A 3-month-old presents with erythematous papulovesicular eruption on the cheeks and extensor surfaces with intense pruritus and a family history of asthma. The most important pathophysiological mechanism in infantile atopic dermatitis is:

• A IgE-mediated mast cell degranulation as the primary initiating event
• B Autoimmune T-cell attack on keratinocytes
• C Deficiency of filaggrin protein leading to impaired skin barrier function with subsequent Th2-skewed inflammation ✓
• D Deficiency of ceramide synthesis causing dry skin only

Explanation

Filaggrin (FLG) gene mutations are the strongest genetic risk factor for atopic dermatitis. Filaggrin deficiency leads to a defective skin barrier (increased TEWL — transepidermal water loss), allowing allergen penetration and microbial colonization (S. aureus), triggering Th2-skewed immune response with IL-4, IL-13, and IgE production. The 'outside-in' hypothesis of barrier dysfunction as the initiating event is now the dominant model. IgE elevation is a consequence, not the primary cause.

Reference: Ghai Essential Pediatrics, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.