Allergic disorders - atopic dermatitis (eczema)
Description
- Chronic relapsing-remitting inflammatory skin disease with impaired epidermal barrier function
- Part of the atopic march - often precedes food allergy, allergic rhinitis, and asthma in childhood
Epidemiology
- ~15-20% of children, ~2-5% of adults (persistent or adult-onset)
- Most (~60%) present in the first year of life
- Strong association with FHx atopy
Aetiopathogenesis
- Filaggrin gene mutations - impaired skin barrier -> transepidermal water loss + allergen/microbial penetration
- Th2-skewed immune response - IL-4, IL-13, IL-31 drive inflammation and pruritus (targets of current biologics)
- Barrier disruption -> colonisation/infection with Staphylococcus aureus -> further inflammation ("itch-scratch cycle")
- Trigger factors: irritants (soap, wool), heat/sweat, aeroallergens, food allergens (esp. infants with moderate-severe disease), stress, dry climate
Diagnosis
Clinical
- Pruritus (always present) + typical morphology/distribution by age:
- Infants - face, scalp, extensor surfaces
- Children/adults - flexural (antecubital/popliteal fossae), neck, hands
- Chronic/relapsing course, personal/family history of atopy
- Severity scoring (e.g. SCORAD, EASI) for treatment escalation decisions
Investigations - rarely needed for diagnosis
- Consider allergy testing (skin prick/specific IgE) if food allergy suspected as a trigger in infants with moderate-severe disease, or for concurrent aeroallergen-driven disease
- Skin swab if secondary bacterial infection suspected
Management
By severity - stepwise
### All severities - foundational
- Regular emollient use (liberal, frequent) - reduces flares and topical steroid requirement
- Avoid known triggers/irritants, lukewarm short showers, soap substitutes
### Mild-moderate
- Topical corticosteroids - potency matched to site/severity (low potency for face/flexures, higher for thickened plaques), used for flares, stepped down once controlled
- Topical calcineurin inhibitors (tacrolimus, pimecrolimus) - steroid-sparing, useful for face/flexures and maintenance ("proactive" twice-weekly use to prevent relapse)
### Moderate-severe, refractory to topical therapy
- Dupilumab (anti-IL-4Ra) - first-line biologic, strong evidence base, approved from age 6 months in many jurisdictions
- Tralokinumab (anti-IL-13) - alternative biologic, fewer ocular side effects than dupilumab
- JAK inhibitors (upadacitinib, abrocitinib) - oral option for refractory disease or when biologics inadvisable/failed; faster onset than biologics but carry a boxed warning (VTE, MACE, malignancy, infection) - reserve for refractory cases after risk discussion
- Phototherapy (narrowband UVB) - alternative for widespread disease without access to systemic agents
- Short courses of oral corticosteroids - avoid as a long-term strategy (rebound flare on cessation)
### Secondary infection
- Treat overt bacterial infection (topical/oral antibiotics targeting S. aureus); routine antibiotic/antiseptic use for colonisation alone is not recommended
- Eczema herpeticum (rapidly spreading vesicles, punched-out erosions, systemic illness) - same-day dermatology/ID referral, IV aciclovir
Associations
- Atopic march - food allergy, allergic rhinitis, asthma
- Secondary bacterial (S. aureus) and viral (eczema herpeticum, molluscum) skin infection
- Sleep disturbance, psychological impact (anxiety, depression), impaired quality of life
- Ocular complications with dupilumab specifically (conjunctivitis, keratitis) - counsel and monitor
Natural history & complications
- Many children improve/resolve by adolescence; a significant minority have persistent or adult-onset disease
- Severity fluctuates with environmental triggers, infection, and stress
- Early effective control may reduce (though does not eliminate) progression along the atopic march
- Biologics/JAK inhibitors have substantially improved outcomes for the moderate-severe refractory population previously limited to immunosuppressants (ciclosporin, methotrexate) or phototherapy alone
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