Dermatology Textbook•Papulosquamous & Eczematous Dermatoses•Eczematous Dermatoses
Pathophysiology & Clinical Features
Atopic dermatitis (AD) is driven by epidermal barrier dysfunction (FLG filaggrin mutations, ceramide deficiency) and type 2 immune polarization (IL-4, IL-13, IL-31, and TSLP).
- Infantile Phase (<2 years): Acute weeping, crusted erythematous papulovesicles on cheeks, forehead, scalp, and extensor limbs (sparing the diaper area).
- Childhood & Adult Phase: Lichenified flexural plaques in antecubital and popliteal fossae, wrists, ankles, and eyelids.
- Complications: Staphylococcus aureus impetiginization and Eczema Herpeticum (punched-out monomorphic umbilicated vesicles requiring urgent oral/IV Acyclovir).
EASI Scoring & Targeted Systemic Escalation
- EASI (Eczema Area and Severity Index): Evaluates Erythema, Edema/Papulation, Excoriation, and Lichenification (0–3 each) across 4 body regions. EASI ≥ 21.1 indicates severe disease.
- Biologics (Dupilumab, Tralokinumab, Lebrikizumab): Safe in high-TB settings; no routine blood monitoring required.
- Oral Selective JAK1 Inhibitors (Upadacitinib 15–30 mg OD, Abrocitinib 100–200 mg OD): Rapid itch relief within 24–48 hours; requires baseline IGRA/TB, HBV/HCV panel, CBC, LFT, and lipids.
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How to Cite
Cutisight. "Atopic Dermatitis: Barrier Dysfunction, EASI & Targeted Therapy." Encyclopedia of Dermatology [Internet]. 2026. Available from: https://cutisight.com/education/papulosquamous/atopic-dermatitis/easi-dupilumab-and-jak-inhibitors
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