Zeiger R S, Heller S
Department of Allergy, Kaiser Permanente Medical Center, San Diego, CA 92111, USA.
J Allergy Clin Immunol. 1995 Jun;95(6):1179-90. doi: 10.1016/s0091-6749(95)70074-9.
The natural history of allergic disease and its potential for prevention merit close examination because of the explosive worldwide increase in the prevalence and morbidity of atopic disorders. This study examines the development of atopy at age 7 years in 165 children in a high-risk cohort, previously reported from birth to age 4 years.
In this prospective, randomized, controlled study of food allergen avoidance in infancy, the prophylactic-treated group consisted of infants whose mothers avoided cow's milk, egg, and peanut during the last trimester of pregnancy and lactation and who, themselves, avoided cow's milk until age 1 year (casein hydrolysate supplementation before age 1), egg until age 2 years, and peanut and fish until age 3 years. The control group consisted of maternal/infant pairs who followed standard feeding practices.
Despite a significant reduction in food allergy and milk sensitization before age 2 years, none of the following differed between the groups at age 7 years: food allergy, atopic dermatitis, allergic rhinitis, asthma, any atopic disease, lung function, food or aeroallergen sensitization, serum IgE level, or presence of nasal eosinophils or nasal basophilic cells. Children with food allergy by 4 years evidenced higher 7-year (current) prevalences of allergic rhinitis and asthma (p < 0.01). Atopic diseases/parameters at age 7 years were shown, by multivariate analysis (p < 0.05), to be associated with several genetic and environmental risk factors (male gender, 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).
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 aeroallergen sensitization despite food allergy prevention in infancy; (3) identify allergy predictive markers; and (4) expand our appreciation of the interactions of genetic and environmental factors in the development of atopy.
由于全球范围内特应性疾病的患病率和发病率呈爆发式增长，过敏性疾病的自然史及其预防潜力值得密切研究。本研究调查了一个高危队列中165名儿童在7岁时特应性的发展情况，该队列此前已报道过从出生到4岁的情况。
在这项关于婴儿期避免食物过敏原的前瞻性、随机、对照研究中，预防性治疗组的婴儿母亲在妊娠晚期和哺乳期避免食用牛奶、鸡蛋和花生，婴儿自身在1岁前避免食用牛奶（1岁前补充酪蛋白水解物），2岁前避免食用鸡蛋，3岁前避免食用花生和鱼类。对照组由遵循标准喂养方式的母婴对组成。
尽管2岁前食物过敏和牛奶致敏率显著降低，但两组在7岁时以下各项并无差异：食物过敏、特应性皮炎、过敏性鼻炎、哮喘、任何特应性疾病、肺功能、食物或空气过敏原致敏、血清IgE水平，或鼻嗜酸性粒细胞或鼻嗜碱性细胞的存在。4岁时有食物过敏的儿童在7岁时（当前）过敏性鼻炎和哮喘的患病率更高（p < 0.01）。多因素分析显示（p < 0.05），7岁时的特应性疾病/参数与多种遗传和环境风险因素（男性、母亲非白人种族和哮喘、家庭吸烟）以及婴儿期的预测性特应性标志物（血清IgE水平升高、鸡蛋、牛奶和花生致敏、鼻嗜酸性粒细胞和鼻嗜碱性细胞）相关。
这些发现有助于：（1）阐明高危儿童特应性疾病的自然史；（2）记录尽管婴儿期预防了食物过敏，但过敏从特应性皮炎、食物过敏和食物致敏发展到呼吸道过敏和空气过敏原致敏的过程；（3）识别过敏预测标志物；（4）加深我们对遗传和环境因素在特应性发展中相互作用的认识。
