Dermatology

Atopic Dermatitis (Eczema)

Chronic pruritic inflammatory skin disease with impaired filaggrin skin barrier and Th2 inflammation; often part of atopic march (asthma, allergic rhinitis).

Last reviewed 2 Jun 2026 - MedicoMedics editorial team

Pathophysiology

Loss-of-function FLG mutations impair skin barrier; Th2 (IL-4, IL-13, IL-31) drives inflammation and pruritus.

Sources: AAD AD 2023; NEJM Dupilumab 2016;375:2335

Presentation

Infants: face and extensor eczema. Children/adults: flexural (antecubital, popliteal) lichenified plaques; xerosis, pruritus; frequent S. aureus superinfection.

Diagnosis

Clinical (Hanifin-Rajka criteria); IgE often elevated. Rule out contact dermatitis, scabies.

Management

Emollients daily, low-mid potency topical corticosteroids for flares, topical calcineurin inhibitors (tacrolimus). Moderate-severe: dupilumab (anti-IL-4Ra), tralokinumab, JAK inhibitors (upadacitinib), phototherapy.

Sample USMLE-style MCQs

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Question 1

A 4-year-old has recurrent itchy flexural eczema and family history of asthma. Best daily maintenance?

References

Primary guidelines and peer-reviewed sources used for this entry. Reviewed 2 Jun 2026 by MedicoMedics editorial team.

Frequently asked

Which cytokines dominate?

IL-4 and IL-13 (Th2).

Best sparing strategy?

Topical calcineurin inhibitors for face/flexures.

First systemic biologic?

Dupilumab.

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