What is atopic dermatitis?

Atopic dermatitis (eczema) is the most common chronic inflammatory skin disease — characterised by intense itch, dry skin and recurring patches of inflamed, weeping or lichenified (thickened) skin. It results from two intersecting defects: skin barrier dysfunction (allowing allergens and irritants to penetrate) and dysregulated type 2 immune inflammation. AD typically begins in early childhood (60% within the first year of life) — but in many patients persists into adolescence and adulthood.

What causes atopic dermatitis?

AD is caused by the interaction of genetic susceptibility (particularly filaggrin gene FLG loss-of-function mutations) and environmental factors. The FLG mutations disrupt the epidermal barrier — reducing natural moisturising factor, raising skin pH, and allowing allergen/irritant penetration. This triggers a type 2 inflammatory response (IL-4, IL-13, IL-31 — causing itch). Environmental factors: early-life antibiotic use; low microbial diversity (hygiene hypothesis); urban living; harsh detergents; and dry climates. Notably, specific food allergies are more often a consequence of AD than a cause.

What is the atopic march?

The atopic march describes the typical progression of allergic diseases in genetically predisposed individuals: (1) Atopic dermatitis in infancy (compromised skin barrier allows transcutaneous allergen sensitisation); (2) Food allergy (sensitised through the skin — IgE-mediated reactions to foods); (3) Allergic rhinoconjunctivitis (hay fever — inhalant allergen sensitisation); (4) Asthma. Not all atopic individuals progress through all stages, but AD increases the risk of each subsequent condition. Early intervention to restore skin barrier (emollients from birth) may prevent the atopic march.

How is atopic dermatitis treated?

Mild AD: regular use of emollients (moisturisers) to restore barrier; topical corticosteroids (TCS) for flares; topical calcineurin inhibitors (tacrolimus, pimecrolimus) for sensitive areas. Moderate AD: higher-potency TCS; phosphodiesterase-4 inhibitors (crisaborole); dupilumab. Severe AD: dupilumab (IL-4Rα mAb); JAK inhibitors (abrocitinib, upadacitinib); lebrikizumab or tralokinumab (anti-IL-13 mAbs). Systemic immunosuppressants (ciclosporin, methotrexate, azathioprine) when biologics are unavailable. Phototherapy (narrowband UVB) for adults.

What is dupilumab and why is it significant?

Dupilumab (Dupixent, Sanofi/Regeneron) — approved since 2017 — was the first targeted biologic for atopic dermatitis and represents a genuine therapeutic revolution. By blocking IL-4Rα (preventing both IL-4 and IL-13 signalling), it addresses the central pathogenic driver of type 2 inflammation. Clinical trials show approximately 75-80% of patients achieve EASI-75 response (75%+ skin clearance) — dramatically better than any previous treatment. It is now also approved for children from 6 months of age. Subcutaneous injection every 2 weeks; excellent safety profile.

How does AD affect children?

In children, severe AD causes: sleep disruption (nocturnal itch — profoundly affecting the whole family); school absenteeism; reduced physical activity; bullying and social exclusion; parental work disruption; and significantly impaired quality of life. Uncontrolled AD in infancy increases risk of subsequent food allergy, asthma and allergic rhinitis (atopic march). Early, aggressive barrier repair and inflammation control are therefore important not only for immediate quality of life but for preventing long-term allergic disease.

How is the mental health impact of AD managed?

Depression affects approximately 20-30% and anxiety approximately 30% of moderate-severe AD patients — driven by chronic pain, sleep loss, disfigurement and social stigma. Effective AD treatment (dupilumab, JAK inhibitors) improves psychological outcomes substantially — treating the skin disease improves mental health. Integrated psychological support — CBT for itch-scratch cycles, sleep hygiene counselling and stigma-focused support — is a recommended part of comprehensive AD management.

Is atopic dermatitis the same as eczema?

"Eczema" is a broader term encompassing several types of inflammatory skin conditions with similar morphology — including atopic dermatitis (the most common), contact dermatitis (allergic and irritant), seborrhoeic dermatitis and others. In common usage, "eczema" is often used interchangeably with "atopic dermatitis." Atopic dermatitis specifically refers to the type associated with the atopic tendency (IgE-mediated sensitisation, association with food allergy, rhinitis and asthma) and typically beginning in early childhood.

How does GMJ News cover atopic dermatitis?

GMJ News covers WHO AD burden data, dupilumab and JAK inhibitor approvals and access, the atopic march, AD in children and the mental health impact. Atopic dermatitis is a significant dermatological condition in Georgia — directly relevant to PHIG's NCD agenda and the Georgian Medical Journal's dermatology and allergy coverage.

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Atopic Dermatitis (Eczema)

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Atopic dermatitis (eczema) — the most common chronic inflammatory skin disease — affects approximately 230 million people globally (including up to 20% of children and 10% of adults) and causes profound suffering through intense pruritus, sleep disruption, skin infection, psychosocial impact and reduced quality of life (WHO). Atopic dermatitis is driven by a type 2 inflammatory pathway (IL-4, IL-13) and skin barrier dysfunction (filaggrin mutations). The biologic therapy revolution — dupilumab (IL-4Rα inhibitor) and JAK inhibitors (abrocitinib, upadacitinib) — has transformed moderate-severe atopic dermatitis management, achieving near-complete skin clearance in the majority of treated patients.

Key messages

230 million people globally

Atopic dermatitis (eczema) — the most common chronic inflammatory skin disease — affects approximately 230 million people globally, including up to 20% of children and 10% of adults, with rising prevalence in LMICs (WHO).

Dupilumab — a transformative biologic

Dupilumab (Dupixent) — an IL-4Rα monoclonal antibody blocking both IL-4 and IL-13 signalling — achieves near-complete skin clearance (EASI-90) in the majority of moderate-severe atopic dermatitis patients, the first true disease-modifying treatment for this condition.

Type 2 inflammation and barrier dysfunction

Atopic dermatitis results from two intersecting defects: skin barrier dysfunction (loss of filaggrin — FLG gene mutations are the strongest genetic risk factor; abnormal lipid composition) allowing allergen penetration; and dysregulated type 2 immune response (Th2 cells, IL-4, IL-13) causing inflammation and itch.

The atopic march

Atopic dermatitis is often the first step in the "atopic march" — the sequential development of allergic diseases: eczema → food allergy → allergic rhinitis → asthma. Preventing skin barrier breakdown in infancy may prevent sensitisation and subsequent allergic diseases.

Profound psychological impact

Chronic pruritus, sleep disruption, disfigurement and social stigma cause depression and anxiety at significantly higher rates in atopic dermatitis patients (approximately 2-3x general population). Sleep disruption from nocturnal itch is a major driver of quality-of-life impairment.

JAK inhibitors expand options

JAK inhibitors (abrocitinib, upadacitinib for adults/adolescents; ruxolitinib cream for mild-moderate) provide additional efficacy options, with rapid itch relief (often within 48 hours). Require blood monitoring for haematological effects and safety screening.

Key statistics

230M

people with atopic dermatitis globally

WHO/EADV

Up to 20%

of children in high-income countries affected

WHO

10%

of adults affected

WHO/EADV

60%

of cases have at least one FLG loss-of-function mutation

Research

Rising

incidence rapidly increasing in LMICs as they industrialise

WHO

2-3x

higher depression/anxiety rates in AD vs general population

WHO/EADV

Atopic dermatitis prevalence (%) in children by country income group — WHO/ISAAC

Source: ISAAC (International Study of Asthma and Allergies in Childhood). Rising in LMICs.

Glossary of key terms

Filaggrin (FLG)
WHO/GeneticsFilaggrin is a structural protein essential for forming the skin's barrier function — compacting corneocytes, binding natural moisturising factor (NMF) and contributing to the skin's acidic pH. Loss-of-function mutations in the FLG gene dramatically increase atopic dermatitis risk; approximately 60% of European AD patients carry FLG mutations.

Type 2 inflammation
WHO/ImmunologyAn immune response pattern driven by Th2 helper cells — producing IL-4, IL-5, IL-13. Central to atopic dermatitis pathogenesis: IL-4 and IL-13 activate the JAK1/TYK2 signalling pathway, driving itch, inflammation and skin barrier disruption. Targeted by dupilumab (anti-IL-4Rα), lebrikizumab and tralokinumab (anti-IL-13), and JAK inhibitors.

Dupilumab (Dupixent)
FDA/EMAA human monoclonal antibody against the IL-4 receptor alpha (IL-4Rα) subunit — blocking both IL-4 and IL-13 signalling. SC injection every 2 weeks. Approved for moderate-severe AD in adults (2017), adolescents (2019) and children ≥6 months (2022). Also approved for asthma, CRSwNP, EoE, PPN.

EASI score
EADV/ClinicalEczema Area and Severity Index — the standard measure of AD severity, combining extent and intensity of four signs (erythema, excoriation, oedema/papulation, lichenification) in four body regions. EASI-50/75/90 responses (50/75/90% improvement) are clinical trial endpoints.

JAK inhibitors (AD)
FDA/EMAAbrocitinib (Cibinqo — JAK1 selective) and upadacitinib (Rinvoq — JAK1 preferential): oral agents approved for moderate-severe AD in adults and adolescents. Provide rapid itch relief (often 24-48 hours). Similar long-term efficacy to dupilumab; require laboratory monitoring and come with FDA boxed warnings (thrombosis, malignancy — though AD-specific risk is likely lower than RA).

Atopic march
WHO/EAACIThe sequential development of allergic diseases in atopic individuals: atopic dermatitis (earliest, often infancy) → food allergy → allergic rhinoconjunctivitis → asthma. The skin barrier defect in AD allows allergen sensitisation, driving subsequent systemic allergic disease. Early skin moisturisation and barrier repair may prevent subsequent sensitisation.