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Dermatology›Condition·Updated Jun 27, 2026·v1

Atopic Dermatitis

Atopic dermatitis is a chronic inflammatory skin disease characterized by pruritus, eczematous lesions, and barrier dysfunction. Diagnosis is clinical using validated criteria. Management follows a stepwise ladder from emollients and topical anti-inflammatories to phototherapy and systemic therapy with biologics or JAK inhibitors. Early recognition of emergencies (eczema herpeticum, erythroderma) is essential. The disease carries significant comorbidity burden including atopic march, cardiovascular disease, and mental health disorders.

High Evidence429 references·9,261 words·38 min read·v1
atopic dermatitiseczemapruritustype 2 inflammationdermatologyfilaggrindupilumabJAK inhibitor

Quick Reference

RxDrug of choiceDupilumab 300 mg subcutaneously every 2 weeks (loading 600 mg) for moderate-to-severe AD after topical failure.
AltAlternativesTralokinumab 300 mg every 2 weeks, lebrikizumab 250 mg every 2 weeks, nemolizumab 30 mg every 4 weeks; oral JAK inhibitors (abrocitinib 100-200 mg daily, upadacitinib 15-30 mg daily).
⊘AvoidLong-term systemic corticosteroids; live vaccines (e.g., smallpox) in active AD; JAK inhibitors in patients with prior VTE, age >65, or high cardiovascular risk.
DxTest of choiceClinical diagnosis using Hanifin and Rajka criteria; dermoscopy for atypical cases; skin biopsy for treatment failure or suspicion of mycosis fungoides.
ScKey scoreEczema Area and Severity Index (EASI), EASI ≥16 defines moderate-to-severe disease; treat-to-target goal EASI ≤7.
→When to referFailure of topical therapy after 12-16 weeks, need for systemic therapy, suspected eczema herpeticum or erythroderma, atypical features suggesting mycosis fungoides.
Atopic dermatitis is a clinical diagnosis managed with a stepwise ladder: emollients, topical anti-inflammatories, phototherapy, then biologics or JAK inhibitors for moderate-to-severe disease; early recognition of emergencies (eczema herpeticum, erythroderma) is critical.
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease driven by epidermal barrier dysfunction and type 2 immune dysregulation, affecting up to 20% of children and 10% of adults globally. The cardinal symptom is intense pruritus, which fuels the itch-scratch cycle and leads to eczematous lesions that evolve from acute vesicles to chronic lichenified plaques. Diagnosis is clinical, based on validated criteria (Hanifin and Rajka or UK Working Party), and severity is quantified using tools like EASI and IGA to guide therapy. Management follows a stepwise ladder: consistent emollient use, topical anti-inflammatories (corticosteroids, calcineurin inhibitors, newer agents), phototherapy, and systemic therapy with biologics (e.g., dupilumab) or JAK inhibitors for moderate-to-severe disease. Early recognition of emergencies such as eczema herpeticum and erythroderma is critical.

Overview and Recommendations

Background

  • •Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease affecting up to 20% of children and 10% of adults globally, with the highest disability burden of any skin condition. It is driven by a self-amplifying cycle of epidermal barrier disruption ( mutations, ) and type 2 immune dysregulation (IL-4, IL-13, IL-31), with colonization and the itch-scratch cycle as amplifying loops.
  • •Loss-of-function mutations in the filaggrin gene (FLG) are the strongest known genetic risk factor (OR 3-5), leading to reduced natural moisturizing factor and increased allergen penetration. Environmental triggers include low humidity, air pollution, obesity, and stress.
  • •AD is a spectrum disease with distinct clinical phenotypes: extrinsic (80-85%, elevated IgE) vs intrinsic (normal IgE), and variants such as head-and-neck AD ( -driven), chronic hand eczema, nummular eczema, prurigo nodularis overlap, and erythrodermic AD. Recognizing these guides therapy.
  • •The atopic march describes the progression from infantile AD to asthma, , and food allergy; early-onset persistent AD carries the highest risk. Early effective therapy with may reduce incident asthma by 38%.

Evaluation

  • •Suspect AD in any patient with intense pruritus, eczematous lesions, and a chronic relapsing course, especially with personal or family history of atopy. The diagnosis is clinical using Hanifin and Rajka criteria (≥3 major: pruritus, typical morphology/distribution, chronic course, atopy; plus ≥3 minor).
  • •Ask about onset age (usually <2 years), itch severity (use Peak Pruritus NRS 0-10), sleep disturbance, triggers (sweat, stress, irritants), and history of asthma, allergic rhinitis, or food allergy.
  • •Examine for morphology: acute (erythematous papules/vesicles with oozing), subacute (dry scaly patches), chronic (lichenified plaques with excoriations). Distribution varies by age: infants face/extensors, children flexural, adults flexural plus head-and-neck or hand eczema.
  • •Look for associated signs: Dennie-Morgan fold, , hyperlinear palms, pityriasis alba, white dermographism.
  • •No confirmatory lab test is required. Dermoscopy shows yellow serous crusts, dotted vessels (<25/mm²), and diffuse white scaling; linear or spermatozoa-like vessels suggest mycosis fungoides and warrant biopsy.
  • •Skin biopsy is reserved for atypical presentations (unilateral, nodular, erythrodermic) or treatment failure; histology shows spongiosis in acute lesions and psoriasiform hyperplasia in chronic lesions, with reduced filaggrin expression.
  • •Assess severity using validated tools: EASI (≥16 moderate-severe), IGA (0-4), PP-NRS (≥4-point reduction meaningful), POEM, DLQI. BSA ≥10% defines moderate-severe in trials.
  • •Consider differentials: psoriasis (sharply demarcated plaques, silvery scale, nail changes), contact dermatitis (patch testing), mycosis fungoides (atypical lymphocytes, clonality), scabies (burrows, interdigital involvement).
  • •In acute deterioration, distinguish (monomorphic vesicles, fever, HSV PCR), erythroderma (>90% BSA, systemic symptoms), and bacterial superinfection (honey-colored crusts, cellulitis).

Management

  • •Initiate consistent emollient therapy (fragrance-free, lipid-rich) at least twice daily to restore barrier function; this is the foundation of all AD management.
  • •For active flares, apply (TCS) once or twice daily: low-potency ( 1%) for face/intertriginous, mid-potency (triamcinolone 0.1%) for trunk/limbs, high-potency (clobetasol 0.05%) for short bursts on lichenified plaques. Taper to twice-weekly maintenance for prone sites.
  • •Topical calcineurin inhibitors ( 0.03%/0.1% ointment, pimecrolimus 1% cream) are steroid-sparing alternatives for sensitive areas; tacrolimus 0.1% is non-inferior to mid-potency TCS.
  • •Newer topical options: roflumilast cream 0.15% once daily (PDE4 inhibitor), tapinarof cream 1% once daily (AhR agonist), and ruxolitinib cream 0.75%/1.5% twice daily (JAK1/2 inhibitor) are approved for mild-to-moderate AD.
  • •For moderate-to-severe AD inadequately controlled with topicals, consider narrowband UVB phototherapy (311-313 nm) three times weekly; it is effective but requires frequent visits.
  • •First-line conventional systemic: 2.5-5 mg/kg/day (divided BID) for rapid onset; monitor BP and renal function. Limit to ≤1 year due to toxicity.
  • •Alternative conventional systemic: 10-25 mg weekly with folic acid 5 mg weekly; slower onset (8-12 weeks) but better long-term safety. Azathioprine and mofetil are third-line.
  • •Biologics are first-line systemic therapy for moderate-severe AD after topical failure. Initiate 600 mg subcutaneously loading dose, then 300 mg every 2 weeks; it blocks IL-4Rα and achieves IGA 0/1 in 36-38% at week 16.
  • •Alternative biologics: tralokinumab 600 mg load then 300 mg every 2 weeks (anti-IL-13), lebrikizumab 500 mg load then 250 mg every 2 weeks (anti-IL-13), nemolizumab 60 mg load then 30 mg every 4 weeks (anti-IL-31RA, especially for pruritus).
  • •Oral JAK inhibitors offer rapid efficacy but carry FDA boxed warnings for MACE, VTE, malignancy, and serious infections. Abrocitinib 100-200 mg daily, upadacitinib 15-30 mg daily, baricitinib 2-4 mg daily. Upadacitinib 30 mg showed superior EASI-75 (71%) vs dupilumab (61%) at week 16.
  • •For acute emergencies: requires IV acyclovir 10 mg/kg every 8 hours; systemic corticosteroids are contraindicated. Erythroderma requires hospitalization, fluid resuscitation, and topical steroids under wet wraps.
  • •Avoid long-term systemic corticosteroids, leukotriene receptor antagonists, probiotics, and house dust mite avoidance as monotherapy; these lack evidence.
  • •Refer to dermatology if no EASI-50 response after 12-16 weeks of adequate topical therapy, if systemic therapy is needed, or if atypical features suggest mycosis fungoides.
  • •Monitor for treatment-specific adverse events: conjunctivitis with dupilumab (5-15%), VTE with JAK inhibitors, renal toxicity with cyclosporine, and infections with all immunosuppressants.

Board Review — High Yield

  • •Hanifin and Rajka criteria, Requires ≥3 major (pruritus, typical morphology/distribution, chronic course, atopy) and ≥3 minor features for diagnosis.
  • •Filaggrin (FLG) mutations, Strongest genetic risk factor (OR 3-5); leads to barrier dysfunction and increased transepidermal water loss.
  • •Eczema herpeticum, Emergency: monomorphic vesicles, fever; treat with IV acyclovir 10 mg/kg q8h; systemic corticosteroids contraindicated.
  • •Dupilumab, First-line biologic for moderate-severe AD; blocks IL-4Rα; IGA 0/1 in ~37% at week 16; associated with conjunctivitis (5-15%).
  • •JAK inhibitor boxed warning, MACE, VTE, malignancy, serious infections; screen for risk factors before use.
  • •Atopic march, Progression from infantile AD to asthma, allergic rhinitis, food allergy; early dupilumab may reduce asthma risk by 38%.
  • •Topical steroid withdrawal (TSW), Intense erythema/burning after abrupt discontinuation of potent TCS; manage with slow taper and calcineurin inhibitors.
  • •EASI score, Validated severity tool; EASI ≥16 = moderate-severe; treat-to-target goal EASI ≤7.
  • •Intrinsic vs extrinsic AD, Extrinsic (80-85%) has elevated IgE; intrinsic has normal IgE, later onset, female predominance.
  • •Phototherapy, Narrowband UVB (311-313 nm) is second-line after topicals; contraindicated in photosensitivity disorders.

Deep Dive — Evidence Details

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