Atopic dermatitis

Lifetime prevalence 15–20% in children, 2–10% in adults. Higher severity and prevalence in Black and Asian children in US studies. Commonly under-recognized as 'mild' in darker skin because visible erythema is attenuated — severity is driven by induration, lichenification, and pruritus impact, not color.

Multifactorial: filaggrin loss-of-function mutations → barrier dysfunction; type 2 immune skew (IL-4, IL-13, IL-31); skin microbiome dysbiosis (Staph aureus dominance); impaired lipid processing. IL-4/IL-13 signaling is the target of dupilumab.

Infantile (0–2y): cheeks, scalp, extensor extremities; oozing, crusting. Diaper area spared.

Childhood (2–12y): flexural (antecubital, popliteal), neck, wrists. Lichenification as chronicity builds.

Adolescent/adult: flexural persists, plus hands, face, eyelids, head-and-neck variant. Prurigo and chronic hand dermatitis phenotypes.

Erythema is unreliable in Fitzpatrick V–VI — describe as violaceous, dusky, hyperpigmented, or grey-brown. Palpate for warmth and induration. Follicular papular variant is common in Black and South Asian patients and can be misread as folliculitis or miliaria. Post-inflammatory hyperpigmentation and hypopigmentation are part of the disease course — counsel early, do not treat as a separate cosmetic issue. Prurigo nodules and lichenification dominate chronic disease and contribute disproportionately to QoL impact.

• Seborrheic dermatitis — greasy scale, scalp/nasolabial distribution, often overlaps in infancy.
• Contact dermatitis — geometric borders, history of exposure.
• Scabies — burrows, family members affected, acral/genital distribution.
• Tinea — annular, scaly, KOH positive.
• CTCL (mycosis fungoides) — adult-onset 'eczema' unresponsive to treatment; biopsy.
• HIES, Wiskott-Aldrich, Netherton — severe early-onset with systemic features.

Clinical diagnosis (Hanifin-Rajka or UK Working Party criteria). Consider KOH, bacterial culture, HSV PCR if flared. Patch testing for refractory cases. Total IgE/specific IgE rarely guides therapy. Biopsy only for atypical/refractory cases to rule out CTCL.

• Emollients twice daily (ceramide- or petrolatum-based; cost matters).
• Topical corticosteroids potency matched to site and severity (low potency face/intertriginous; mid-to-high elsewhere; short courses).
• Topical calcineurin inhibitors (tacrolimus 0.03%/0.1%, pimecrolimus 1%) — non-steroid option for face, eyelids, genital.
• Bathing + trigger avoidance — lukewarm baths, gentle cleansers, identify contact triggers.
• Wet wraps for flares in children.

• Dupilumab (IL-4Rα) — first-line systemic; approved ≥6 months. Watch for conjunctivitis, head-and-neck flares.
• JAK inhibitors (upadacitinib, abrocitinib, topical ruxolitinib) — rapid efficacy; screen per REMS (TB, lipids, VTE risk).
• Tralokinumab (IL-13) — alternative biologic.
• Phototherapy (nbUVB) — durable, steroid-sparing.
• Traditional immunosuppressants (MTX, cyclosporine, MMF) — when biologics unavailable.

~60% of children clear by adolescence; ~40% persist into adulthood. Atopic march: AD → food allergy → asthma → allergic rhinitis. Severity and quality-of-life impact are highest in the SoC adult phenotype with prurigo/lichenification.

• In darker skin, 'mild erythema' can mask severe disease. Grade severity by induration, lichenification, and pruritus — not color.
• Post-inflammatory dyspigmentation is part of AD. Address it proactively in patient counseling.
• 'Steroid phobia' is common — address it directly; undertreatment perpetuates disease.
• Sudden monomorphic vesicles: think eczema herpeticum, treat empirically.
• Adult 'eczema' refractory to treatment → biopsy to exclude CTCL.

Chronic condition, not curable but controllable. Daily moisturizer is the foundation. Flares expected — step up, don't start over. Post-inflammatory color changes will fade but take months. In Black and South Asian skin, follicular bumps are the disease, not a separate problem.