Eczema

Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder characterized by a dysfunctional epidermal barrier and immune dysregulation. The primary pathogenic mechanism involves loss-of-function mutations in the filaggrin (FLG) gene (present in 20-50% of AD patients), which encodes a structural protein essential for keratinocyte differentiation and the formation of the stratum corneum. Deficient filaggrin results in increased transepidermal water loss (TEWL), elevated skin pH, and impaired antimicrobial peptide production, creating an 'outside-in' barrier defect that permits allergen penetration and microbial colonization (particularly Staphylococcus aureus, which colonizes >90% of AD lesional skin). The immune response in AD is biphasic: the acute phase is driven by Th2 cytokines (IL-4, IL-13, IL-31) that promote IgE class switching, eosinophil recruitment, and intense pruritus; the chronic phase involves Th1 cytokines (IFN-gamma) producing epidermal thickening (lichenification). IL-31 is the primary mediator of itch in AD, acting on neural IL-31 receptors to generate the itch-scratch cycle that perpetuates skin damage. The 'atopic march' describes the temporal progression from AD in infancy to allergic rhinitis and asthma in childhood, reflecting systemic Th2 immune polarization initiated by transcutaneous allergen sensitization through the defective skin barrier. The clinician evaluates disease severity using validated tools (SCORAD, EASI), prescribes stepwise therapy from emollients through topical and systemic immunomodulators, and identifies complicating infections.