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Environmental peanut exposure increases the risk of peanut sensitization in high‐risk children

机译:环境花生暴露会增加高危儿童花生致敏的风险

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Summary Background High household peanut consumption is associated with the development of peanut allergy, especially when peanut allergic cases are compared against atopic controls; thus, environmental peanut exposure (EPE) may be a risk factor for peanut sensitization and allergy. In this study, we explored the relationship between EPE and school‐age peanut sensitization in a population‐based cohort. Methods Maternal bed dust was collected postnatally, and EPE was quantified using a polyclonal peanut ELISA. Peanut sensitization was assessed by specific IgE to peanut extract and sIgE to peanut protein component allergens Ara h 1, 2 or 3?≥?0.35kU/L (primary peanut sensitization). Initial nested case‐control analysis was performed comparing peanut‐sensitized cases against high‐risk controls (matched for parental atopy) (n?=?411) using a conditional regression analysis. This was followed by whole cohort analysis (n?=?1878) comparing EPE against peanut sIgE sensitization at ages 4 and 8?years using generalized estimating equations and against primary peanut sensitization at age 8?years using a logistic regression model. Finally, a subgroup analysis was performed comparing the impact of EPE in peanut‐sensitized vs egg‐sensitized, peanut‐tolerant individuals using logistic regression analysis. Levels of EPE were compared between groups using the Mann‐Whitney U test. Results In the nested case‐control analysis, a higher level of EPE around birth was associated with peanut‐specific IgE sensitization at age 4?years (OR=1.41, 95% CI:1.05‐1.90) and primary peanut sensitization at age 8?years (OR=2.11, 95% CI:1.38‐3.22) compared against high‐risk controls. When the whole BAMSE cohort was assessed, EPE was no longer associated with peanut sensitization; however, on subgroup analysis, EPE was associated with primary peanut sensitization when compared against egg‐sensitized peanut‐tolerant controls with an adjusted odds ratio of 1.44 per unit EPE (95% CI:1.06‐1.94). There was no significant interaction between EPE and FLG loss‐of‐function mutations, egg sensitization at age 4?years, infantile eczema or parental atopy on peanut sensitization. Conclusions Higher levels of environmental exposure to peanut in the first few months of life appear to increase the probability of developing school‐age peanut sensitization in atopic children (based on egg sensitization and parental atopy).
机译:摘要背景技术高家庭花生消耗与花生过敏的发展有关,特别是当花生过敏病例与特应性控制进行比较;因此,环境花生暴露(EPE)可能是花生致敏和过敏的危险因素。在这项研究中,我们探讨了EPE与学龄花生致敏关系的基于人口的队列。方法出现产妇床粉尘,使用多克隆花生ELISA定量EPE。通过特定的IgE对花生提取物和SiGe来评估花生致敏,对花生蛋白组分过敏原ara H 1,2或3?≥?0.35ku / L(初级花生致敏)。使用条件回归分析进行比较对与高风险控制(匹配的父母Atopate)进行比较进行初始嵌套病例控制分析。随后是整个队列分析(n?= 1878),将Epe与花生SiGe致敏在4和8岁以下使用广义估算方程的年份进行比较,以及使用逻辑回归模型的8岁时初级花生敏化。最后,进行了使用Logistic回归分析的对比较PEAE在花生敏化的对蛋清敏化的水的影响的亚组分析。使用Mann-Whitney U测试在组之间比较EPE水平。导致嵌套病例对照分析,出生周围更高水平的EPE与花生特异性的IgE致敏与年龄为4年龄(或= 1.41,95%CI:1.05-1.90)和8岁时的初级花生致敏相关?年(或= 2.11,95%CI:1.38-3.22)与高风险控制相比。当评估整个BAMSE队列时,EPE不再与花生敏化相关;然而,在亚组分析上,与蛋清敏化花生耐受对照进行比较时,EPE与初级花生致敏与每单位EPE每单位EPE的调整率为1.44(95%CI:1.06-1.94)进行比较。 EPE和FLG失去功能突变之间没有显着的相互作用,4岁的鸡蛋致敏于4年,婴儿湿疹或治疗花生致敏的父母的特性。结论生命中最初几个月的花生水平较高,似乎增加了在特应性儿童中发展学龄花生致敏的可能性(基于鸡蛋致敏和父母的特性)。

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