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首页> 外文期刊>Annals of allergy, asthma, and immunology >Relationship between childhood atopy and wheeze: what mediates wheezing in atopic phenotypes?
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Relationship between childhood atopy and wheeze: what mediates wheezing in atopic phenotypes?

机译:儿童特应性与喘息之间的关系:特应性表型由什么介导喘息?

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BACKGROUND: The nature of the relationship between childhood wheeze and atopy remains uncertain. OBJECTIVE: To characterize childhood wheeze among atopic phenotypes in a longitudinal birth cohort study. METHODS: A whole population birth cohort (N = 1,456) was recruited in 1989. Children were seen at birth and at 1, 2, 4, and 10 years of age to obtain information on asthma and allergic disease development and relevant risk factors for these states. Skin prick testing at ages 4 (n = 980) and 10 (n = 1,036) years was used to define atopic phenotypes. Wheezing in these states was characterized, and logistic regression was used to identify independent risk factors for wheeze onset in different atopic phenotypes. RESULTS: Wheeze ever occurred in 37% of never atopics, 38% of early childhood atopics, 65% of chronic childhood atopics, and 52% of delayed childhood atopics. Chronic childhood atopics had significant wheezing morbidity and bronchial hyperresponsiveness. Their wheezing was associated with male sex, early eczema, family history of eczema, and early tobacco exposure. Never atopic wheeze was related to maternal asthma, parental smoking, and respiratory tract infections. Exclusive breastfeeding protected against early childhood atopic wheeze. Maternal asthma, family history of urticaria, and dog ownership increased delayed childhood atopic wheeze. CONCLUSIONS: In many respects, chronic childhood atopy is the atopic phenotype associated with the most significant forms of childhood wheezing. In such children, heritable drive, allergens, and synergy with other environmental triggers seem to be crucial determinants of wheeze onset. Where such sensitization is absent, numerous environmental factors plus genetic predisposition may assume importance for wheezing.
机译:背景:儿童喘息与特应性之间关系的性质仍不确定。目的:在纵向出生队列研究中表征特应性表型中的儿童喘息。方法:于1989年招募了整个人口的出生队列(N = 1456)。在出生时,1、2、4和10岁时对儿童进行了观察,以获取有关哮喘和过敏性疾病发展的信息以及相关的危险因素状态。使用4岁(n = 980)和10岁(n = 1,036)岁的皮肤点刺测试来定义特应性表型。对这些状态下的喘息进行了表征,并采用逻辑回归分析确定了不同特应性表型引起喘息发作的独立危险因素。结果:37%的永无特应性,38%的儿童早期特应性,65%的慢性儿童特应性和52%的儿童特应性迟发性喘息。儿童慢性特应性哮喘有明显的喘息发病率和支气管高反应性。他们的喘息与男性,早期湿疹,湿疹家族史和早期吸烟有关。特应性喘息从未与母亲哮喘,父母吸烟和呼吸道感染有关。纯母乳喂养可防止儿童早期特应性喘息。孕产妇哮喘,荨麻疹家族史和犬只所有权增加会延迟儿童特应性喘息。结论:在许多方面,慢性儿童特应性表型是与儿童哮喘最重要形式相关的特应性表型。在这类儿童中,遗传性驱动力,过敏原以及与其他环境触发因素的协同作用似乎是喘息发作的关键决定因素。在缺乏这种致敏的地方,许多环境因素加上遗传易感性可能对喘息起着重要作用。

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