Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease characterized by pruritus, eczematous lesions, and a disrupted skin barrier. It arises from a multifactorial interplay of genetic predisposition (e.g., filaggrin mutations), type 2 inflammation, environmental triggers, and microbiome dysbiosis. Management centers on barrier repair, anti-inflammatory therapy (topical and systemic), itch control, trigger mitigation, infection prevention, and patient education. Biologic and JAK inhibitor therapies have transformed care for moderate-to-severe disease.
Epidemiology
- Global prevalence ~15–20% in children, 5–10% in adults; prevalence varies by region and urbanization.
- Onset typically in early childhood; up to 20–40% persist into adulthood.
- Strong associations: food allergy (especially early childhood), allergic rhinitis, asthma (atopic march).
Pathophysiology
- Barrier dysfunction: filaggrin and other epidermal structural protein defects increase transepidermal water loss and allergen penetration.
- Immune dysregulation: type 2 skewing (IL-4, IL-13, IL-31, TSLP, IL-22) drives inflammation and itch.
- Microbiome: Staphylococcus aureus colonization exacerbates flares; reduced microbial diversity.
- Neural component: chronic itch with central sensitization; IL-31 implicated.
- Phenotypes endotype-specific differences across age, ethnicity, and anatomic sites.
Clinical Features
- Pruritus is universal; sleep disturbance common.
- Age-specific morphology and distribution:
- Infant: cheeks, scalp, extensor surfaces.
- Childhood: flexural involvement (antecubital, popliteal).
- Adult: chronic lichenified plaques, head/neck, hands, flexural, nipples; prurigo nodules in some.
- Skin findings: xerosis, eczematous plaques, excoriations, lichenification; secondary impetiginization possible.
Diagnosis
- Clinical diagnosis; no single definitive test.
- Typical criteria (e.g., UK Working Party) include pruritus plus flexural dermatitis, chronic/relapsing course, personal/family atopy, xerosis.
- Evaluate for secondary infection when exudate/crusts present.
- Consider patch testing if refractory or atypical distribution suggests allergic contact dermatitis overlap.
Severity Assessment
- Common indices: SCORAD, EASI, POEM; IGA for trials/practice.
- Quality-of-life instruments (DLQI, CDLQI) are valuable adjuncts.
Differential Diagnosis
- Contact dermatitis (allergic/irritant), psoriasis, scabies, seborrheic dermatitis (infants), tinea, immunodeficiency, cutaneous T-cell lymphoma (adults with recalcitrant disease), nummular eczema.
Management
- Foundational skin care
- Daily emollients (liberal, fragrance-free; creams/ointments preferred).
- Lukewarm short baths/showers; gentle cleansers; avoid harsh soaps.
- Trigger management: wool, fragrances, smoke, extremes of humidity/temperature.
- Topical anti-inflammatory therapy
- Topical corticosteroids (TCS): potency matched to site/age/severity; use fingertip unit guidance; proactive weekend therapy to high-risk areas reduces relapses.
- Topical calcineurin inhibitors (TCIs: tacrolimus, pimecrolimus): steroid-sparing for face, folds; proactive maintenance.
- Topical PDE4 inhibitor (crisaborole) for mild-to-moderate disease.
- Newer topicals (where available): topical JAK inhibitors (ruxolitinib) for mild-to-moderate AD.
- Itch and sleep
- Optimize inflammation control first. Non-sedating antihistamines have limited benefit for itch unless comorbid urticaria; short-term sedating antihistamines may aid sleep.
- Infection control
- Treat clinical bacterial infection with appropriate antibiotics; consider dilute bleach baths in recurrent infections.
- Herpetic superinfection (eczema herpeticum) requires prompt antiviral therapy.
- Phototherapy
- Narrowband UVB for moderate disease refractory to topicals; consider logistical access.
- Systemic therapy (moderate–severe, refractory)
- Biologics: dupilumab (IL-4Rα inhibitor), tralokinumab (IL-13 inhibitor).
- Oral JAK inhibitors: upadacitinib, abrocitinib, baricitinib—rapid efficacy; monitor for class-specific risks (infections, lipids, thrombosis risk stratification).
- Conventional immunosuppressants (where biologics/JAKs not available): cyclosporine (short-term), methotrexate, azathioprine, mycophenolate—monitor labs and adverse effects.
- Education and adherence
- Written action plans, demonstration of fingertip units, flare vs maintenance regimens, and expectations.
Special Populations
- Pediatrics: emollients first-line; careful TCS potency; dupilumab approved down to 6 months in many regions.
- Pregnancy: prefer TCS/TCIs; phototherapy; dupilumab has emerging safety data but shared decision-making required.
- Skin of color: dyspigmentation risk and papular/follicular variants more common; address PIH proactively.
Emerging Directions
- Microbiome-targeted approaches, topical biologics, allergen immunomodulation, personalized endotype-driven therapy.
References (recent guidelines and key reviews)
- Wollenberg A, et al. European Task Force on Atopic Dermatitis (ETFAD) and ESCD/EADV Guidelines Update, 2023–2024.
- Drucker AM, et al. AAD Guidelines of Care for the Management of Atopic Dermatitis, 2023–2024 updates.
- Sidbury R, et al. Joint Task Force Practice Parameter Update, 2023.
- Thyssen JP, et al. Lancet/NEJM reviews 2022–2024 on AD pathogenesis and therapeutics.