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.

Clinical Manifestations

Infantile Seborrheic Dermatitis

• 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.

Adolescent Seborrheic Dermatitis

• 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.

Associated Systemic Conditions

• 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.

Differential Diagnosis

Therapeutic Management Protocol

Infantile Disease Management

Adolescent Disease Management