国际妇产科学杂志 ›› 2019, Vol. 46 ›› Issue (6): 641-644.

• 综述 • 上一篇    下一篇

未足月胎膜早破发病机制研究进展

张赐敏,张龑   

  1. 100191 北京大学第三医院妇产科
  • 收稿日期:2019-06-19 修回日期:2019-08-01 出版日期:2019-12-15 发布日期:2019-12-15
  • 通讯作者: 张龑,E-mail:zhangyan01@126.com E-mail:zhangcimin@126.com
  • 基金资助:
     

Research Progress in the Pathogenesis of Preterm Premature Rupture of Fetal Membranes

ZHANG Ci-min,ZHANG Yan   

  1. Department of Obstetrics and Gynecology,Peking University Third Hospital,Beijing 100191,China
  • Received:2019-06-19 Revised:2019-08-01 Published:2019-12-15 Online:2019-12-15
  • Contact: ZHANG Yan,E-mail:zhangyan01@126.com E-mail:zhangcimin@126.com
  • Supported by:
     

摘要: 未足月胎膜早破(PPROM)是一种常见且棘手的产科并发症,是早产的常见原因,若不能及时处理,会严重威胁母儿生命。在许多低、中等收入国家,PPROM产生的最大影响是早产所导致新生儿死亡。许多因素与PPROM的发生有关,如感染、子宫过度增大、吸烟、遗传相关疾病等,它们所导致胎膜降解和破裂的通路是重叠的。PPROM的发病机制十分复杂,最近的研究表明炎性细胞因子和基质金属蛋白酶(MMPs)的激活、氧化应激和羊膜细胞凋亡是导致PPROM的主要途径。综述PPROM发病机制的研究进展,通过讨论导致胎膜弱化的危险因素以及机制,为降低PPROM发生率提供线索和方法。

关键词: 胎膜早破, 炎症, 氧化性应激, 基质金属蛋白酶类, 细胞凋亡

Abstract: Preterm premature rupture of fetal membranes (PPROM) is a common and troublesome obstetric complications. It causes many preterm births. And if it is not handled in time, it would seriously threaten the mothers and infants. In many low- and middle-income countries, the biggest impact of PPROM is neonatal death caused by premature birth. Many factors are related to the occurrence of PPROM, such as infection, uterine overdistention, smoking and genetic. Their pathways to membrane degradation and ultimate rupture overlap. The etiology and pathogenesis of PPROM are very complicated. Recent investigations identify matrix metalloproteinases (MMPs), amniotic cell apoptosis, and oxidative stress as primary mechanisms in these processes. This article reviews the latest research progresses on the pathogenesis of PPROM. By discussing the risk factors and mechanism of membrane weakening, which can provide clues to reduce the incidence of PPROM.

Key words: Fetal membranes, premature rupture, Inflammation, Oxidative stress, Matrix metalloproteinases, Apoptosis

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