Seborrheic Dermatitis

Epidemiology

• Prevalence in the general population: 2.35% to 11.30%, with most estimates around 5%.
• Two peaks: infants (onset as early as 2 weeks of life; peak at 3 months) and adults (peak in the 4th-6th decades).
• Male predominance at all ages.
• Prevalence rises sharply in immunosuppression: up to 83% in HIV/AIDS patients, with severity worsening as CD4 counts drop.
• Higher incidence in Parkinson disease, cerebrovascular accidents, and other neurologic conditions.
• Worsens in cold, dry climates; may improve with sun exposure.
• Drug-associated forms reported with neuroleptics, atypical antipsychotics, dupilumab, and tyrosine kinase inhibitors.

Pathogenesis

1. Malassezia (Pityrosporum)

• Malassezia globosa and M. restricta are considered the most important species (14 species total identified in the genus).
• Lipophilic yeasts that colonize sebaceous gland-rich skin. Antifungal therapy suppresses SD, supporting a causal role.
• However, there is no simple quantitative relationship between yeast density and severity - unaffected skin can carry a similar load.
• A mycelial (pathogenic) form, as seen in pityriasis versicolor, has not been detected in SD lesions.
• Malassezia metabolizes sebum triglycerides into unsaturated fatty acids (e.g., oleic acid), which may disrupt the epidermal barrier and trigger inflammation.

2. Sebaceous Gland Activity

• Distribution of lesions mirrors sebaceous gland-dense areas.
• SD appears when sebaceous activity is high (neonates due to maternal hormones; puberty/young adults; older adults).

3. Individual Immune Response

• SD is much more severe and prevalent in immunosuppressed patients.
• Lesional skin shows increased IL-1α, IL-1β, IL-4, IL-12, TNF-α, and IFN-γ.
• CD4+/CD8+ ratio alterations noted in some patients.
• Increased IgA and IgG antibodies in serum, but antibody levels against Malassezia specifically are not consistently elevated.
• Increased histamine and oxidative stress (reactive oxygen species) also implicated.

Clinical Features

Distribution

• Scalp: greasy scales, dandruff - most commonly involved
• Face: nasolabial folds, eyebrows, upper eyelids, glabella, forehead, postauricular areas
• Ears: external auditory canal and auricle
• Trunk: sternal chest (petaloid/arcuate lesions), upper back, umbilicus
• Intertriginous areas: axillae, inguinal folds (less scale, more erythema - easily mistaken for intertrigo)
• Rarely: erythroderma in severe cases

Morphology

• Erythematous patches or plaques with greasy, yellowish scale
• Ranges from mild pinkish scaling to thick adherent crusts
• In dark-skinned individuals: lesions may appear hypopigmented rather than erythematous
• Symptoms: pruritus, burning, tingling
• Course is chronic and relapsing; worsens in winter

Associated conditions

• Pityrosporum folliculitis: diffuse papulopustular eruption at the periphery
• Blepharitis: lid margin involvement
• Infantile SD ("cradle cap"): greasy yellow scale on scalp with mild erythema; in diaper area, overlaps with infantile psoriasis ("seborpsoriasis")

Diagnosis

Histology (if needed)

• Spongiosis, parakeratosis, crusting at follicular ostia
• Superficial perivascular lymphocytic infiltrate
• Presence of Malassezia on skin biopsy

Differential Diagnosis

Treatment

Infantile SD

• Mild cases: baby oil or mineral oil applied to scalp, gentle combing, mild shampoo - sufficient in most cases.
• Moderate/severe: topical antifungal (ketoconazole 2% cream) ± short courses of low-potency topical corticosteroids.
• Avoid strong keratolytic shampoos or mechanical scale removal.

Adult SD - First Line

• Topical azoles are the mainstay: ketoconazole 2% shampoo (scalp) or cream (body), response rate 75%-90% in double-blind trials.
• Scalp: fluocinolone acetonide 0.01% solution/gel, twice daily x 3-4 weeks; then ketoconazole 2% shampoo daily or every other day for maintenance.
• Face: hydrocortisone 2.5% cream, twice daily x 1-2 weeks initially; then ketoconazole 2% cream as needed.
• Ciclopirox olamine: both antifungal and anti-inflammatory; equally effective as shampoo or cream in randomized trials.
• Low-potency topical corticosteroids: rapid inflammation suppression; found equally efficacious to topical azoles in Cochrane analysis - useful for initial control.

Adult SD - Second Line

• Zinc pyrithione, selenium sulfide, coal tar shampoos
• Topical calcineurin inhibitors (tacrolimus, pimecrolimus): steroid-sparing option, especially useful on the face to avoid atrophy
• Emollients (important adjunct)

Maintenance

• SD relapses if maintenance therapy is not continued. M. furfur has a slow proliferation rate; relapses typically appear after 2 to several weeks. Maintenance therapy should follow this interval.
• Weekly or biweekly antifungal shampoo is a practical maintenance approach.

Systemic Therapy

• Reserved for severe or frequently relapsing disease: weekly fluconazole, itraconazole, or ketoconazole (note: ketoconazole has more activity against M. furfur than other azoles in vitro).
• In HIV patients: topical ketoconazole is first-line per WHO guidelines; add topical corticosteroids for severe/unresponsive cases. ART itself may improve SD. Oral antibiotics if bacterial superinfection present. Prolonged treatment courses often required.

Special Populations

HIV/AIDS

• Prevalence up to 83%, severity tracks inversely with CD4 count.
• Extensive scalp, axillae, groin, flexural involvement; thick greasy yellow scalp scale; frequent bacterial superinfection; may progress to erythroderma.
• Often refractory to standard therapy; frequent relapse.
• ART itself can improve SD.

Parkinson Disease and Neurologic Conditions

• SD is significantly more prevalent; the dopaminergic pathway and sebum production are proposed mechanisms.

Infants

• Self-limited in most cases; resolves within the first 1-2 years of life.
• Possible association with later development of adult SD or atopic dermatitis.

Seborrheic Dermatitis: Treatments

General Measures (All Patients)

• Emollients (mineral oil, vegetable oil, petroleum jelly) loosen and soften scales
• Gentle combing/brushing to remove adherent scale - avoid aggressive scraping (worsens inflammation)
• For scalp shampoos: lather and leave in place 3-5 minutes before rinsing to maximize effect
• Identify and address triggers: cold/dry climate, stress, certain medications (neuroleptics, antipsychotics)

Topical Antifungals (First-Line)

• SOR: A evidence - Shampoos containing ketoconazole, selenium sulfide, or zinc pyrithione are effective for scalp SD.
• SOR: B evidence - Ketoconazole 2% cream/gel is safe and effective for facial SD.

Topical Corticosteroids (First-Line, Adjunct)

• Found equally efficacious to topical azoles in Cochrane analysis for total clearance.
• Best used for initial rapid control of erythema, pruritus, and scaling; not ideal for long-term monotherapy.
• Beware of rebound flares on discontinuation.

Critical warning: High-potency corticosteroids must not be used on the face - risk of steroid-induced rosacea, perioral dermatitis, telangiectasia, and skin atrophy.

Topical Calcineurin Inhibitors (Second-Line / Steroid-Sparing)

• Tacrolimus 0.1% and pimecrolimus 1% cream
• Block calcineurin, preventing inflammatory cytokine production in T-lymphocytes
• No statistically significant difference from topical corticosteroids in short-term clearance trials
• Advantages over corticosteroids: no risk of telangiectasia, skin atrophy, or steroid rosacea - preferred for the face in long-term or maintenance use
• Useful for maintenance therapy to prevent relapse
• Long-term safety still under monitoring (theoretical lymphoma/malignancy concern with systemic calcineurin inhibitors, though topical risk appears very low)

Medicated Shampoos (OTC, Scalp-Focused)

Keratolytics

• Salicylic acid - loosens adherent scale before antifungal or steroid application
• Urea/propylene glycol/lactic acid combination - shown highly effective for scalp SD in studies
• Caution in neonates: selenium sulfide and salicylic acid carry risk of percutaneous absorption in infants

Systemic Therapy (Severe / Refractory Cases)

Emerging / Novel Therapies

• Topical PDE4 inhibitors (e.g., crisaborole, roflumilast): clinical trials completed as of 2024; data emerging as a potential new class for SD
• Narrow-band UVB phototherapy: shown safe and effective in open-label prospective studies; works via immunomodulatory and anti-inflammatory mechanisms
• Tea tree oil: randomized single-blind study showed benefit in severity, pruritus, and greasiness; antifungal activity against M. furfur confirmed in vitro

Infantile SD - Specific Approach

• Keratolytics (salicylic acid, selenium sulfide) are dangerous in neonates due to percutaneous absorption.
• Licochalcone 0.025% lotion (plant extract) shown comparable to hydrocortisone 1% in one study.
• Dietary controls and vitamin supplementation are not beneficial in infantile SD.
• Secondary bacterial or fungal infection: appropriate systemic antibiotics/antifungals.

HIV/AIDS Patients

• First-line: topical ketoconazole (WHO guidelines)
• Refractory/severe: add topical corticosteroids ± oral antifungals (ketoconazole preferred over fluconazole/itraconazole for M. furfur activity)
• ART itself may improve SD independently
• Oral antibiotics when bacterial superinfection is present
• Prolonged treatment courses often required; expect frequent relapse

Maintenance Strategy

• M. furfur has a slow proliferation rate; relapses typically emerge 2 to several weeks after stopping treatment
• Maintenance intervals should mirror this rhythm (e.g., antifungal shampoo 2x/week, or weekly fluconazole for severe cases)
• Topical calcineurin inhibitors are preferred for long-term facial maintenance (avoid steroid side effects)