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Eczema (Atopic Dermatitis): Origins, Immune Dysregulation & Triggers
Atopic dermatitis (eczema) is a chronic relapsing inflammatory skin disease driven by skin barrier defect + immune dysregulation.
Core Pathogenesis
- Barrier Defect: FLG (filaggrin) mutations → impaired stratum corneum → ↑ TEWL, ↑ allergen penetration, ↓ antimicrobial peptides.
- Type 2 Immune Skewing: Th2/Th22 cytokines (IL-4, IL-13, IL-31, IL-22) → IgE ↑, eosinophilia, pruritus, lichenification.
- Neuroimmune Crosstalk: IL-31, TSLP → itch-scratch cycle → further barrier damage.
- Microbiome Dysbiosis: S. aureus dominance → superantigens, toxins → inflammation.
Triggers (Flare Precipitants)
- Environmental: Low humidity, heat, sweat, wool/synthetic fabrics, detergents
- Allergens: Dust mite, pet dander, pollen, food (esp. children: egg, milk, peanut)
- Psychological: Stress (↑ cortisol → barrier impairment)
- Infections: Viral (eczema herpeticum), bacterial
Management Pyramid
- Foundation: Emollients 2×/day (ceramide-rich, ointment > cream), gentle cleansing, trigger avoidance.
- Topical Anti-Inflammatories: Corticosteroids (appropriate potency/area), calcineurin inhibitors (tacrolimus, pimecrolimus) for face/folds/maintenance.
- Crisaborole (PDE4 inhibitor), Ruxolitinib (JAK inhibitor) — non-steroidal options.
- Systemic (Moderate-Severe): Dupilumab (IL-4Rα), tralokinumab (IL-13), upadacitinib/abrocitinib (JAK1) — transformative.
- Phototherapy: Narrowband UVB.
- Bleach Baths: ½ cup/40 gal 2×/wk — reduces S. aureus load.
Eczema is a systemic immune-barrier disorder — not just "dry skin." Modern biologics target root pathways.
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