Epidemiology

  • Onset of symptoms usually occurs at 3–6 months of age.
  • Disease often improves with age.

Etiology


Pathophysiology

  • Multifactorial, involving genetic predisposition, immune dysregulation, and environmental factors leading to a defective epidermal barrier.
  • Key genetic factor: Loss-of-function mutations in the filaggrin (FLG) gene are present in up to 30% of patients, impairing skin barrier function and moisture retention.
  • Immune dysregulation: Characterized by a Th2-dominant inflammatory response, leading to increased IgE production and eosinophilia.
  • Barrier dysfunction: A compromised stratum corneum leads to increased transepidermal water loss (TEWL), resulting in dry, itchy skin (xerosis) that is more susceptible to irritants and allergens.

Clinical features

Tip

  • The symptoms of atopic dermatitis are variable and often change in the course of a lifetime. Pruritus and dry skin are usually the main symptoms.
  • Most patients have a history of other atopic disorders
  • Flares with low humidity (eg, winter months) or excessive heat
  • Main symptoms: intense pruritus and dry skin
  • Infantile AD (age < 2 years)
    • Eczema involving the face, head, and extensor surfaces of the extremities that usually spares the diaper area
    • May present initially with features similar to seborrheic dermatitis, e.g., cradle cap
    • Dennie-Morgan fold: increased folds below the eye
      • as a result of eyelid dermatitis
    • Occasionally, lesions appear on the trunk.
  • Childhood AD (age 2–12 years)
    • Eczema: flexural creases (antecubital fossa and popliteal fossa), skin folds, extensor surface of hands
    • Lesions usually become lichenified (thickening of the skin with accentuated skin markings).
  • Adult/adolescent AD (age > 12 years)
    • Lichenified lesions and pruritus of flexor surfaces of the extremities
    • Antecubital fossae are frequently involved.
    • Adult AD may also present as nummular eczema.
  • Associated skin findings in AD
    • Atopic triad: a triad of asthma, allergic rhinitis, and atopic dermatitis that is linked to allergen-triggered IgE-mast cell activation
    • Food allergies
    • Keratosis pilaris: keratinized hair follicles (rough bumps) typically distributed over extensor arms and thighs
    • Hertoghe sign: thinning or loss of the outer third of the eyebrows

Diagnostics

  • Atopy
    • Personal and/or family history
    • Immunoglobulin E reactivity (↑ serum IgE)
    • Comorbid atopic diseases (i.e., asthma, allergic rhinitis, allergic conjunctivitis, and food allergies)

Treatment