THE DEVELOPMENT AND PREDICTION OF ATOPY IN HIGH-RISK CHILDREN - FOLLOW-UP AT AGE 7 YEARS IN A PROSPECTIVE RANDOMIZED STUDY OF COMBINED MATERNAL AND INFANT FOOD ALLERGEN AVOIDANCE

Background: The natural history of allergic disease and its potential for prevention merit close examination because of the explosive worldw ide increase in the prevalence and morbidity of atopic disorders. This study examines the development of atopy at age 7 years in 165 childre n in a high-risk cohort, previously reported from birth to age 4 years . Methods: In this prospective, randomized controlled study of food al lergen avoidance in infancy, the prophylactic-treated group consisted of infants whose mothers avoided cow's milk; egg, and peanut during th e last trimester of pregnancy and lactation and who, themselves, avoid ed cow's milk until age 1 year (casein hydrolysate supplementation bef ore age 1), egg until age 2 years, and peanut and Fish until age 3 yea rs. The control group consisted of maternal/infant pairs who followed standard feeding practices. Results: Despite a significant reduction i n food allergy and milk sensitization before age 2 years, none of the following differed between the groups at age 7 years: food allergy, at opic dermatitis, allergic rhinitis, asthma, any atopic disease, lung f unction, food or aeroallergen sensitization, serum IgE level, or prese nce of nasal eosinophils or nasal basophilic cells. Children with food allergy by 4 years evidenced higher 7-year (current) prevalences of a llergic rhinitis and asthma (p < 0.01). Atopic diseases/parameters at age 7 years were shown, by multivariate analysis (p < 0.05), to be ass ociated with several genetic and environmental risk factors (male gend er, maternal nonwhite ethnicity and asthma, and household smoking), as well as predictive atopic markers during infancy (elevated serum IgE level; egg cow's milk, and peanut sensitization; and nasal eosinophils and nasal basophilic cells). Conclusions: These findings help to: (1) elucidate the natural history of atopic disease in high-risk children ; (2) document the progression of allergy from atopic dermatitis, food allergy, and food sensitization to respiratory allergy and aeroallerg en sensitization despite food allergy prevention in infancy; (3) ident ify allergy predictive markers; and (4) expand our appreciation of the interactions of genetic and environmental factors in the development of atopy.