Atopic dermatitis (eczema) management guide: barrier repair, steroids, and biologics

Atopic dermatitis (AD) — commonly called eczema — is the most common chronic inflammatory skin disease, affecting 15–20% of children and 2–10% of adults globally. It is not simply dry skin; it is a complex immune-mediated condition driven by barrier dysfunction and type 2 (Th2) immune dysregulation. Here's the complete management framework.

Understanding atopic dermatitis

The triad: barrier dysfunction + immune dysregulation + sensitization

AD pathogenesis involves three interacting components:

Barrier dysfunction (filaggrin):
Filaggrin loss-of-function mutations are present in ~30% of AD patients — the strongest single genetic risk factor. Filaggrin is essential for forming the cornified cell envelope and generating natural moisturizing factors. Without it, the skin barrier is porous: transepidermal water loss is elevated, pH rises (disrupting enzyme activity), and allergens and irritants penetrate to immune cells in the dermis.

Type 2 immune activation:
Damaged keratinocytes release thymic stromal lymphopoietin (TSLP), IL-25, and IL-33 → activate innate lymphoid cells type 2 (ILC2) and dendritic cells → Th2 lymphocyte polarization → IL-4, IL-13, IL-31 production. IL-4 and IL-13 drive IgE production and further barrier deterioration. IL-31 is the primary itch mediator — the "itch-scratch cycle" perpetuates barrier damage.

Sensitization and triggers:
The porous barrier allows percutaneous sensitization to environmental allergens (house dust mite, pet dander, pollen, food proteins). In sensitized individuals, allergen contact triggers IgE-mediated mast cell degranulation → acute flare.

The itch-scratch cycle

IL-31 → peripheral itch sensory neurons → scratching → physical barrier damage → keratinocyte activation → more TSLP/IL-33 → more Th2 → more IL-31. Breaking this cycle is central to AD management. Even non-lesional atopic skin has elevated TEWL and sub-clinical inflammation compared to non-atopic skin.

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The proactive maintenance model

AD management has shifted from reactive treatment (only treating flares) to proactive maintenance — treating both active and subclinical disease:

Reactive approach: Apply treatment at flare onset; stop when flare resolves → frequent cycles of repeated inflammation → increased sensitization and skin damage over time
Proactive approach: After clearing a flare, continue intermittent topical treatment to previously-affected areas 2× weekly (even when skin appears clear) → prevents subclinical inflammation from escalating to clinical flare

Berth-Jones et al. (2003): Proactive fluticasone propionate 0.05% twice weekly vs. vehicle demonstrated significantly fewer relapses (6.8 vs. 12.8 over 20 weeks). The proactive model is now standard in European and US guidelines.

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Step 1: Barrier repair (the foundation of all AD management)

Moisturization is not optional or adjunctive — it is the primary treatment for mild AD and the foundation of all management levels:

Emollients applied liberally and frequently — minimum twice daily; immediately post-bathing (within 3 minutes) while skin is still damp
Volume: 250–500g per week for adults with significant involvement; under-application is the most common failure
Formulation: Fragrance-free, preservative-minimized ceramide-containing cream or ointment (Vanicream, CeraVe Moisturizing Cream, Aveeno Eczema Therapy, Eucerin Original). Ointments (petrolatum-base) provide greatest occlusion but may be less acceptable to patients
The 1:1:1 physiological lipid ratio: Ceramide:cholesterol:fatty acid in this ratio produces fastest TEWL normalization (Mao-Qiang 1996, Journal of Investigative Dermatology)
Fragrance avoidance: Fragrance is the leading contact sensitizer in AD patients; all skincare and laundry products should be fragrance-free

Bathing guidance: Lukewarm (not hot) water; 5–10 minutes maximum; gentle fragrance-free wash; pat dry (not rub); apply emollient within 3 minutes of exiting bath.

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Step 2: Topical corticosteroids (TCS)

TCS are the first-line treatment for active AD flares. Potency selection is the critical skill:

Potency ladder

| Class | Potency | Examples | Where to use |
|---|---|---|---|
| VII (lowest) | Mild | Hydrocortisone 0.5–1% | Face, eyelids, skin folds, infants |
| V–VI | Moderate | Triamcinolone 0.025%, desonide 0.05% | Trunk and limbs in children; face short-term |
| III–IV | Mid-high | Triamcinolone 0.1%, mometasone furoate 0.1% | Trunk and limbs in adults; thick lichenified skin |
| I–II (highest) | Very potent | Clobetasol propionate 0.05%, betamethasone dipropionate | Palms, soles; severe lichenified plaques; maximum 2 weeks |

Rules:
Use the lowest potency effective for the body site and patient age
Never high-potency steroids on face, eyelids, or skin folds — skin is thinner, systemic absorption is higher, atrophy risk is significant
Application: Thin layer once or twice daily to active lesions only (not healthy skin); fingertip unit (FTU) guides quantity
Duration: Use until lesion clears, then switch to proactive maintenance (2×/week) or taper

Side effects of prolonged inappropriate TCS use: Skin atrophy, striae, telangiectasia, perioral dermatitis, steroid-induced rosacea, HPA axis suppression (rare but possible with potent steroids over large body surface area).

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Step 3: Topical calcineurin inhibitors (TCIs)

TCIs are steroid-sparing alternatives — no skin atrophy risk, making them preferred for chronic use on the face and skin folds:

Tacrolimus 0.03% (children) / 0.1% (adults) — Protopic ointment
Pimecrolimus 1% — Elidel cream; slightly less potent than tacrolimus; better tolerability profile

Mechanism: Inhibit calcineurin → prevent nuclear factor of activated T cells (NFAT) translocation → block IL-2 and other Th2 cytokine transcription → suppress local T cell activation.

Evidence: Eichenfield et al. (2002, JAAD): tacrolimus 0.1% superior to vehicle for moderate-severe AD at all body sites including face; tacrolimus 0.03% and pimecrolimus 1% both superior to 1% hydrocortisone for facial AD.

Application: To active lesions 2× daily; may be used for proactive maintenance 2×/week on traditionally affected areas. Burning/stinging on application common in first few days and then resolves.

FDA black box warning (2006): Theoretical malignancy risk (based on animal studies at much higher doses); never substantiated in humans in 20+ years of post-marketing. Current evidence does not support avoidance based on malignancy concern. Pediatric approval for pimecrolimus ≥2 years; tacrolimus 0.03% ≥2 years.

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Step 4: Crisaborole (Eucrisa)

Phosphodiesterase 4 (PDE4) inhibitor — 2% ointment; FDA-approved for mild-to-moderate AD ≥2 years. Non-steroidal, non-TCI option. Less potent than tacrolimus but provides an additional non-steroidal option. Stinging on application in ~4% of patients.

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Step 5: Biologics (moderate-to-severe AD)

Dupilumab (Dupixent) — the landmark advance

Dupilumab is a monoclonal antibody targeting the IL-4Rα receptor — blocking both IL-4 and IL-13 signaling simultaneously. It directly addresses the central Th2 driver of AD.

*Simpson et al. (2016, New England Journal of Medicine)* — pivotal LIBERTY AD SOLO trials: dupilumab 300 mg SC Q2W vs. placebo in adults with moderate-severe AD → IGA 0/1 (clear/almost clear) in 38% vs. 10% (placebo); EASI-75 (75% improvement) in 44% vs. 12%.

FDA approvals: Adults 2019; children 6–11 years 2022; 6 months–5 years 2023. The broadest biologic approval in AD.

Side effects: Conjunctivitis (most common — 10–28%; manage with ophthalmologist; usually resolves or manageable); injection site reactions; facial redness ("dupilumab head-and-neck dermatitis" — management: low-potency topical steroid or TCI; often resolves over time).

Tralokinumab (Adbry)

IL-13 specific monoclonal antibody (vs. dupilumab's dual IL-4/13 blockade). FDA-approved for adults with moderate-severe AD 2022. Comparable efficacy to dupilumab with slightly different side effect profile (conjunctivitis rate lower).

Lebrikizumab (Ebglyss)

IL-13 monoclonal antibody; EU-approved 2023; US approval 2023. ADVOCATE trials demonstrate EASI-75 ~58% at week 16.

JAK inhibitors (oral)

Abrocitinib (Cibinqo) — JAK1 selective; FDA-approved 2022 for adults with moderate-severe AD
Upadacitinib (Rinvoq) — JAK1 selective; FDA-approved 2022; also approved for adolescents ≥12 years

JAK inhibitors act faster than biologics (clinical response within 2–4 weeks vs. 8–16 weeks for dupilumab) but carry class effects: infection risk, thromboembolism (boxed warning class), herpes zoster reactivation. Used for patients needing rapid response or biologic failures.

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Trigger identification and avoidance

Beyond treatment, identifying and managing triggers reduces flare frequency:

House dust mite: Encasings for mattress/pillow; wash bedding weekly at 60°C; reduce carpet and soft furnishings
Pet allergen: If sensitized, reduce bedroom exposure; HEPA filters; hand washing after contact
Fragrance: Laundry detergent, fabric softener, soap — all fragrance-free
Wool/synthetic fabrics: Cotton next to skin; avoid wool direct contact
Sweat: Shower promptly after exercise; apply emollient post-shower
Stress: Psychosocial stress activates the HPA axis and mast cells — well-documented AD trigger
Certain foods: In young children with AD, egg and milk are the most common food triggers; formal IgE testing recommended before elimination (non-specific elimination diets without evidence cause nutritional harm)

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