In New Zealand, eczema is managed by dermatologists. Eczema is a chronic, relapsing inflammatory skin disease driven by a defective epidermal barrier and a type 2 immune response that produces intense itch, dry skin, and scaling rashes. The term most often refers to atopic dermatitis, the dominant form, which affects roughly 20% of children and 2-10% of adults in high-income countries and an estimated 204 million people worldwide.
Eczema is the everyday term for atopic dermatitis (ICD-10: L20), the most common chronic inflammatory dermatosis worldwide, with the broader ICD-10 category L30 covering other and unspecified dermatitis subtypes. Pathologically it is a barrier-immune disease: filaggrin loss-of-function mutations (carried by 10-50% of moderate-to-severe patients of European ancestry), ceramide depletion, and increased transepidermal water loss break the stratum corneum, while a T-helper 2 (Th2) skewed immune response releases interleukin-4, interleukin-13, and interleukin-31 — the cytokines that drive itch, lichenification, and Staphylococcus aureus overgrowth. Disease severity is graded with validated tools such as the Eczema Area and Severity Index (EASI), the Scoring Atopic Dermatitis (SCORAD) index, and the validated Investigator Global Assessment for atopic dermatitis (vIGA-AD). Eczema is also an umbrella label for related dermatitides — contact dermatitis (irritant and allergic), dyshidrotic eczema, nummular eczema, seborrheic dermatitis, and stasis dermatitis — which share scaling, erythema, and pruritus but differ in trigger, distribution, and mechanism.
The key symptoms of Eczema are: Intense, persistent itch (pruritus) that worsens at night and is severe enough to disturb sleep in roughly 60% of moderate-severe patients — the cardinal symptom and the one most strongly tied to quality-of-life impairment., Dry, rough, scaly skin (xerosis) with reduced elasticity from increased transepidermal water loss, present even between flares., Erythematous papules and papulovesicles that may weep clear fluid during acute flares, classically on the cheeks and scalp in infants., Lichenification — thickened, leathery skin with exaggerated skin markings — over chronically scratched flexural surfaces such as the antecubital and popliteal fossae, neck, and ankles in older children and adults., Excoriations, fissures, and crusting from repeated scratching, with frequent secondary bacterial infection (golden crust suggests Staphylococcus aureus impetiginization)., Age-dependent distribution: cheeks, scalp, and extensor surfaces in infants under 2; flexural creases of elbows, knees, wrists, and ankles in older children; hands, eyelids, and neck in adults., Sleep disturbance, irritability, and daytime fatigue from nocturnal itch — measured on validated scales such as the Patient-Oriented Eczema Measure (POEM)..
Eczema is a clinical diagnosis — no single laboratory test confirms it. Dermatologists and primary-care clinicians use the UK Working Party refinement of the Hanifin-Rajka criteria: an itchy skin condition plus three or more of (1) history of flexural involvement, (2) personal or family history of atopy, (3) generally dry skin in the last year, (4) onset before age 2, or (5) visible flexural dermatitis. Severity is graded with the Eczema Area and Severity Index (EASI), SCORAD, the Patient-Oriented Eczema Measure (POEM), and the vIGA-AD. Patch testing is indicated when distribution suggests allergic contact dermatitis (eyelids, hands, perianal area, isolated regions that flare with specific products) or when established atopic dermatitis fails to respond to standard therapy. Skin biopsy is rarely needed but is performed to exclude cutaneous T-cell lymphoma, psoriasis, or other mimickers in atypical or treatment-resistant adult cases. Total serum IgE is elevated in 70-80% of moderate-severe patients but is non-specific. Targeted food-allergy testing (specific IgE or skin-prick) is reserved for infants with moderate-severe eczema and a convincing history of immediate reactions — broad untargeted panels generate false positives and drive harmful elimination diets. The decisive differentials to keep in mind are scabies in any new-onset severely itchy eruption (especially in households with multiple itchy members), psoriasis when plaques are well-demarcated with silvery scale, contact dermatitis when distribution maps to an exposure, and cutaneous lymphoma in long-standing adult disease that fails escalating therapy.
Eczema is a chronic relapsing-remitting disease, but most childhood cases improve significantly with age — roughly 50-60% of children meet criteria for clinical remission by adolescence, and 30-40% have persistent or recurrent disease in adulthood. Predictors of persistence include early severe disease, filaggrin loss-of-function variants, sensitization to multiple allergens, and onset before 3 months of age. With current therapy, well-controlled patients achieve clear or almost-clear skin for most of the year, sleep well, and have minimal impact on school or work. Biologic-treated moderate-severe patients achieve EASI-75 in roughly 50-70% at week 16 and many maintain that response over years on continued dosing. Eczema itself does not shorten life, but the disease carries measurable burden: increased risk of depression (about 1.3-1.5 fold), anxiety, suicidal ideation in severe disease, growth impairment in poorly controlled children, and a 2-3 fold increased risk of cutaneous infection. The atopic march — progression from eczema to food allergy, asthma, and allergic rhinitis — affects 60-80% of moderate-severe pediatric patients, reinforcing the case for early effective barrier and inflammation control.
Refer to dermatology when first-line topical therapy fails after 4-6 weeks, when more than 10% of body surface area is involved, when sleep is regularly disrupted, when there are repeated skin infections, when systemic therapy or phototherapy is being considered, or when there is diagnostic uncertainty versus psoriasis, cutaneous T-cell lymphoma, or scabies. Pediatric patients with moderate-severe disease benefit from combined dermatology-allergy review to address food allergy, asthma, and growth.
Find specialists →An acute eczema flare typically responds within days of restarting topical corticosteroid or calcineurin inhibitor: visible redness drops within 3-5 days, itch within 5-10 days, and most flares resolve within 2-4 weeks. Lichenified plaques take longer — 4-12 weeks of consistent therapy plus emollient. Once dupilumab is started, half of responders see meaningful itch reduction within 2-4 weeks and peak response is reached around week 16; tralokinumab and lebrikizumab follow similar kinetics. Oral JAK inhibitors act fastest, with measurable itch relief in 24-48 hours. Proactive maintenance (twice-weekly topical anti-inflammatory plus daily emollient) is continued indefinitely to prevent relapse.
Exercise is encouraged and improves quality of life despite the irritant effect of sweat. Wear breathable cotton or moisture-wicking fabrics, shower lukewarm within an hour, and reapply emollient afterwards. Chlorinated pools are tolerated by most; rinse and moisturize immediately after swimming. Avoid prolonged hot showers and saunas during active flares.
Look for a board-certified dermatologist with experience prescribing biologics (dupilumab, tralokinumab) and oral JAK inhibitors, access to patch testing for atopic patients with possible contact allergy, and a clinic that uses validated severity tools (EASI, POEM, vIGA-AD) at every visit. Continuity matters — eczema is a long-game disease; a clinician who knows your trigger profile and treatment history will out-perform episodic specialist visits.
Medically reviewed by AIHealz Medical Editorial Board · May 12, 2026
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