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
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Psoriasis | Well-demarcated silvery plaques, extensor | Clinical |
| Seborrhoeic dermatitis | Scalp, nasolabial folds, greasy scale | Clinical |
| Scabies | Burrows, finger webs, nocturnal itch, contacts affected | Dermoscopy, scraping |
| Contact dermatitis | Distribution follows contactant | Patch testing |
| Immunodeficiency (Wiskott-Aldrich, hyper-IgE) | Severe eczema + recurrent infections + thrombocytopenia | Immunology 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) |
|---|---|
| Pruritus | Xerosis (dry skin) |
| Typical morphology and distribution | Elevated serum IgE |
| Chronic/relapsing course | Early age of onset |
| Personal/family history of atopy | Ichthyosis/keratosis pilaris |
| Dennie-Morgan infraorbital folds | |
| Wool intolerance |
NICE Treatment Stepladder
| Step | Treatment |
|---|---|
| 1 | Emollients |
| 2 | Mild topical corticosteroid |
| 3 | Moderate topical corticosteroid / TCI |
| 4 | Potent topical corticosteroid / TCI |
| 5 | Phototherapy / systemic / biologics |