Atopic Dermatitis (Eczema): Causes, Symptoms, Treatment, and Prevention

Atopic dermatitis (AD) is a chronic, relapsing, pruritic inflammatory skin disease affecting 10-20% of children and 1-3% of adults. It's the "atopic march" starter (→ asthma, allergic rhinitis).

Pathogenesis

• Skin barrier defect: Filaggrin (FLG) mutations → impaired stratum corneum → ↑ TEWL, allergen penetration.
• Immune dysregulation: Th2/Th22/Th17 skewing → IL-4, IL-13, IL-31, TSLP → inflammation, itch.
• Microbiome: S. aureus dominance → superantigens, biofilms.

Clinical Features

• Age-dependent distribution: infants (face, extensor), children (flexural), adults (hands, eyelids, flexural).
• Intense pruritus (worse at night) → lichenification, excoriations.
• Xerosis, erythema, papules, vesicles, crusting.
• Associated: Dennie-Morgan lines, keratosis pilaris, ichthyosis vulgaris.

Treatment Ladder

1. Foundation: Daily emollients (ointments > creams > lotions) within 3 min post-bath. Ceramide-dominant formulations.
2. Mild: Low-potency TCIs (tacrolimus 0.03%, pimecrolimus 1%) or low-potency steroids (hydrocortisone 2.5%) for face/folds.
3. Moderate: Mid-potency steroids (triamcinolone 0.1%) for body; TCIs for maintenance.
4. Severe: High-potency steroids short-term → transition to TCIs/phototherapy/systemics.
5. Phototherapy: NB-UVB (first-line systemic-sparing).
6. Systemics: Dupilumab (IL-4Rα, ≥6mo), upadacitinib/abrocitinib (JAKi, ≥12y), methotrexate, cyclosporine, azathioprine.

Flare Prevention

• Bleach baths (½ cup/40 gal tub, 2x/week) for S. aureus colonization.
• Identify/avoid triggers (allergens, irritants, heat, stress).
• Fragrance-free, dye-free products.
• Humidifier in winter.

AD is controllable. New biologics/JAK inhibitors offer transformative control for moderate-severe disease.