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产前因素与哮喘的发展

Prenatal factors and the development of asthma.

作者信息

Kumar Rajesh

机构信息

Division of Allergy and Immunology, Children's Memorial Hospital, Chicago, Illinois, USA.

出版信息

Curr Opin Pediatr. 2008 Dec;20(6):682-7. doi: 10.1097/MOP.0b013e3283154f26.

DOI:10.1097/MOP.0b013e3283154f26
PMID:19005336
Abstract

PURPOSE OF REVIEW

There is increasing evidence that both prenatal and perinatal events influence both allergic diseases and early-life respiratory morbidity.

RECENT FINDINGS

Studies in the last year have suggested that in-utero exposures including tobacco smoke exposure, dietary exposures including vitamin D, and prenatal infection and exposure to microbial products may modulate both atopy and respiratory disease. There have been studies revealing gene x environment interactions between inflammatory pathway genes and in-utero smoke exposure. There have also been studies which have revealed that prenatal exposure to endotoxin may be protective. On the other hand, a recent study also suggested that chorioamnionitis may increase the risk of recurrent wheezing in combination with preterm birth. Finally, two separate large cohort studies evaluated maternal diet in pregnancy and suggested that vitamin D levels may be protective against asthma and wheezing.

SUMMARY

There is epidemiological evidence for multiple prenatal factors impacting early-life respiratory morbidity. The mechanisms of these factors need further investigation and may act via various pathways which include effects on lung development, allergic and nonallergic inflammation, and airway remodeling. It remains to be determined if some of these early-life factors which predispose to wheezing will all translate into increased risk of asthma.

摘要

综述目的

越来越多的证据表明,产前和围产期事件会影响过敏性疾病和早期呼吸道疾病。

最新发现

去年的研究表明,子宫内暴露(包括接触烟草烟雾)、饮食暴露(包括维生素D)、产前感染以及接触微生物产物可能会调节特应性和呼吸道疾病。有研究揭示了炎症途径基因与子宫内烟雾暴露之间的基因-环境相互作用。也有研究表明,产前接触内毒素可能具有保护作用。另一方面,最近一项研究还表明,绒毛膜羊膜炎可能会增加早产合并反复喘息的风险。最后,两项独立的大型队列研究评估了孕期母亲的饮食,结果表明维生素D水平可能对哮喘和喘息具有保护作用。

总结

有流行病学证据表明多种产前因素会影响早期呼吸道疾病。这些因素的作用机制需要进一步研究,可能通过多种途径起作用,包括对肺发育、过敏性和非过敏性炎症以及气道重塑的影响。这些易导致喘息的早期因素是否都会转化为哮喘风险的增加,仍有待确定。

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