Seborrheic Dermatitis in Skin of Color: Clinical Considerations

cells per high power field. In addition, the high therapeutic efficacy of antifungal agents in the treatment of SD seems to support Malessezia yeast as a contributing factor.¹¹ The host immune response has been proposed to play a role in the pathogenesis of SD. SD is more common in immunosup- pressed patients than immunocompetent patients with rates up to 83% in the former versus 1-3% in the latter.¹¹The presentation of HIV-associated SD is distinct, and has unique clinical and his- topathological features. HIV-infected patients may present with erythroderma or may develop concurrent Kaposi varicelliform eruption, also known as eczema herpeticum, both of which may be recalcitrant to standard treatment and tend to recur much more frequently.¹² This clinical presentation of SD may be a marker of underlying HIV infection and should prompt the clinician to screen for HIV status. In a study comparing lesional skin in SD patients to non-lesional skin in healthy controls,¹³ it was found that SD involves a strong inflammatory reaction with an increase in NK1+ and CD16+ cells, complement activation, and increased inflammatory interleukins. It has also been shown thatT-cell function is depressed in patients with SD while natural killer cell, IgA or IgG antibody levels may be increased.⁸ Together these findings highlight an immune or inflammatory reaction in patients with SD, possibly towards Malessezia yeast.

SD is generally a clinical diagnosis based on the typical location and morphology of lesions. In adults, the classic presentation of SD consists of erythematous patches with greasy scales on areas of the body highly populated with sebaceous glands: scalp, glabella, eyebrows, nasolabial folds, paranasal skin, cheeks, bearded areas of the face, upper chest, back, and skin flexures.¹¹ HIV-associated SD may be quite extensive, spreading well beyond the commonly affected sites.¹⁴ In children, SD typically presents as thick white or yellow greasy scale on the scalp, commonly called “cradle cap.” SD may be asymptomatic or can be intensely itchy. Darker-skinned adults may have additional presentations of SD including hypopigmentation in the classic areas of involvement (Figure 1) and underlying erythema may be difficult to appreciate.¹⁵ This population may also present with arcuate and petaloid lesions that commonly involve the hairline but may affect other areas of the face.¹⁶ This form of SD, called “petaloid seborrheic dermatitis,” appears as polycyclic coalescing rings that are pink or hypopigmented with minimal scale.¹⁷ The associated hypopigmentation typically improves with treatment¹⁸ and is thought to result from inhibition of melanocyte tyrosinase function and pigment production by yeast metabolites.¹⁸ In children of color SD generally does not have the standard “cradle cap” appearance that is seen in Caucasians. Children of color often present with erythema, flaking, and hypopigmen- tation of the affected areas and overlying atopic dermatitis, which accentuates hypopigmentation (Figure 2).¹⁹ Meanwhile, adolescents of Hispanic, Asian, and African origin may present similarly to adults, with hypopigmented scaly plaques on the eyebrow and perinasal region.²⁰ The differential diagnosis for SD is lengthy (Table 1) and includes psoriasis, atopic and contact dermatitis, and rosacea.³ In children, tinea capitis, particularly the seborrheic type, is an important diagnostic consideration for scalp involvement as it is more common than SD in black and Hispanic children.²¹ Langerhans cell histiocytosis is an additional consideration in children.³ If uncertain, a biopsy can be obtained demonstrating parakeratosis in the epidermis, spongiosis, and plugged follicular ostia.²²