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坏死性小肠结肠炎的发病机制与预防。

Pathogenesis and prevention of necrotizing enterocolitis.

机构信息

Centre for Reviews and Dissemination, Hull York Medical School, University of York, Heslington, York, UK.

出版信息

Curr Opin Infect Dis. 2011 Jun;24(3):183-9. doi: 10.1097/QCO.0b013e328345d5b5.

Abstract

PURPOSE OF REVIEW

Necrotizing enterocolitis (NEC) remains the most common serious acquired gastrointestinal disorder affecting preterm infants. Here we review recent advances in our understanding of the pathogenesis of this multifactorial condition and consider the implications for practice and research.

RECENT FINDINGS

NEC is an important cause of mortality and serious morbidity in preterm infants. The risk is inversely proportional to gestational age and weight at birth. Fetal growth restriction and compromise may be additional specific risk factors. NEC, particularly severe NEC requiring surgical intervention and NEC with invasive infection, is associated with acute morbidity and mortality and adverse neurodevelopmental outcomes. The principal modifiable postnatal risk factors for NEC in preterm infants relate to enteral feeding practices including formula milk feeding, early and rapid advancement of enteral feed volumes, and exposure to H2-receptor antagonists.

SUMMARY

Our understanding of the pathogenesis of this condition remains incomplete. With the exception of feeding with human milk, only limited evidence is currently available to support interventions to prevent NEC. Promising strategies that merit further evaluation in randomized controlled trials include the use of prebiotics and probiotics and the avoidance of exposure to H2-receptor antagonists.

摘要

目的综述

坏死性小肠结肠炎(NEC)仍然是影响早产儿最常见的严重获得性胃肠道疾病。本文综述了我们对这种多因素疾病发病机制的最新认识,并探讨了其对实践和研究的意义。

最近的发现

NEC 是早产儿死亡和严重发病率的重要原因。风险与胎龄和出生体重成反比。胎儿生长受限和损害可能是另外的特定危险因素。NEC,尤其是需要手术干预的严重 NEC 和伴有侵袭性感染的 NEC,与急性发病率和死亡率以及不良神经发育结局相关。早产儿发生 NEC 的主要可改变的产后危险因素与肠内喂养实践有关,包括配方奶喂养、早期和快速增加肠内喂养量以及暴露于 H2 受体拮抗剂。

总结

我们对该疾病发病机制的认识仍然不完整。除了母乳喂养外,目前仅有限的证据支持预防 NEC 的干预措施。值得进一步在随机对照试验中评估的有前途的策略包括使用益生元和益生菌以及避免暴露于 H2 受体拮抗剂。

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