Atopic Dermatitis: Definition & Epidemiology - Itchy Beginnings
- Definition: A chronic, relapsing, intensely pruritic inflammatory skin condition.
- Epidemiology:
- Common in childhood; often begins in infancy (first 6 months).
- Global prevalence: 10-20% in children, 1-3% in adults.
- Indian studies show childhood prevalence ranging from 2.7% to over 20% in different regions.
- Strongly linked to personal or family history of atopy (asthma, allergic rhinitis).
- Often the initial step in the 'atopic march'.
⭐ Atopic dermatitis is often the first manifestation of the 'atopic march' (eczema → allergic rhinitis → asthma).
Atopic Dermatitis: Pathophysiology - Barrier Breakdown
- Genetic Factors:
- Key: Filaggrin (FLG) gene mutations impair skin barrier protein formation.
- Other susceptibility loci also contribute.
- Immune Dysregulation:
- Dominant Th2 immune response (e.g., IL-4, IL-13, IL-31).
- Results in ↑ IgE production by B-cells.
- Eosinophilia often present.
- Epidermal Barrier Dysfunction:
- ↓ Ceramides & other lipids, weakening intercellular matrix.
- ↑ Transepidermal Water Loss (TEWL), leading to xerosis.
- Impaired barrier allows easier allergen/microbe penetration.

⭐ Mutations in the filaggrin (FLG) gene are a major predisposing factor for atopic dermatitis, leading to impaired skin barrier function.
Atopic Dermatitis: Clinical Manifestations - The Eczema Map
-
Pruritus: Cardinal symptom; often paroxysmal, worse at night.
-
Age-Dependent Presentation:
Age Group Morphology Distribution Infantile (0-2 yrs) Vesicles, papules, oozing, crusting; acute Face (cheeks, forehead, chin), scalp, extensor surfaces; spares diaper area. 📌 Face, Extensors, Scalp (FES) Childhood (2-12 yrs) Lichenified plaques, papules; subacute/chronic Flexural areas (antecubital, popliteal fossae), wrists, ankles, neck. Adult (>12 yrs) Lichenification, dry, fissured skin; chronic Flexures, hands, face (periorbital, perioral), neck, upper trunk. -
Associated Features:
- Xerosis (dry skin) - universal.
- Dennie-Morgan folds (infraorbital folds).
- Hertoghe's sign (thinning/loss of lateral eyebrows).
- Keratosis pilaris (follicular papules, upper arms, thighs).
- Pityriasis alba (hypopigmented patches, face, neck).
⭐ Infantile atopic dermatitis typically affects the face (cheeks, forehead, chin) and extensor surfaces, characteristically sparing the diaper area.
Atopic Dermatitis: Diagnosis & Management - Soothe & Control
-
Diagnosis:
- Hanifin & Rajka criteria: Pruritus + ≥3 major/minor criteria.
- Major: Typical morphology/distribution (flexural adult; facial/extensor infant), personal/family history of atopy, chronic/relapsing dermatitis.
- Minor: Xerosis, ichthyosis/palmar hyperlinearity/keratosis pilaris, Dennie-Morgan infraorbital fold, ↑serum IgE, early age of onset.
- DDx: Seborrheic dermatitis, contact dermatitis, psoriasis, scabies.
- Hanifin & Rajka criteria: Pruritus + ≥3 major/minor criteria.
-
Management: Stepwise approach.
- Baseline: Emollients (liberal, frequent), trigger avoidance (irritants, allergens).
⭐ Emollients are the cornerstone of atopic dermatitis management, used liberally and frequently even during remission to maintain skin barrier function.
- Mild AD: Low-potency Topical Corticosteroids (TCS) (e.g., hydrocortisone 1%). Topical Calcineurin Inhibitors (TCIs) (e.g., tacrolimus 0.03%, pimecrolimus) for sensitive areas/long-term.
- Moderate AD: Medium-potency TCS (e.g., betamethasone valerate 0.1%). TCIs. Antihistamines for pruritus. Wet wraps for acute flares.
- Severe AD: High-potency TCS (e.g., clobetasol propionate 0.05%). Phototherapy (NB-UVB). Systemic therapy: cyclosporine (3-5 mg/kg/day), azathioprine, methotrexate, biologics (e.g., Dupilumab).

- Complications:
- Eczema herpeticum (HSV superinfection) ⚠️ Medical emergency.
- Impetiginization (bacterial superinfection, e.g., Staph. aureus).
- Erythroderma.
High‑Yield Points - ⚡ Biggest Takeaways
- Type I Hypersensitivity; strong family history of atopy (asthma, allergic rhinitis).
- Classic distribution: Infants (cheeks, extensors), Children/Adults (flexures like antecubital/popliteal fossae).
- Intense pruritus is hallmark, driving the itch-scratch cycle.
- Key features: xerosis (dry skin), lichenification (from chronic scratching).
- Filaggrin (FLG) gene mutations are a major predisposing factor, impairing skin barrier.
- Diagnosis is clinical; Hanifin and Rajka criteria are often used (major & minor).
- Management cornerstones: emollients, topical corticosteroids or calcineurin inhibitors, and trigger avoidance.
Continue reading on Oncourse
Sign up for free to access the full lesson, plus unlimited questions, flashcards, AI-powered notes, and more.
CONTINUE READING — FREEor get the app