Atopic March, Skin Barrier Dysfunction, and Prevention Strategies in Atopic Dermatitis

The talk reviews the atopic march, describing how atopic dermatitis often begins in infancy and can precede food allergy, asthma, allergic rhinitis, and other allergic disease. The speaker explains evidence that skin barrier dysfunction, especially filaggrin-related abnormalities and early immune activation in even non-lesional skin, can drive systemic allergic responses through increased antigen penetration, Th2 inflammation, and alarmin release. He highlights risk factors such as early persistent or severe eczema, polysensitization, parental atopy, skin barrier defects, and environmental triggers. Prevention strategies are discussed, including emollients, topical anti-inflammatories, early dietary approaches, microbiome manipulation, and targeting type 2 inflammation. However, the evidence for emollients alone is mixed: smaller studies showed benefit, but larger trials often did not, possibly because treatment started too late, adherence was low, and inflammation may already be present before visible eczema. Studies using early intensive topical steroids reduced food allergy but raised safety concerns, including growth retardation. Multi-omic and lipid studies suggest that atopic dermatitis with food allergy may represent a distinct endotype with disorganized, short-chain lipids and greater immune activation. Overall, the speaker concludes that skin moisturization is important but unlikely to prevent the atopic march alone; combined anti-inflammatory treatment and potentially systemic biologics may be needed, along with more precision-medicine approaches to identify who will benefit from each intervention.