TextbookDermatologyAtopic Dermatitis

Atopic Dermatitis

Chronic relapsing inflammatory skin condition representing the most common form of eczema. Part of the atopic triad with asthma and allergic rhinitis. Characterised by intensely pruritic, dry, erythematous skin in a flexural distribution. Pathogenesis involves filaggrin gene mutations causing epidermal barrier dysfunction and Th2-mediated immune dysregulation.

Key Facts

Filaggrin (FLG) gene mutations: strongest genetic risk factor; present in ~30% of atopic dermatitis patients in European populations Atopic triad: atopic dermatitis → food allergy → asthma → allergic rhinitis (atopic march) Diagnostic criteria (Hanifin & Rajka): pruritus + ≥3 of: flexural distribution, personal/family atopy, dry skin, onset <2 years S. aureus colonisation: >90% of AD skin — flares often associated with bacterial superinfection Emollients 250–500g/week: foundation of all treatment; reduce flare frequency by 50% Wet wraps: for acute severe flares — emollient/dilute steroid under wet bandages Dupilumab (anti-IL-4Rα): first biologic approved; SOLO 1 & 2 trials showed 75% reduction in EASI score; NICE TA534 Quality of life: AD has greater QoL impact than many chronic diseases; associated with anxiety, depression, sleep disturbance

Overview

Key Facts

Atopic dermatitis is the most common inflammatory skin disease. Understanding the filaggrin-barrier defect model and the Th2 immune pathway is essential for rational treatment decisions.

Epidemiology

  • UK prevalence: 15–20% of children; 2–5% of adults
  • 60% develop symptoms in first year of life; 90% by age 5
  • Increasing prevalence worldwide (especially in developed countries)
  • Stronger maternal than paternal heritability

Aetiology

  • Genetic: FLG mutations (epidermal barrier), IL-4/IL-13 pathway polymorphisms
  • Environmental triggers: house dust mite, pet dander, food allergens (egg, milk — especially in young children), irritants (soap, detergents)
  • Microbiome: S. aureus dominance; reduced microbial diversity
  • Psychosocial: stress worsens disease

Pathophysiology

  • FLG deficiency → defective cornified envelope → impaired skin barrier → increased TEWL + allergen penetration
  • Th2 skewing: IL-4, IL-13 → IgE class switching, further barrier disruption
  • IL-31 → itch → scratch → barrier damage → more inflammation (itch-scratch cycle)
  • Chronic: Th1/Th22 involvement → lichenification

Clinical Presentation

Age-Related Distribution

  • Infants: face, scalp, extensor surfaces; weeping, crusting
  • Children: flexures (antecubital, popliteal fossae), wrists, ankles; dry, lichenified
  • Adults: hands, face, flexures; may be lichenified or nummular (discoid)

Severity Assessment

  • Mild: areas of dry skin, infrequent itch
  • Moderate: areas of dry skin, frequent itch, redness ± excoriations
  • Severe: widespread dry skin, incessant itch, extensive redness, lichenification, bleeding, oozing

Complications

  • Eczema herpeticum: widespread HSV — punched-out erosions, fever; EMERGENCY
  • Secondary bacterial infection: S. aureus — crusting, pustules
  • Growth restriction: in children on prolonged systemic steroids

Red Flags

  • Eczema herpeticum (punched-out erosions + systemic illness)
  • Erythroderma (>90% BSA)
  • Failure to thrive in infant with severe eczema

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
PsoriasisWell-demarcated silvery plaques, extensorClinical
Seborrhoeic dermatitisScalp, nasolabial folds, greasy scaleClinical
ScabiesBurrows, finger webs, nocturnal itch, contacts affectedDermoscopy, scraping
Contact dermatitisDistribution follows contactantPatch testing
Immunodeficiency (Wiskott-Aldrich, hyper-IgE)Severe eczema + recurrent infections + thrombocytopeniaImmunology workup

Diagnosis / Investigation

Clinical Diagnosis

  • Usually clinical; Hanifin & Rajka criteria

If Indicated

  • Skin swab: if infected (MC&S for S. aureus; viral PCR for HSV)
  • Specific IgE / skin prick tests: if food allergy suspected (children <2 with moderate-severe AD)
  • Total IgE: often elevated (non-specific)
  • SCORAD/EASI/POEM scores: validated severity tools for monitoring
  • Patch testing: if allergic contact dermatitis component suspected
  • Skin biopsy: rarely needed; shows spongiotic dermatitis

Management

Complete Emollient Therapy

  • 250–500g/week; apply frequently, especially after bathing
  • Ointments (Epaderm, emulsifying ointment) for very dry skin
  • Creams (Diprobase, Cetraben) for less dry/daytime use
  • Soap substitute for washing

Topical Anti-Inflammatory

  • Mild: hydrocortisone 1% OD-BD (face, children)
  • Moderate: clobetasone butyrate 0.05%
  • Potent: betamethasone valerate 0.1% (body — short courses for flares)
  • Topical calcineurin inhibitors: tacrolimus 0.03%/0.1%, pimecrolimus 1% (face, flexures, long-term maintenance)
  • Proactive maintenance: TCI or low-potency steroid 2×/week to previously affected areas

Adjunct Therapies

  • Wet wraps: emollient ± dilute steroid under wet tubular bandages (acute flares)
  • Bandages: ichthammol, zinc
  • Antihistamines: sedating (hydroxyzine, chlorphenamine) at night for itch — non-sedating have no proven benefit in AD

Systemic (Specialist)

  • Phototherapy: narrowband UVB
  • Ciclosporin: 3–5mg/kg/day — rapid onset; monitor renal function and BP
  • Methotrexate: 10–25mg weekly (slower onset than ciclosporin)
  • Azathioprine: 1–3mg/kg/day (check TPMT first)
  • Dupilumab: 600mg loading then 300mg SC every 2 weeks — SOLO 1&2, LIBERTY AD trials
  • JAK inhibitors: baricitinib 4mg OD, upadacitinib 15–30mg OD, abrocitinib 100–200mg OD

Referral Criteria

  • Dermatology: moderate-severe AD not responding to optimised topical therapy
  • Urgent: eczema herpeticum, erythroderma
  • Allergy: suspected food allergy (children), contact allergy (patch testing)

Prognosis

  • 60% of childhood AD clears by adolescence
  • 20% have lifelong disease (more likely with FLG mutations, early onset, severe disease)
  • AD in childhood increases asthma risk by 3-fold
  • QoL impact: comparable to diabetes and heart disease (DLQI studies)
  • Dupilumab: sustained improvement at 52 weeks in >60% of patients

Other Relevant Information

Hanifin & Rajka Diagnostic Criteria

Major (need pruritus + 3 minor)Minor Criteria (examples)
PruritusXerosis (dry skin)
Typical morphology and distributionElevated serum IgE
Chronic/relapsing courseEarly age of onset
Personal/family history of atopyIchthyosis/keratosis pilaris
Dennie-Morgan infraorbital folds
Wool intolerance

NICE Treatment Stepladder

StepTreatment
1Emollients
2Mild topical corticosteroid
3Moderate topical corticosteroid / TCI
4Potent topical corticosteroid / TCI
5Phototherapy / systemic / biologics