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Atopic Dermatitis

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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. Atopic dermatitis skin barrier and immune dysfunction

⭐ 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 GroupMorphologyDistribution
    Infantile (0-2 yrs)Vesicles, papules, oozing, crusting; acuteFace (cheeks, forehead, chin), scalp, extensor surfaces; spares diaper area. 📌 Face, Extensors, Scalp (FES)
    Childhood (2-12 yrs)Lichenified plaques, papules; subacute/chronicFlexural areas (antecubital, popliteal fossae), wrists, ankles, neck.
    Adult (>12 yrs)Lichenification, dry, fissured skin; chronicFlexures, 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.
  • 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).

Topical Steroid Potency Comparison by Class

  • 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.

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