.75 contact hours, of which 0.25 are Pharmacology contact hours. Earn FREE CE Contact Hours Online
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. Conflicts of interest: None to report. Dr. Maymone and Dr. Watchmaker should be considered as colead authors. Correspondence: Neelam A. Vashi, MD, Boston University School of Medicine, Department of Dermatology, 609 Albany St., J108, Boston, MA 02118; e-mail: [email protected]. J Pediatr Health Care. (2019) 33, 727-737 0891-5245/$36.00 Copyright © 2019 Published by Elsevier Inc. on behalf of National Association of Pediatric Nurse Practitioners. https://doi.org/10.1016/j.pedhc.2019.04.019
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Contact Hours for this online activity are FREE for NAPNAP Members. Non-Members will be charged a fee of $10 to receive contact hours for this online activity through PedsCESM. Payment can be made by credit card through PedsCESM. 1. To take the Posttest for this article and earn contact hours, please go to PedsCESM at ce.napnap.org. 2. In the Course Catalog, search for the name of the CE article. 3. If you already have an account with PedsCESM, log in using your username and password. If you are a NAPNAP member, log in with your username and password. If you are a first-time user and NAPNAP nonmember, click on “New Customer? Click Here.” 4. Once you have successfully passed the Posttest and completed the evaluation form, you will be able to print out your certificate immediately.
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
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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. J Pediatr Health Care. (2019) 33, 727−737
KEY WORDS Pediatrics, dermatology, skin of color, ethnic skin
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 (Silverberg, DuranMcKinster, & Tay, 2015). According to the U.S. Census Bureau, by 2044, people with skin of color will represent 50.3% of the U.S. population (Colby & Ortman, 2015). 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, Kenner-Bell, Ricketts, & Kundu, 2016). This article will also briefly address differences in pathophysiology and treatment modalities in those with richly pigmented skin (Table 2). ACNE Regardless of race or Regardless of race ethnicity, acne is one of or ethnicity, acne is the most common skin one of the most disorders observed in children and adolescents. common skin A retrospective cohort disorders observed study showed that acne in children and was among the top three most common dermatoadolescents. logic diagnoses in African American and Asian adolescents (Perkins, Cheng, Hillebrand, Miyamoto, & Kimball, 2011). TABLE 1. Fitzpatrick skin scale Type I Type II Type III Type IV Type V Type VI
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Always burns, never tans Usually burns, tans minimally Sometimes mildly burns, tans uniformly Burns minimally, always tans well Very rarely burns, tans very easily Never burns
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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 (Silverberg et al., 2015). 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 et al., 2011; Robles & Berg, 2007). 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, 2018). 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, Brooks, & Callender, 2003; Halder & Nootheti, 2003). 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 & Callender, 2010; Yin & McMichael, 2014). 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 creambased vehicle. Additionally, certain retinoid formulations, such as adapalene and micronized forms, have been shown to be well tolerated in skin of color (Silverberg, DuranMcKinster, & Tay, 2015). 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, 2011). Alexis et al. (2014) 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 treatmentrelated PIH were observed (Alexis, Johnson, Kerrouche, & Callender, 2014). 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, 2012). 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,
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TABLE 2. Common 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
Atopic dermatitis
Varies (infantile atopic dermatitis has onset < 2 years of age)
Pityriasis alba
3−16 years of age
Tinea versicolor
Adolescence
Progressive macular hypomelanosis Traction alopecia
Adolescence
Infantile atopic dermatitis: eczematous dermatitis on cheeks and extensor surfaces Childhood atopic dermatitis: subacute and chronic dermatitis predominantly on flexural areas Poorly defined, hypopigmented macules and patches with minimal scale, typically on face 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 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 Scaly, brown, thin papules that coalesce into reticulated plaques, often on central chest and back Skin-colored to hyperpigmented firm plaques that extend beyond wound margins
Topical antibiotics (clindamycin, erythromycin), topical benzoyl peroxide, topical retinoids, oral tetracyclines Oral contraceptives and spironolactone (females only) Isotretinoin for severe cases Topical steroids, topical calcineurin inhibitors, phosphodiaterase-4 inhibitors, systemic medication or phototherapy for severe disease
Adolescence/adulthood
Confluent and reticulated papillomatosis
Adolescence
Keloids
Adolescence
2014). Antibiotics such as tetracycline derivatives are used in moderate to severe acne because of their antimicrobial and antiinflammatory properties (Spann 2011). 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 (Silverberg, Duran-McKinster, & Tay, 2015). 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 & Callender, 2010).
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Emollients, low-potency topical steroids, topical calcineurin inhibitors, sun protection
Topical antifungals (ketoconazole), selenium sulfide shampoo Systemic antifungals for severe disease Photoprotective measures
Benzoyl peroxide, topical antibiotics, oral antibiotics, phototherapy Discontinuation of tight hairstyles, avoidance of chemical relaxers and heat styling, topical steroids, intralesional steroids, sub-antimicrobial doses of oral antibiotics
Oral minocycline (first line) Isotretinoin
Topical and intralesional steroids, intralesional injection of interferon or 5-fluorouracil, cryotherapy, surgical excision, laser therapy, silicone gel sheets, pressure application, or combination treatment
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, 2014). 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, 2012; Grimes & Callender, 2006). Strict sun
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FIGURE 1. Acne vulgaris.
FIGURE 2. Atopic dermatitis.
(This figure appears in color online at www.jpedhc.org)
(This figure appears in color online at www.jpedhc.org) 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 & Al-Yousef, 2018). 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 et al., 2018). 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, Jaworski, & Mina-Osorio, 2018). 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, Feldman, Gupta, & Fleischer, 2002). 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 730
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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 et al., 2018) . 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 (Julian-Gonzalez et al., 2012). 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 (Julian-Gonzalez et al., 2012). 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 & Hay, 2002). Moreover, dark-skinned patients may deem their atopic symptoms as less severe than those with lighter skin types (Zhao et al., 2017). 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 et al., 2018; Quiggle et al., 2015). In addition, African Americans have reduced ceramide levels and increased transepidermal water loss, which contributes to xerosis (Vachiramon, Tey, Thompson, & Yosipovitch, 2012). Children born outside the United States have lower risk of AD than U.S.-born children; however, children born outside
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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, Simpson, Durkin, & Joks, 2013). 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, Reich, & Szepietowski, 2017; Pustisek, Vurnek Zivkovic, & Situm, 2016). 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 et al., 2014). 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, 2018). Recalcitrant AD may require systemic treatment or phototherapy (Ortiz-Salvador & Perez-Ferriols, 2017). Crisaborole, a phosphodiaesterase-4 inhibitor, is a promising nonsteroid alternative for treatment of mild to moderate AD in children older than 2 years (Paller et al., 2016). 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, Michalek, Pawlowska-Kisiel, Olszewska, & Rudnicka, 2015).
FIGURE 3. Pityriasis alba.
(This figure appears in color online at www.jpedhc.org)
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 & Givler, 2018).
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 et al., 2015). 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 & Givler, 2018).
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 Even though PA is sunscreens (zinc oxide, benign and may titanium dioxide) that undergo are typically recommended for atopic spontaneous patients may be cosremission, it can be metically difficult to particularly tolerate for patients with darker skin types. bothersome for Low-potency topical those with darker corticosteroids and calphototypes. cineurin inhibitors have also shown good response (Miazek et al., 2015).
Pathogenesis Environmental factors such as sun exposure, long and frequent baths, and mechanical exfoliation appear to be predisposing factors in susceptible skin. African American
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
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pigmentation are often the presenting complaint, especially in patients with skin of color (Kallini, Riaz, & Khachemoune, 2014). 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, Alzayir, Abdulghani, & Osman, 2001; Kallini et al., 2014). 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 yellowgreen fluorescence in one third of cases (Kallini et al., 2014). TV commonly affects adolescents and young adults but may also occur in children. It is especially prevalent in tropical climates and during summer months. 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 FIGURE 4. Tinea versicolor.
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 & Passi, 1978). 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 et al., 2014). 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 et al., 2001). 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 (MartínezMartínez, Azana-Defez, Rodriguez-Vazquez, Faura-Berruga, & Escario-Travesedo, 2012). 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, Wuennenberg, Foote, Aires, & Rajpara, 2017). 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
FIGURE 5. Progressive macular hypomelanosis.
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(This figure appears in color online at www.jpedhc.org)
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because the condition may be more noticeable in darkerskinned individuals.
alopecia areata, trichotillomania, frontal fibrosing alopecia, infectious folliculitis, and syphilis (Castelo-Soccio, 2014).
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, Relyveld, Kingswijk, de Man, & Menke, 2004).
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 et al., 2013; Lawson et al., 2017).
Treatment Treatment options include topical and oral antibiotics, topical benzoyl peroxide, and ultraviolet light irradiation (Thng, Long, Chuah, & Tan, 2016). 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, 2018). 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 & Miteva, 2018; Pulickal & Kaliyadan, 2018). 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, Price, Zedek, & Mirmirani, 2011). The diagnosis is usually clinical, but difficult cases may require a skin biopsy. Differential diagnoses include tinea capitis, FIGURE 6. Traction alopecia.
(This figure appears in color online at www.jpedhc.org)
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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 Behavioral changes of topical or intralemay be particularly sional corticosteroids or sub-antimicrobial challenging for doses of oral antibiotpatients with ics. Behavioral changes may be particularly traction alopecia. challenging for patients with traction alopecia. Prognosis of this preventable condition will depend largely on the stage of the disease (Bolognia, 2018). 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, 2018). 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, Kang, Lee, & Kim, 2015). 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, Tey, & Chong, 2016). 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 et al., 2016). Fungal staining results are usually negative, and this condition typically does not respond to antifungal treatment. Histologically, CARP is
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FIGURE 7. Confluent and reticulated papillomatosis. Image courtesy of Dr. Brandi Kenner-Bell.
FIGURE 8. Keloid.
(This figure appears in color online at www.jpedhc.org)
(This figure appears in color online at www.jpedhc.org) 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, Loo, & Tan, 2018). Both oral and topical retinoids can also be tried for treatment failure with antibiotics (Lim et al., 2016). 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, Tsosie, Williams, Edwards, & Russell, 2014), with the highest prevalence in those of African descent (Glass, 2017). 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. 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, Simeone, Scaramuzzi, Parisi, & Guglielmi, 2011). 734
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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 et al., 2014). Keloids and hypertrophic scars are also genetically associated with human leukocyte antigens HLA-B14, HLA-B21, HLA-BW16, HLABW35, HLA-DR5, and HLA-DQW3 and blood group A (Laurentaci, & Dioguardi, 1977). 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, 2017). 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 & Shenefelt, 1999). Treatment Treatment includes surgical therapies, topical and intralesional steroids, intralesional injection of interferon or 5fluorouracil, cryotherapy, surgical excision, laser therapy, silicone gel sheeting, or combination treatment (Hsu, Luan & Tsai, 2017; Patel, Bialey, & Yakuboff, 2012). 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, Waller, & Davis, 2005). For patients requiring surgical intervention, preoperative radiation therapy has been used as a preventative measure, but benefits must outweigh the risks.
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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). SUPPLEMENTARY MATERIALS Supplementary material associated with this article can be found in the online version at https://doi.org/10.1016/j. pedhc.2019.04.019. REFERENCES Al Qarqaz, F., & Al-Yousef, A. (2018). Skin microneedling for acne scars associated with pigmentation in patients with dark skin. Journal of Cosmetic Dermatology, 17, 390–395. Alexis, A. F. (2014). Acne vulgaris in skin of color: Understanding nuances and optimizing treatment outcomes. Journal of Drugs in Dermatology, 13(6), s61–s65. Alexis, A. F., Johnson, L. A., Kerrouche, N., & Callender, V. D. (2014). 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, 13, 170– 174. Aljabre, S. H., Alzayir, A. A., Abdulghani, M., & Osman, O. O. (2001). Pigmentary changes of tinea versicolor in dark-skinned patients. International Journal of Dermatology, 40, 273–275. Ben-Gashir, M. A., & Hay, R. J. (2002). Reliance on erythema scores may mask severe atopic dermatitis in black children compared with their white counterparts. British Journal of Dermatology, 147, 920–925. Billero, V., & Miteva, M. (2018). Traction alopecia: The root of the problem. Clinical, Cosmetic and Investigational Dermatology, 11, 149–159. Bolognia, J. L., Schaffer, J. V., & Cerroni, L. (2018). Dermatology (4th ed.). Edinburgh: Elsevier. Callender, V. D. (2012). 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, 11, 643–648. Castelo-Soccio, L. (2014). Diagnosis and management of alopecia in children. Pediatric Clinics of North America, 61, 427–442. Colby, S. L., & Ortman, J. M. (2015). Projections of the size and composition of the U.S. population: 2014 to 2060. Washington, DC: U.S. Census Bureau. Retrieved from https://www.census.gov/ content/dam/Census/library/publications/2015/demo/p251143.pdf Davis, E. C., & Callender, V. D. (2010). A review of acne in ethnic skin: Pathogenesis, clinical manifestations, and management strategies. Journal of Clinic and Aesthetic Dermatology, 3, 24–38. Eichenfield, L. F., Tom, W. L., Chamlin, S. L., Feldman, S. R., Hanifin, J. M., Simpson, E. L., & Sidbury, R. (2014). Guidelines of care for the management of atopic dermatitis: Section 1. Diagnosis and assessment of atopic dermatitis. Journal of the American Academy of Dermatology, 70, 338–351. English, R. S., & Shenefelt, P. D. (1999). Keloids and hypertrophic scars. Dermatologic Surgery, 25, 631–638. Givler, D. N., & Givler, A. (2018). Pityriasis alba. Treasure Island, FL: StatPearls Publishing. Glass, D. A., 2nd. (2017). Current understanding of the genetic causes of keloid formation. Journal of Investigative Dermatology Symposium Proceedings, 18(2), S50–S53.
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Grimes, P., & Callender, V. (2006). Tazarotene cream for postinflammatory hyperpigmentation and acne vulgaris in darker skin: A double-blind, randomized, vehicle-controlled study. Cutis, 77 (1), 45–50. Halder, R. M., Brooks, H. L., & Callender, V. D. (2003). Acne in ethnic skin. Dermatologic Clinics, 21, 609–615. Halder, R. M., & Nootheti, P. K. (2003). Ethnic skin disorders overview. Journal of the American Academy of Dermatology, 48(6), S143–S148. Hsu, K.-C., Luan, C.-W., & &Tsai, Y.-W. (2017). Review of silicone gel sheeting and silicone gel for the prevention of hypertrophic scars and keloids. Wounds, 29(5), 154–158. Janumpally, S. R., Feldman, S. R., Gupta, A. K., & Fleischer, A. B. (2002). In the United States, blacks and Asian/ Pacific Islanders are more likely than whites to seek medical care for atopic dermatitis. Archives of Dermatology, 138, 634–637. Ji, J. H., Park, T.-S., Lee, H.-J., Kim, Y.-D., Pi, L.-Q., Jin, X.-H., & Lee, W.-S. (2013). The ethnic differences of the damage of hair and integral hair lipid after ultra violet radiation. Annals of Dermatology, 25, 54–60. n-Go nzalez, R. E., Orozco-Covarrubias, L., Duran-McKinster, C., Julia ez-de-Ocariz, M. Palacios-Lopez, C., Ruiz-Maldonado, R., & Sa (2012). Less common clinical manifestations of atopic dermatitis: prevalence by age. Pediatric Dermatology, 29, 580–583. Kallini, J. R., Riaz, F., & Khachemoune, A. (2014). Tinea versicolor in dark-skinned individuals. International Journal of Dermatology, 53(2), 137–141. Lane, J. E., Waller, J. L., & Davis, L. S. (2005). Relationship between age of ear piercing and keloid formation. Pediatrics, 115, 1312–1314. Laurentaci, G., & Dioguardi, D. (1977). HLA antigens in keloids and hypertrophic scars. Archives of Dermatology, 113, 1726. Lawson, C. N., Hollinger, J., Sethi, S., Rodney, I., Sarkar, R., Dlova, N., & Callender, V. D. (2017). Updates in the understanding and treatments of skin & hair disorders in women of color. International Journal of Women’s Dermatology, 3(1 Suppl.), S21–S37. Lee, S. W., Loo, C. H., & Tan, W. C. (2018). Confluent and reticulated papillomatosis: Case series of 3 patients from Kedah, Malaysia and literature review. Medical Journal of Malaysia, 73, 338–339. Lim, J. H.-L., Tey, H. L., & Chong, W.-S. (2016). Confluent and reticulated papillomatosis: Diagnostic and treatment challenges. Clinical, Cosmetic and Investigational Dermatology, 9, 217–223. Marciniak, J., Reich, A., & Szepietowski, J. C. (2017). Quality of life of parents of children with atopic dermatitis. Acta Dermato Venereologica, 97, 711–714. Margolis, D. J., Mitra, N., Gochnauer, H., Wubbenhorst, B., D’Andrea, K., Kraya, A., . . . Nathanson, K. L. (2018). Uncommon filaggrin variants are associated with persistent atopic dermatitis in african americans. Journal of Investigative Dermatology, 138, 1501–1506. ~a-Defez, J. M., Rodríguez-Vazquez, M., Martínez-Martínez, M. L., Azan Faura-Berruga, C., & Escario-Travesedo, E. (2012). Progressive macular hypomelanosis. Pediatric Dermatology, 29, 460–462. Miazek, N., Michalek, I., Pawlowska-Kisiel, M., Olszewska, M., & Rudnicka, L. (2015). Pityriasis alba—Common disease, enigmatic entity: Up-to-date review of the literature. Pediatric Dermatology, 32, 786–791. Nazzaro-Porro, M., & Passi, S. (1978). Identification of tyrosinase inhibitors in cultures of Pityrosporum. Journal of Investigative Dermatology, 71, 205–208. rez-Ferriols, A. (2017). Phototherapy in Ortiz-Salvador, J. M., & Pe atopic dermatitis. Advances in Experimental Medicine and Biology, 996, 279–286. Paller, A. S., Tom, W. L., Lebwohl, M. G., Blumenthal, R. L., Boguniewicz, M., Call, R. S., . . . Hebert, A. A. (2016). Efficacy and safety of crisaborole ointment, a novel, nonsteroidal
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phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. Journal of the American Academy of Dermatology, 75(3), 494–503. Park, Y. J., Kang, H. Y., Lee, E.-S., & Kim, Y. C. (2015). Differentiating confluent and reticulated papillomatosis from acanthosis nigricans. Journal of Cutaneous Pathology, 42, 944–952. Patel, P. A., Bailey, J. K., & Yakuboff, K. P. (2012). Treatment outcomes for keloid scar management in the pediatric burn population. Burns, 38, 767–771. Perkins, A. C., Cheng, C. E., Hillebrand, G. G., Miyamoto, K., & Kimball, A. B. (2011). 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, 25, 1054–1060. Pflederer, R. T., Wuennenberg, J. P., Foote, C., Aires, D., & Rajpara, A. (2017). Use of Wood’s lamp to diagnose progressive macular hypomelanosis. Journal of the American Academy of Dermatology, 77(4), e99–e100. Pulickal, J. K., & Kaliyadan, F. (2018). Alopecia, traction. Treasure Island, FL: StatPearls Publishing. Pustisek, N., Vurnek Zivkovic, M., & Situm, M. (2016). Quality of life in families with children with atopic dermatitis. Pediatric Dermatology, 33, 28–32. Quiggle, A. M., Goodwin, Z. A., Marfatia, T. R., Kumar, M. G., Ciliberto, H., Bayliss, S. J., & de Guzman Strong, C. (2015). Low filaggrin monomer repeats in African American pediatric patients with moderate to severe atopic dermatitis. JAMA Dermatology, 151, 557–559. Robles, D. T., & Berg, D. (2007). Abnormal wound healing: Keloids. Clinics in Dermatology, 25, 26–32. Samrao, A., Price, V. H., Zedek, D., & Mirmirani, P. (2011). The “Fringe Sign”—A useful clinical finding in traction alopecia of the marginal hair line. Dermatology Online Journal, 17(11), 1. Shen, L. Y., Kenner-Bell, B. M., Ricketts, J., & Kundu, R. V. (2016). Ethnic skin: Kids are not just little people. Clinics in Dermatology, 34, 690–697. Siegfried, E. C., Jaworski, J. C., & Mina-Osorio, P. (2018). A systematic scoping literature review of publications supporting treatment guidelines for pediatric atopic dermatitis in contrast to clinical practice patterns. Dermatologic Therapy (Heidelb), 8, 349–377.
CE QUESTIONS 1. The presence of erythema may be harder to appreciate in a Fitzpatrick skin type IV patient compared with a Fitzpatrick skin type II patient. a. True b. False 2. Which of the following is not correct regarding acne? a. Cutibacterium acnes plays a pathogenic role in the development of acne. b. Isotretinoin is first-line treatment for comedonal acne. c. African American female patients with acne have a higher level of inflammation histologically compared with non-Black counterparts. d. Patients with skin of color are more likely to have acne scars and postinflammatory hyperpigmentation. 3. Topical retinoids and topical antibiotics should not be used to treat acne in patients with darker skin, given
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Silverberg, J. I., Simpson, E. L., Durkin, H. G., & Joks, R. (2013). Prevalence of allergic disease in foreign-born American children. JAMA Pediatrics, 167, 554–560. Silverberg, N. B., Duran-McKinster, C., Tay, Y.-K. (Eds.). (2015). Pediatric skin of color. New York, NY: Springer. Spann, C. T. (2011). Ten tips for treating acne vulgaris in Fitzpatrick skin types IV-VI. Journal of Drugs in Dermatology, 10, 654– 657. Thng, S. T. G., Long, V. S. H., Chuah, S. Y., & Tan, V. W. D. (2016). Efficacy and relapse rates of different treatment modalities for progressive macular hypomelanosis. Indian Journal of Dermatology, Venereology and Leprology, 82, 673–676. Troiano, M., Simeone, A., Scaramuzzi, G., Parisi, S., & Guglielmi, G. (2011). Giant keloid of left buttock treated with post-excisional radiotherapy. Journal of Radiology Case Report, 5, 8–15. Vachiramon, V., Tey, H. L., Thompson, A. E., & Yosipovitch, G. (2012). Atopic dermatitis in African American children: addressing unmet needs of a common disease. Pediatric Dermatology, 29, 395– 402. Velez Edwards, D. R., Tsosie, K. S., Williams, S. M., Edwards, T. L., & Russell, S. B. (2014). Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans. Human Genetics, 133, 1513–1523. Vemula, S., Maymomne, M. B. C., Secemsky, E. A., Widjajahakim, R., Patzelt, N. M., Saade, D., & Vashi, N. A. (2018). Assessing the safety of superficial chemical peels in darker skin: A retrospective study. Journal of the American Academy of Dermatology, 79, 508–513. Westerhof, W., Relyveld, G. N., Kingswijk, M. M., de Man, P., & Menke, H. E. (2004). Propionibacterium acnes and the pathogenesis of progressive macular hypomelanosis. Archives of Dermatology, 140, 210–214. Yin, N. C., & McMichael, A. J. (2014). Acne in patients with skin of color: Practical management. American Journal of Clinical Dermatology, 15, 7–16. Zhao, C. Y., Hao, E. Y., Oh, D. D., Daniel, B. S., Martin, L. K., Su, J. C., . . . Murrell, D. F. (2017). A comparison study of clinician-rated atopic dermatitis outcome measures for intermediate- to dark-skinned patients. Britsh Journal of Dermatology, 176, 985–992.
the risk of hyperpigmentation associated with these medications. a. True b. False 4. A 10-year-old African American patient presents to your office with acne predominantly located on her forehead. Which of the following components of your history is most important in determining the cause of this patient’s acne? a. Onset of menarche b. Family history of acne c. Hair products used d. Sunscreen use 5. Which of the following are common sites of involvement for infantile (<2 years of age) atopic dermatitis? a. Bilateral antecubital fossae b. Bilateral popliteal fossae c. Cheeks
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d. Buttocks 6. Children with darker skin tend to have a more papular variant of atopic dermatitis. a. True b. False 7. A 5-year-old Iranian boy presents to your office with ill-defined, hypopigmented patches on bilateral cheeks. There is minimal associated erythema and little to no associated pruritus. What is the most likely diagnosis? a. Pityriasis alba b. Tinea versicolor c. Atopic dermatitis d. Progressive macular hypomelanosis 8. A 13-year-old Haitian female presents to your office with hypopigmented scaly macules on the neck and back. What is the most likely diagnosis? a. Pityriasis alba
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b. Tinea versicolor c. Progressive macular hypomelanosis d. Atopic dermatitis 9. Early-stage traction alopecia is reversible. a. True b. False 10. A 17-year-old Hispanic female presents to your office with brown papules that coalesce into a reticular pattern across her central chest. What is the best initial treatment option for this patient? a. Isotretinoin b. Topical clindamycin c. Better sun protection d. Oral minocycline Answers available online at ce.napnap.org.
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Pharmacology Continuing Education
Common Skin Disorders in Pediatric Skin of Color Mayra B.C. Maymone, DDS, MD, DSc, Jacqueline D. Watchmaker, MD, Michelle Dubiel, MD, Stephen A. Wirya, MD, Lisa Y. Shen, MD, & Neelam A. Vashi, MD INSTRUCTIONS To obtain continuing education credit: 1. Read the article carefully. 2. Read each question and determine the correct answer. 3. Visit PedsCESM, ce.napnap.org, to complete the online Posttest and evaluation. 4. You must receive 70% correct responses to receive the certificate. 5. Tests will be accepted until December 31, 2020.
OBJECTIVES 1. Discuss common skin conditions in pediatric patients with darker skin types.
Mayra B.C. Maymone, Trainee, Department of Dermatology, Boston University School of Medicine, Boston, MA.
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. Posttest Questions Contact hours: 0.75 Passing score: 70% This continuing education activity is administered by the National Association of Pediatric Nurse Practitioners (NAPNAP) as an Agency providing continuing education credit. Individuals who complete this program and earn a 70% or higher score on the Posttest will be awarded 0.75 contact hours, of which 0.25 are Pharmacology contact hours. Earn FREE CE Contact Hours Online
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. Conflicts of interest: None to report. Dr. Maymone and Dr. Watchmaker should be considered as colead authors. Correspondence: Neelam A. Vashi, MD, Boston University School of Medicine, Department of Dermatology, 609 Albany St., J108, Boston, MA 02118; e-mail: [email protected]. J Pediatr Health Care. (2019) 33, 727-737 0891-5245/$36.00 Copyright © 2019 Published by Elsevier Inc. on behalf of National Association of Pediatric Nurse Practitioners. https://doi.org/10.1016/j.pedhc.2019.04.019
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Contact Hours for this online activity are FREE for NAPNAP Members. Non-Members will be charged a fee of $10 to receive contact hours for this online activity through PedsCESM. Payment can be made by credit card through PedsCESM. 1. To take the Posttest for this article and earn contact hours, please go to PedsCESM at ce.napnap.org. 2. In the Course Catalog, search for the name of the CE article. 3. If you already have an account with PedsCESM, log in using your username and password. If you are a NAPNAP member, log in with your username and password. If you are a first-time user and NAPNAP nonmember, click on “New Customer? Click Here.” 4. Once you have successfully passed the Posttest and completed the evaluation form, you will be able to print out your certificate immediately.
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
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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. J Pediatr Health Care. (2019) 33, 727−737
KEY WORDS Pediatrics, dermatology, skin of color, ethnic skin
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 (Silverberg, DuranMcKinster, & Tay, 2015). According to the U.S. Census Bureau, by 2044, people with skin of color will represent 50.3% of the U.S. population (Colby & Ortman, 2015). 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, Kenner-Bell, Ricketts, & Kundu, 2016). This article will also briefly address differences in pathophysiology and treatment modalities in those with richly pigmented skin (Table 2). ACNE Regardless of race or Regardless of race ethnicity, acne is one of or ethnicity, acne is the most common skin one of the most disorders observed in children and adolescents. common skin A retrospective cohort disorders observed study showed that acne in children and was among the top three most common dermatoadolescents. logic diagnoses in African American and Asian adolescents (Perkins, Cheng, Hillebrand, Miyamoto, & Kimball, 2011). TABLE 1. Fitzpatrick skin scale Type I Type II Type III Type IV Type V Type VI
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Always burns, never tans Usually burns, tans minimally Sometimes mildly burns, tans uniformly Burns minimally, always tans well Very rarely burns, tans very easily Never burns
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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 (Silverberg et al., 2015). 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 et al., 2011; Robles & Berg, 2007). 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, 2018). 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, Brooks, & Callender, 2003; Halder & Nootheti, 2003). 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 & Callender, 2010; Yin & McMichael, 2014). 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 creambased vehicle. Additionally, certain retinoid formulations, such as adapalene and micronized forms, have been shown to be well tolerated in skin of color (Silverberg, DuranMcKinster, & Tay, 2015). 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, 2011). Alexis et al. (2014) 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 treatmentrelated PIH were observed (Alexis, Johnson, Kerrouche, & Callender, 2014). 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, 2012). 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,
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TABLE 2. Common 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
Atopic dermatitis
Varies (infantile atopic dermatitis has onset < 2 years of age)
Pityriasis alba
3−16 years of age
Tinea versicolor
Adolescence
Progressive macular hypomelanosis Traction alopecia
Adolescence
Infantile atopic dermatitis: eczematous dermatitis on cheeks and extensor surfaces Childhood atopic dermatitis: subacute and chronic dermatitis predominantly on flexural areas Poorly defined, hypopigmented macules and patches with minimal scale, typically on face 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 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 Scaly, brown, thin papules that coalesce into reticulated plaques, often on central chest and back Skin-colored to hyperpigmented firm plaques that extend beyond wound margins
Topical antibiotics (clindamycin, erythromycin), topical benzoyl peroxide, topical retinoids, oral tetracyclines Oral contraceptives and spironolactone (females only) Isotretinoin for severe cases Topical steroids, topical calcineurin inhibitors, phosphodiaterase-4 inhibitors, systemic medication or phototherapy for severe disease
Adolescence/adulthood
Confluent and reticulated papillomatosis
Adolescence
Keloids
Adolescence
2014). Antibiotics such as tetracycline derivatives are used in moderate to severe acne because of their antimicrobial and antiinflammatory properties (Spann 2011). 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 (Silverberg, Duran-McKinster, & Tay, 2015). 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 & Callender, 2010).
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Emollients, low-potency topical steroids, topical calcineurin inhibitors, sun protection
Topical antifungals (ketoconazole), selenium sulfide shampoo Systemic antifungals for severe disease Photoprotective measures
Benzoyl peroxide, topical antibiotics, oral antibiotics, phototherapy Discontinuation of tight hairstyles, avoidance of chemical relaxers and heat styling, topical steroids, intralesional steroids, sub-antimicrobial doses of oral antibiotics
Oral minocycline (first line) Isotretinoin
Topical and intralesional steroids, intralesional injection of interferon or 5-fluorouracil, cryotherapy, surgical excision, laser therapy, silicone gel sheets, pressure application, or combination treatment
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, 2014). 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, 2012; Grimes & Callender, 2006). Strict sun
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FIGURE 1. Acne vulgaris.
FIGURE 2. Atopic dermatitis.
(This figure appears in color online at www.jpedhc.org)
(This figure appears in color online at www.jpedhc.org) 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 & Al-Yousef, 2018). 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 et al., 2018). 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, Jaworski, & Mina-Osorio, 2018). 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, Feldman, Gupta, & Fleischer, 2002). 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 730
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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 et al., 2018) . 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 (Julian-Gonzalez et al., 2012). 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 (Julian-Gonzalez et al., 2012). 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 & Hay, 2002). Moreover, dark-skinned patients may deem their atopic symptoms as less severe than those with lighter skin types (Zhao et al., 2017). 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 et al., 2018; Quiggle et al., 2015). In addition, African Americans have reduced ceramide levels and increased transepidermal water loss, which contributes to xerosis (Vachiramon, Tey, Thompson, & Yosipovitch, 2012). Children born outside the United States have lower risk of AD than U.S.-born children; however, children born outside
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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, Simpson, Durkin, & Joks, 2013). 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, Reich, & Szepietowski, 2017; Pustisek, Vurnek Zivkovic, & Situm, 2016). 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 et al., 2014). 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, 2018). Recalcitrant AD may require systemic treatment or phototherapy (Ortiz-Salvador & Perez-Ferriols, 2017). Crisaborole, a phosphodiaesterase-4 inhibitor, is a promising nonsteroid alternative for treatment of mild to moderate AD in children older than 2 years (Paller et al., 2016). 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, Michalek, Pawlowska-Kisiel, Olszewska, & Rudnicka, 2015).
FIGURE 3. Pityriasis alba.
(This figure appears in color online at www.jpedhc.org)
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 & Givler, 2018).
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 et al., 2015). 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 & Givler, 2018).
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 Even though PA is sunscreens (zinc oxide, benign and may titanium dioxide) that undergo are typically recommended for atopic spontaneous patients may be cosremission, it can be metically difficult to particularly tolerate for patients with darker skin types. bothersome for Low-potency topical those with darker corticosteroids and calphototypes. cineurin inhibitors have also shown good response (Miazek et al., 2015).
Pathogenesis Environmental factors such as sun exposure, long and frequent baths, and mechanical exfoliation appear to be predisposing factors in susceptible skin. African American
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
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pigmentation are often the presenting complaint, especially in patients with skin of color (Kallini, Riaz, & Khachemoune, 2014). 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, Alzayir, Abdulghani, & Osman, 2001; Kallini et al., 2014). 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 yellowgreen fluorescence in one third of cases (Kallini et al., 2014). TV commonly affects adolescents and young adults but may also occur in children. It is especially prevalent in tropical climates and during summer months. 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 FIGURE 4. Tinea versicolor.
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 & Passi, 1978). 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 et al., 2014). 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 et al., 2001). 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 (MartínezMartínez, Azana-Defez, Rodriguez-Vazquez, Faura-Berruga, & Escario-Travesedo, 2012). 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, Wuennenberg, Foote, Aires, & Rajpara, 2017). 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
FIGURE 5. Progressive macular hypomelanosis.
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(This figure appears in color online at www.jpedhc.org)
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because the condition may be more noticeable in darkerskinned individuals.
alopecia areata, trichotillomania, frontal fibrosing alopecia, infectious folliculitis, and syphilis (Castelo-Soccio, 2014).
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, Relyveld, Kingswijk, de Man, & Menke, 2004).
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 et al., 2013; Lawson et al., 2017).
Treatment Treatment options include topical and oral antibiotics, topical benzoyl peroxide, and ultraviolet light irradiation (Thng, Long, Chuah, & Tan, 2016). 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, 2018). 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 & Miteva, 2018; Pulickal & Kaliyadan, 2018). 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, Price, Zedek, & Mirmirani, 2011). The diagnosis is usually clinical, but difficult cases may require a skin biopsy. Differential diagnoses include tinea capitis, FIGURE 6. Traction alopecia.
(This figure appears in color online at www.jpedhc.org)
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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 Behavioral changes of topical or intralemay be particularly sional corticosteroids or sub-antimicrobial challenging for doses of oral antibiotpatients with ics. Behavioral changes may be particularly traction alopecia. challenging for patients with traction alopecia. Prognosis of this preventable condition will depend largely on the stage of the disease (Bolognia, 2018). 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, 2018). 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, Kang, Lee, & Kim, 2015). 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, Tey, & Chong, 2016). 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 et al., 2016). Fungal staining results are usually negative, and this condition typically does not respond to antifungal treatment. Histologically, CARP is
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FIGURE 7. Confluent and reticulated papillomatosis. Image courtesy of Dr. Brandi Kenner-Bell.
FIGURE 8. Keloid.
(This figure appears in color online at www.jpedhc.org)
(This figure appears in color online at www.jpedhc.org) 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, Loo, & Tan, 2018). Both oral and topical retinoids can also be tried for treatment failure with antibiotics (Lim et al., 2016). 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, Tsosie, Williams, Edwards, & Russell, 2014), with the highest prevalence in those of African descent (Glass, 2017). 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. 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, Simeone, Scaramuzzi, Parisi, & Guglielmi, 2011). 734
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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 et al., 2014). Keloids and hypertrophic scars are also genetically associated with human leukocyte antigens HLA-B14, HLA-B21, HLA-BW16, HLABW35, HLA-DR5, and HLA-DQW3 and blood group A (Laurentaci, & Dioguardi, 1977). 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, 2017). 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 & Shenefelt, 1999). Treatment Treatment includes surgical therapies, topical and intralesional steroids, intralesional injection of interferon or 5fluorouracil, cryotherapy, surgical excision, laser therapy, silicone gel sheeting, or combination treatment (Hsu, Luan & Tsai, 2017; Patel, Bialey, & Yakuboff, 2012). 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, Waller, & Davis, 2005). For patients requiring surgical intervention, preoperative radiation therapy has been used as a preventative measure, but benefits must outweigh the risks.
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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). SUPPLEMENTARY MATERIALS Supplementary material associated with this article can be found in the online version at https://doi.org/10.1016/j. pedhc.2019.04.019. REFERENCES Al Qarqaz, F., & Al-Yousef, A. (2018). Skin microneedling for acne scars associated with pigmentation in patients with dark skin. Journal of Cosmetic Dermatology, 17, 390–395. Alexis, A. F. (2014). Acne vulgaris in skin of color: Understanding nuances and optimizing treatment outcomes. Journal of Drugs in Dermatology, 13(6), s61–s65. Alexis, A. F., Johnson, L. A., Kerrouche, N., & Callender, V. D. (2014). 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, 13, 170– 174. Aljabre, S. H., Alzayir, A. A., Abdulghani, M., & Osman, O. O. (2001). Pigmentary changes of tinea versicolor in dark-skinned patients. International Journal of Dermatology, 40, 273–275. Ben-Gashir, M. A., & Hay, R. J. (2002). Reliance on erythema scores may mask severe atopic dermatitis in black children compared with their white counterparts. British Journal of Dermatology, 147, 920–925. Billero, V., & Miteva, M. (2018). Traction alopecia: The root of the problem. Clinical, Cosmetic and Investigational Dermatology, 11, 149–159. Bolognia, J. L., Schaffer, J. V., & Cerroni, L. (2018). Dermatology (4th ed.). Edinburgh: Elsevier. Callender, V. D. (2012). 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, 11, 643–648. Castelo-Soccio, L. (2014). Diagnosis and management of alopecia in children. Pediatric Clinics of North America, 61, 427–442. Colby, S. L., & Ortman, J. M. (2015). Projections of the size and composition of the U.S. population: 2014 to 2060. Washington, DC: U.S. Census Bureau. Retrieved from https://www.census.gov/ content/dam/Census/library/publications/2015/demo/p251143.pdf Davis, E. C., & Callender, V. D. (2010). A review of acne in ethnic skin: Pathogenesis, clinical manifestations, and management strategies. Journal of Clinic and Aesthetic Dermatology, 3, 24–38. Eichenfield, L. F., Tom, W. L., Chamlin, S. L., Feldman, S. R., Hanifin, J. M., Simpson, E. L., & Sidbury, R. (2014). Guidelines of care for the management of atopic dermatitis: Section 1. Diagnosis and assessment of atopic dermatitis. Journal of the American Academy of Dermatology, 70, 338–351. English, R. S., & Shenefelt, P. D. (1999). Keloids and hypertrophic scars. Dermatologic Surgery, 25, 631–638. Givler, D. N., & Givler, A. (2018). Pityriasis alba. Treasure Island, FL: StatPearls Publishing. Glass, D. A., 2nd. (2017). Current understanding of the genetic causes of keloid formation. Journal of Investigative Dermatology Symposium Proceedings, 18(2), S50–S53.
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Grimes, P., & Callender, V. (2006). Tazarotene cream for postinflammatory hyperpigmentation and acne vulgaris in darker skin: A double-blind, randomized, vehicle-controlled study. Cutis, 77 (1), 45–50. Halder, R. M., Brooks, H. L., & Callender, V. D. (2003). Acne in ethnic skin. Dermatologic Clinics, 21, 609–615. Halder, R. M., & Nootheti, P. K. (2003). Ethnic skin disorders overview. Journal of the American Academy of Dermatology, 48(6), S143–S148. Hsu, K.-C., Luan, C.-W., & &Tsai, Y.-W. (2017). Review of silicone gel sheeting and silicone gel for the prevention of hypertrophic scars and keloids. Wounds, 29(5), 154–158. Janumpally, S. R., Feldman, S. R., Gupta, A. K., & Fleischer, A. B. (2002). In the United States, blacks and Asian/ Pacific Islanders are more likely than whites to seek medical care for atopic dermatitis. Archives of Dermatology, 138, 634–637. Ji, J. H., Park, T.-S., Lee, H.-J., Kim, Y.-D., Pi, L.-Q., Jin, X.-H., & Lee, W.-S. (2013). The ethnic differences of the damage of hair and integral hair lipid after ultra violet radiation. Annals of Dermatology, 25, 54–60. n-Go nzalez, R. E., Orozco-Covarrubias, L., Duran-McKinster, C., Julia ez-de-Ocariz, M. Palacios-Lopez, C., Ruiz-Maldonado, R., & Sa (2012). Less common clinical manifestations of atopic dermatitis: prevalence by age. Pediatric Dermatology, 29, 580–583. Kallini, J. R., Riaz, F., & Khachemoune, A. (2014). Tinea versicolor in dark-skinned individuals. International Journal of Dermatology, 53(2), 137–141. Lane, J. E., Waller, J. L., & Davis, L. S. (2005). Relationship between age of ear piercing and keloid formation. Pediatrics, 115, 1312–1314. Laurentaci, G., & Dioguardi, D. (1977). HLA antigens in keloids and hypertrophic scars. Archives of Dermatology, 113, 1726. Lawson, C. N., Hollinger, J., Sethi, S., Rodney, I., Sarkar, R., Dlova, N., & Callender, V. D. (2017). Updates in the understanding and treatments of skin & hair disorders in women of color. International Journal of Women’s Dermatology, 3(1 Suppl.), S21–S37. Lee, S. W., Loo, C. H., & Tan, W. C. (2018). Confluent and reticulated papillomatosis: Case series of 3 patients from Kedah, Malaysia and literature review. Medical Journal of Malaysia, 73, 338–339. Lim, J. H.-L., Tey, H. L., & Chong, W.-S. (2016). Confluent and reticulated papillomatosis: Diagnostic and treatment challenges. Clinical, Cosmetic and Investigational Dermatology, 9, 217–223. Marciniak, J., Reich, A., & Szepietowski, J. C. (2017). Quality of life of parents of children with atopic dermatitis. Acta Dermato Venereologica, 97, 711–714. Margolis, D. J., Mitra, N., Gochnauer, H., Wubbenhorst, B., D’Andrea, K., Kraya, A., . . . Nathanson, K. L. (2018). Uncommon filaggrin variants are associated with persistent atopic dermatitis in african americans. Journal of Investigative Dermatology, 138, 1501–1506. ~a-Defez, J. M., Rodríguez-Vazquez, M., Martínez-Martínez, M. L., Azan Faura-Berruga, C., & Escario-Travesedo, E. (2012). Progressive macular hypomelanosis. Pediatric Dermatology, 29, 460–462. Miazek, N., Michalek, I., Pawlowska-Kisiel, M., Olszewska, M., & Rudnicka, L. (2015). Pityriasis alba—Common disease, enigmatic entity: Up-to-date review of the literature. Pediatric Dermatology, 32, 786–791. Nazzaro-Porro, M., & Passi, S. (1978). Identification of tyrosinase inhibitors in cultures of Pityrosporum. Journal of Investigative Dermatology, 71, 205–208. rez-Ferriols, A. (2017). Phototherapy in Ortiz-Salvador, J. M., & Pe atopic dermatitis. Advances in Experimental Medicine and Biology, 996, 279–286. Paller, A. S., Tom, W. L., Lebwohl, M. G., Blumenthal, R. L., Boguniewicz, M., Call, R. S., . . . Hebert, A. A. (2016). Efficacy and safety of crisaborole ointment, a novel, nonsteroidal
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phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. Journal of the American Academy of Dermatology, 75(3), 494–503. Park, Y. J., Kang, H. Y., Lee, E.-S., & Kim, Y. C. (2015). Differentiating confluent and reticulated papillomatosis from acanthosis nigricans. Journal of Cutaneous Pathology, 42, 944–952. Patel, P. A., Bailey, J. K., & Yakuboff, K. P. (2012). Treatment outcomes for keloid scar management in the pediatric burn population. Burns, 38, 767–771. Perkins, A. C., Cheng, C. E., Hillebrand, G. G., Miyamoto, K., & Kimball, A. B. (2011). 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, 25, 1054–1060. Pflederer, R. T., Wuennenberg, J. P., Foote, C., Aires, D., & Rajpara, A. (2017). Use of Wood’s lamp to diagnose progressive macular hypomelanosis. Journal of the American Academy of Dermatology, 77(4), e99–e100. Pulickal, J. K., & Kaliyadan, F. (2018). Alopecia, traction. Treasure Island, FL: StatPearls Publishing. Pustisek, N., Vurnek Zivkovic, M., & Situm, M. (2016). Quality of life in families with children with atopic dermatitis. Pediatric Dermatology, 33, 28–32. Quiggle, A. M., Goodwin, Z. A., Marfatia, T. R., Kumar, M. G., Ciliberto, H., Bayliss, S. J., & de Guzman Strong, C. (2015). Low filaggrin monomer repeats in African American pediatric patients with moderate to severe atopic dermatitis. JAMA Dermatology, 151, 557–559. Robles, D. T., & Berg, D. (2007). Abnormal wound healing: Keloids. Clinics in Dermatology, 25, 26–32. Samrao, A., Price, V. H., Zedek, D., & Mirmirani, P. (2011). The “Fringe Sign”—A useful clinical finding in traction alopecia of the marginal hair line. Dermatology Online Journal, 17(11), 1. Shen, L. Y., Kenner-Bell, B. M., Ricketts, J., & Kundu, R. V. (2016). Ethnic skin: Kids are not just little people. Clinics in Dermatology, 34, 690–697. Siegfried, E. C., Jaworski, J. C., & Mina-Osorio, P. (2018). A systematic scoping literature review of publications supporting treatment guidelines for pediatric atopic dermatitis in contrast to clinical practice patterns. Dermatologic Therapy (Heidelb), 8, 349–377.
CE QUESTIONS 1. The presence of erythema may be harder to appreciate in a Fitzpatrick skin type IV patient compared with a Fitzpatrick skin type II patient. a. True b. False 2. Which of the following is not correct regarding acne? a. Cutibacterium acnes plays a pathogenic role in the development of acne. b. Isotretinoin is first-line treatment for comedonal acne. c. African American female patients with acne have a higher level of inflammation histologically compared with non-Black counterparts. d. Patients with skin of color are more likely to have acne scars and postinflammatory hyperpigmentation. 3. Topical retinoids and topical antibiotics should not be used to treat acne in patients with darker skin, given
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Silverberg, J. I., Simpson, E. L., Durkin, H. G., & Joks, R. (2013). Prevalence of allergic disease in foreign-born American children. JAMA Pediatrics, 167, 554–560. Silverberg, N. B., Duran-McKinster, C., Tay, Y.-K. (Eds.). (2015). Pediatric skin of color. New York, NY: Springer. Spann, C. T. (2011). Ten tips for treating acne vulgaris in Fitzpatrick skin types IV-VI. Journal of Drugs in Dermatology, 10, 654– 657. Thng, S. T. G., Long, V. S. H., Chuah, S. Y., & Tan, V. W. D. (2016). Efficacy and relapse rates of different treatment modalities for progressive macular hypomelanosis. Indian Journal of Dermatology, Venereology and Leprology, 82, 673–676. Troiano, M., Simeone, A., Scaramuzzi, G., Parisi, S., & Guglielmi, G. (2011). Giant keloid of left buttock treated with post-excisional radiotherapy. Journal of Radiology Case Report, 5, 8–15. Vachiramon, V., Tey, H. L., Thompson, A. E., & Yosipovitch, G. (2012). Atopic dermatitis in African American children: addressing unmet needs of a common disease. Pediatric Dermatology, 29, 395– 402. Velez Edwards, D. R., Tsosie, K. S., Williams, S. M., Edwards, T. L., & Russell, S. B. (2014). Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans. Human Genetics, 133, 1513–1523. Vemula, S., Maymomne, M. B. C., Secemsky, E. A., Widjajahakim, R., Patzelt, N. M., Saade, D., & Vashi, N. A. (2018). Assessing the safety of superficial chemical peels in darker skin: A retrospective study. Journal of the American Academy of Dermatology, 79, 508–513. Westerhof, W., Relyveld, G. N., Kingswijk, M. M., de Man, P., & Menke, H. E. (2004). Propionibacterium acnes and the pathogenesis of progressive macular hypomelanosis. Archives of Dermatology, 140, 210–214. Yin, N. C., & McMichael, A. J. (2014). Acne in patients with skin of color: Practical management. American Journal of Clinical Dermatology, 15, 7–16. Zhao, C. Y., Hao, E. Y., Oh, D. D., Daniel, B. S., Martin, L. K., Su, J. C., . . . Murrell, D. F. (2017). A comparison study of clinician-rated atopic dermatitis outcome measures for intermediate- to dark-skinned patients. Britsh Journal of Dermatology, 176, 985–992.
the risk of hyperpigmentation associated with these medications. a. True b. False 4. A 10-year-old African American patient presents to your office with acne predominantly located on her forehead. Which of the following components of your history is most important in determining the cause of this patient’s acne? a. Onset of menarche b. Family history of acne c. Hair products used d. Sunscreen use 5. Which of the following are common sites of involvement for infantile (<2 years of age) atopic dermatitis? a. Bilateral antecubital fossae b. Bilateral popliteal fossae c. Cheeks
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d. Buttocks 6. Children with darker skin tend to have a more papular variant of atopic dermatitis. a. True b. False 7. A 5-year-old Iranian boy presents to your office with ill-defined, hypopigmented patches on bilateral cheeks. There is minimal associated erythema and little to no associated pruritus. What is the most likely diagnosis? a. Pityriasis alba b. Tinea versicolor c. Atopic dermatitis d. Progressive macular hypomelanosis 8. A 13-year-old Haitian female presents to your office with hypopigmented scaly macules on the neck and back. What is the most likely diagnosis? a. Pityriasis alba
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b. Tinea versicolor c. Progressive macular hypomelanosis d. Atopic dermatitis 9. Early-stage traction alopecia is reversible. a. True b. False 10. A 17-year-old Hispanic female presents to your office with brown papules that coalesce into a reticular pattern across her central chest. What is the best initial treatment option for this patient? a. Isotretinoin b. Topical clindamycin c. Better sun protection d. Oral minocycline Answers available online at ce.napnap.org.
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