BACKGROUND: Large, prospective population-based studies on clinical course, development of tolerance, and risk for other atopy in children with cow's milk allergy (CMA) are lacking. OBJECTIVE: We investigated the development of tolerance and the risk for asthma, rhinoconjunctivitis, atopic dermatitis, and sensitization in children with CMA followed to school age. METHODS: We followed 118 children with CMA until recovery and repeatedly measured their sensitization to cow's milk (CM). At age 8.6 years, 94 allergic subjects and 80 control subjects from the same cohort were studied for atopic diseases and sensitization. In addition, the parents of 12 allergic subjects and 26 control children returned a questionnaire on atopy, respectively. RESULTS: IgE-mediated CMA was detected in 86 (73%) children; at age 8.6 years, 13 (15%) had persistent CMA. All children with IgE-negative CMA were tolerant by age 5.0 years (P < .0001). Risk factors for persistent CMA at age 2.0 years were sensitization to CM at age 1.6 years (odds ratio, 6.3; 95% CI, 2.6-15.2), urticaria at diagnostic challenge (odds ratio, 3.3; 95% CI, 1.4-7.8), CM exposure at the maternity hospital (odds ratio, 3.2; 95% CI, 1.4-7.8), and early sensitization to egg (odds ratio, 2.8; 95% CI, 1.2-6.6). By age 8.6 years, children with IgE-positive CMA more frequently had asthma (31% vs 13%, P < or = .01), rhinoconjunctivitis (66% vs 21%, P < or = .001), atopic eczema (81% vs 26%, P < or = .001), and sensitization to any allergen (88% vs 39%, P < or = .001) than control subjects. CMA and family history of atopy were independent risk factors for atopic diseases, and CMA was also a risk factor for sensitization to inhalant allergens. CONCLUSION: IgE-mediated CMA often persists to school age and is a risk factor for other atopy; non-IgE-mediated CMA, by contrast, is a benign infantile condition.
BACKGROUND: Large, prospective population-based studies on clinical course, development of tolerance, and risk for other atopy in children with cow's milk allergy (CMA) are lacking. OBJECTIVE: We investigated the development of tolerance and the risk for asthma, rhinoconjunctivitis, atopic dermatitis, and sensitization in children with CMA followed to school age. METHODS: We followed 118 children with CMA until recovery and repeatedly measured their sensitization to cow's milk (CM). At age 8.6 years, 94 allergic subjects and 80 control subjects from the same cohort were studied for atopic diseases and sensitization. In addition, the parents of 12 allergic subjects and 26 control children returned a questionnaire on atopy, respectively. RESULTS: IgE-mediated CMA was detected in 86 (73%) children; at age 8.6 years, 13 (15%) had persistent CMA. All children with IgE-negative CMA were tolerant by age 5.0 years (P < .0001). Risk factors for persistent CMA at age 2.0 years were sensitization to CM at age 1.6 years (odds ratio, 6.3; 95% CI, 2.6-15.2), urticaria at diagnostic challenge (odds ratio, 3.3; 95% CI, 1.4-7.8), CM exposure at the maternity hospital (odds ratio, 3.2; 95% CI, 1.4-7.8), and early sensitization to egg (odds ratio, 2.8; 95% CI, 1.2-6.6). By age 8.6 years, children with IgE-positive CMA more frequently had asthma (31% vs 13%, P < or = .01), rhinoconjunctivitis (66% vs 21%, P < or = .001), atopic eczema (81% vs 26%, P < or = .001), and sensitization to any allergen (88% vs 39%, P < or = .001) than control subjects. CMA and family history of atopy were independent risk factors for atopic diseases, and CMA was also a risk factor for sensitization to inhalant allergens. CONCLUSION: IgE-mediated CMA often persists to school age and is a risk factor for other atopy; non-IgE-mediated CMA, by contrast, is a benign infantile condition.
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