Seborrheic dermatitis (SD) is an inflammatory skin disorder that largely affects infants and adults.^1,2 SD often presents with yellow and/or white greasy scaling and erythema on highly sebaceous areas (e.g., scalp, face, chest, back, groin).^1,3–5 Erythema can be difficult to determine in individuals with skin of color. Additionally, patients with skin of color may present with hypopigmentation and petaloid or arcuate lesions, which commonly appear on the hairline but may also affect other parts of the face. Petaloid SD is characterized by coalescing, pink/hypopigmented rings with little scale.⁵ Infants with SD often present with “cradle cap,” which is characterized by thick, yellow, greasy scaling on the scalp, particularly in White infants,^1,4 whereas infants of color might experience erythema, hypopigmentation, and flaking.⁵ Infants with SD might also present with comorbid atopic dermatitis.^1,5 

In most cases, infantile SD occurs within the first three months of life and resolves spontaneously within one year, whereas adult SD has a relapsing-remitting disease course. Mild, asymptomatic SD is common in infants. Common symptoms of adult-onset SD include pruritus (itching) and burning. Adults with SD often have no history of atopic dermatitis.¹ Dandruff is a mild, noninflammatory form of SD.^1,3

Pathophysiology and Risk Factors

SD involves lipid secretion, colonization by Malassezia (a yeast), and underlying susceptibility. Sebaceous glands secrete lipid onto the skin, and Malassezia colonizes these lipid-rich areas. Malassezia then secretes lipase, which produces free fatty acids and lipid peroxides; this incites an inflammatory response from the immune system—cytokines are produced, and keratinocyte (skin cell) proliferation and differentiation thus occurs. Then, the skin barrier is disrupted, which leads to erythema, scaling, and itch.²

Age, male sex, high sebaceous gland activity, immunodeficiency (e.g., human immunodeficiency virus-acquired immunodeficiency syndrome [HIV-AIDS], lymphoma), neuropsychiatric disorders (e.g., Parkinson’s disease [PD], stroke), and exposure to certain medications (e.g., immunosuppressants, dopamine antagonists) are some known risk factors for SD.^1,2

Androgens and adrenal corticosteroids play a role in sebaceous gland activity and lipid composition, thereby promoting Malassezia growth, which might explain the male predominance in SD.² SD is very common in HIV-AIDS, affecting about 35 percent of patients with HIV infection and 85 percent of patients with AIDS (vs. worldwide prevalence of about 5%).¹ Patients with HIV-AIDS often present with more severe SD than others,^1,2 and sudden onset of severe SD might be a sign of HIV-AIDS.¹ Immune dysregulation might explain the increased prevalence of SD in patients with HIV-AIDS. Furthermore, SD may present differently in this patient population, with a more generalized distribution, lesion development in atypical locations, more severe and generalized inflammation, and greater thickness and greasiness of scale.² Compared to SD lesions in individuals without PD, SD lesions in patients with PD have been shown to contain a higher density of Malassezia yeast, likely caused by parasympathetic system hyperactivity, which increases sebum production. Furthermore, facial immobility due to neurological conditions, such as PD or stroke, can result in sebum accumulation, which contributes to SD.² 

Treatment

SD treatment varies based on patient age, disease severity, and the area of affected skin. 

Topical antifungals, such as ketoconazole, ciclopirox, and sertaconazole, are recommended for the treatment of adult SD of the face and body; topical calcineurin inhibitors, such as pimecrolimus and tacrolimus, may be used off-label for this condition.^3,4,6 Topical calcineurin inhibitors have been shown to effectively treat hypopigmentation in patients with skin of color.⁵ Topical corticosteroids may be used as anti-inflammatory agents, but long-term use is not recommended due to adverse effects.^3,4,6 

Infantile scalp SD can typically be treated with emollients to loosen scales, which can then be gently removed.^4,6 In adults, over-the-counter shampoos containing ingredients such as zinc pyrithione, pine/coal tar, or selenium sulfide can be used to treat scalp SD.^1,3,4 Ketoconazole 1% shampoo is available over the counter, whereas ketoconazole 2% shampoo requires a prescription and is typically used for the treatment of moderate-to-severe SD.⁶ Ciclopirox 1% shampoo is another antifungal treatment option for scalp SD.^4,6 Additionally, foam (ketoconazole) and gel (ketoconazole and ciclopirox) formulations are available. Topical corticosteroids, which have anti-inflammatory properties, can work quickly to decrease erythema, scaling, and itch, but can cause side effects, such as atrophy and telangiectasia, and thus are not recommended for long-term use.⁶ Many over-the-counter shampoos are recommended for use twice weekly, whereas prescription shampoos may require daily use.⁴ Topical vehicles other than shampoos may be more beneficial among individuals who require less frequent hair washing. In individuals with skin of color, shampoos for SD might cause dryness, which could then lead to hair damage; use of heat or chemical relaxers further increases this risk. Pomades and oils have been associated with scalp irritation and thus should be avoided.⁵

For refractory or severe SD, oral systemic treatment with antifungals (e.g., itraconazole, terbinafide) may be effective. Antiretroviral therapy might help to improve SD in patients with HIV-AIDS.^1,6 Patients with PD treated with L-dopa might experience SD improvement.^1,2 Systemic therapies should not be used in patients with PD due to potential neurological side effects.⁶

Sources

1. Tucker D, Masood S. Seborrheic Dermatitis. [Updated 2024 Mar 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024. Available from: https://www.ncbi.nlm.nih.gov/books/NBK551707/
2. Adalsteinsson JA, Kaushik S, Muzumdar S, et al. An update on the microbiology, immunology and genetics of seborrheic dermatitis. Exp Dermatol. 2020;29(5):481–489. 
3. James WD, Elston DM, Treat JR, et al. Seborrheic dermatitis, psoriasis, recalcitrant palmoplantar eruptions, pustular dermatitis, and erythroderma. In: James WD, Elston DM, Treat JR, et al. Andrews’ Diseases of the Skin: Clinical Dermatology, 13th edition. Elsevier; 2020:191–204.
4. Clark GW, Pope SM, Jaboori KA. Diagnosis and treatment of seborrheic dermatitis. Am Fam Physician. 2015;91(3):185–190. 
5. Elgash M, Dlova N, Ogunleye T, Taylor SC. Seborrheic dermatitis in skin of color: clinical considerations. J Drugs Dermatol. 2019;18(1):24–27. 
6. Dall’Oglio F, Nasca MR, Gerbino C, Micali G. An overview of the diagnosis and management of seborrheic dermatitis. Clin Cosmet Investig Dermatol. 2022;15:1537–1548.