Fox Adam T, Sasieni Peter, du Toit George, Syed Huma, Lack Gideon
King's College London, the Medical Research Council and Asthma UK Centre in Allergic Mechanisms of Asthma, Division of Asthma, Allergy and Lung Biology, Guy's and St Thomas' National Health Service Foundation Trust, London, United Kingdom.
J Allergy Clin Immunol. 2009 Feb;123(2):417-23. doi: 10.1016/j.jaci.2008.12.014.
Most children with peanut allergy (PA) react on first known oral exposure to peanut. Recent data suggest cutaneous exposure as a route of sensitization.
This study aimed to establish the relevant route of peanut exposure in the development of allergy.
Questionnaires were administered to children with PA and to high-risk controls (with egg allergy) and controls without allergy. Questionnaires were completed before subjects were aware of their PA status, avoiding recall bias. Questionnaires recorded maternal peanut consumption during pregnancy, breast-feeding, and the first year of life. Peanut consumption was determined among all household members, allowing quantification of environmental household exposure (household peanut).
Median weekly household peanut in the 133 PA cases was significantly elevated (18.8 g) compared with 150 controls without allergy (6.9 g) and 160 high-risk controls (1.9 g). There were no differences in infant peanut consumption between groups. Differences in maternal peanut consumption during pregnancy (and lactation) were significant but become nonsignificant after adjusting for household peanut. A dose-response relationship was observed between environmental (nonoral) peanut exposure and the development of PA, which was strongest for peanut butter. Early oral exposure to peanut in infants with high environmental peanut exposure may have had a protective effect against the development of PA.
High levels of environmental exposure to peanut during infancy appear to promote sensitization, whereas low levels may be protective in atopic children. No effect of maternal peanut consumption during pregnancy or lactation is observed, supporting the hypothesis that peanut sensitization occurs as a result of environmental exposure.
大多数花生过敏（PA）儿童在首次已知口服接触花生时会产生反应。近期数据表明皮肤接触是一种致敏途径。
本研究旨在确定花生暴露在过敏发展过程中的相关途径。
对患有PA的儿童、高危对照（对鸡蛋过敏）和无过敏对照进行问卷调查。在受试者知晓自己的PA状态之前完成问卷，以避免回忆偏差。问卷记录了母亲在孕期、哺乳期和婴儿一岁时的花生摄入量。确定所有家庭成员的花生摄入量，以便量化家庭环境中的花生暴露量（家庭花生）。
133例PA病例的家庭花生周摄入量中位数（18.8克）显著高于150名无过敏对照（6.9克）和160名高危对照（1.9克）。各组婴儿花生摄入量无差异。孕期（及哺乳期）母亲花生摄入量的差异显著，但在调整家庭花生暴露量后变得不显著。观察到环境（非口服）花生暴露与PA发生之间存在剂量反应关系，其中花生酱的这种关系最强。在家庭花生暴露量高的婴儿中，早期口服花生可能对PA的发生有保护作用。
婴儿期环境中高水平的花生暴露似乎会促进致敏，而低水平暴露可能对特应性儿童有保护作用。未观察到孕期或哺乳期母亲食用花生的影响，支持花生致敏是环境暴露所致的假说。
