Seborrheic Dermatitis

Etiology And Pathogenesis

Represents chronic inflammatory disease manifesting primarily in infancy and adolescence.
Cutaneous distribution directly parallels size, distribution, and activity of sebaceous glands.
Exact etiology remains unknown.
Malassezia furfur (commensal yeast) heavily incriminated in disease pathogenesis.
Cutaneous inflammation potentially results from direct fungal action, fungal by-products, or exaggerated host immune response.
Adolescent manifestation strictly follows puberty, indicating distinct sex hormone influence.
Relationship between infantile and adolescent forms remains unclear; infantile disease does not predict adolescent recurrence.

Onset typically occurs within first 4 weeks of life.
Illness remains self-limiting, generally resolving by 12 weeks to 1 year of age.
Initial manifestation frequently involves diffuse or focal scaling and crusting of scalp, clinically termed cradle cap.
Characterized by yellow-orange, greasy scales and crusts overlying erythema.
Lesions frequently expand to involve face, neck, retroauricular areas, axillae, umbilicus, and diaper area.
Cutaneous lesions generally remain nonpruritic in infants.
Postinflammatory pigmentary changes (hypopigmentation) commonly observed in darker skin tones.
Intractable seborrhea-like dermatitis associated with chronic diarrhea and failure to thrive mandates urgent evaluation for systemic immune dysfunction.
Chronic treatment-resistant pattern occasionally indicates underlying Langerhans cell histiocytosis.

Disease onset universally follows puberty.
Follows chronic relapsing course, generally lacking spontaneous resolution.
Disease remains more localized, confined primarily to scalp, chest, and intertriginous areas.
Scalp manifestations vary from diffuse brawny scaling to focal thick, oily, yellow crusts with underlying erythema.
Frequently involves marginal blepharitis and external auditory canal inflammation.
Severe cases exhibit prominent erythema and scaling at frontal hairline, medial eyebrows, nasolabial folds, and retroauricular folds.
Red, scaly plaques frequently appear in axillae, inguinal region, gluteal cleft, and umbilicus.
Extremity plaques often appear more eczematous, less erythematous, and poorly demarcated.
Pruritus highly variable, ranging from absent to marked.
Accompanying hair loss remains distinctly uncommon.

Represents frequent cutaneous manifestation of Acquired Immunodeficiency Syndrome.
Human Immunodeficiency Virus infected patients exhibit thick, greasy scalp scales and large hyperkeratotic erythematous plaques on face, chest, and genitals.

Diagnostic Entity	Distinguishing Clinical Features
Atopic Dermatitis	Characterized by acute weeping, severe pruritus; often clinically indistinguishable from seborrheic dermatitis in early infancy.
Psoriasis	Exhibits bright red, scaly, well-demarcated plaques; highly persistent; strong family history common.
Langerhans Cell Histiocytosis	Presents with treatment-resistant, infiltrative, crusted, hemorrhagic papules in groin, axillae, scalp; accompanied by systemic signs including hepatosplenomegaly and anemia.
Candidiasis	Involves intertriginous and convex surfaces; features bright-red plaques with diagnostic satellite pustules.
Irritant Diaper Dermatitis	Strictly spares intertriginous creases; localized strictly to convex contact surfaces.

Therapeutic Modality	Specific Clinical Recommendations
General Skin Care	Emollients, baby oil, gentle shampooing utilizing nonmedicated baby shampoo.
Mechanical Scale Removal	Pretreatment with oil followed by gentle brushing removes thick cradle cap crusts effectively.
Refractory Lesions	Apply 2% ketoconazole shampoo or cream twice daily.
Inflammatory Lesions	Short course of mild, low-potency topical corticosteroids applied once daily for 1 week.
Steroid Sparing Agents	Topical calcineurin inhibitors (pimecrolimus or tacrolimus) hasten clinical subsidence.

Target Anatomical Area	Specific Pharmacologic Interventions
Scalp (First-Line Therapy)	Antifungal shampoos (selenium sulfide, ketoconazole, ciclopirox, zinc pyrithione, salicylic acid, tar) utilized several times weekly to daily.
Scalp (Inflamed Lesions)	Mid-potency topical corticosteroids (fluocinolone 0.01% oil or triamcinolone 0.1% lotion) applied once daily for 2-4 weeks.
Facial Lesions	Low-potency topical corticosteroid cream combined continuously with topical antifungals (ketoconazole 2% cream/shampoo).
Trunk And Extremity Lesions	Mid-potency topical corticosteroid cream combined continuously with topical antifungals.
Second-Line Options	Topical calcineurin inhibitors; potent keratolytic agents including urea.
Severe Refractory Disease	Oral antifungal agents utilized in severe adult cases; comprehensive pediatric data remains lacking.
Long-Term Maintenance	Antifungal shampoo utilized strictly twice-weekly significantly reduces clinical relapse risk.