国际妇产科学杂志 ›› 2023, Vol. 50 ›› Issue (4): 405-408.doi: 10.12280/gjfckx.20230106

• 产科生理及产科疾病:综述 • 上一篇    下一篇

子痫前期发病机制的研究进展

梁结明, 刘国成()   

  1. 510010 广州,广东省妇幼保健院
  • 收稿日期:2023-02-19 出版日期:2023-08-15 发布日期:2023-08-15
  • 通讯作者: 刘国成,E-mail:hnliuguocheng@126.com
    审校者

Research Progress on the Pathogenesis of Preeclampsia

LIANG Jie-ming, LIU Guo-cheng()   

  1. Guangdong Women and Children Hospital, Guangzhou 510010, China
  • Received:2023-02-19 Published:2023-08-15 Online:2023-08-15
  • Contact: LIU Guo-cheng, E-mail: hnliuguocheng@126.com

摘要:

子痫前期(preeclampsia)发病率高,进展迅速,是一种累及母体多系统的妊娠期高血压综合征。据统计,子痫前期每年可导致全球超过7万孕妇和50万胎儿死亡,给全球的医疗卫生保健系统造成严重的负担。然而,目前子痫前期的发病机制尚未明确,普遍认为子痫前期的发病与胎盘滋养细胞侵袭不足导致子宫-胎盘血管重塑异常及母体系统性炎症反应激活有关。已有大量的研究表明胎盘缺血和缺氧、氧化应激、血管生成与功能失衡、免疫失调、炎症反应、母体心血管功能障碍是子痫前期发病机制的重要组成部分。综述上述方面在子痫前期发病机制中的研究进展,以期从多个方面了解子痫前期的发生、发展,有助于子痫前期的早期诊断和干预,改善母婴结局。

关键词: 先兆子痫, 炎症, 胎盘, 血管重塑, 发病机制

Abstract:

Preeclampsia is a multi-system hypertensive disorder in pregnancy with high morbidity and rapid progress. According to the statistics, preeclampsia causes more than 70 000 maternal deaths and 500 000 fetal deaths in the world annually, imposing a serious burden to the global health care system. However, the pathogenesis of preeclampsia is still unclear. It is generally believed that the development of preeclampsia is related to abnormal uterine-placental vascular remodeling caused by insufficient invasion of placental trophoblast cells and activation of maternal systemic inflammatory response. Numerous studies have demonstrated that placenta ischemia and hypoxia, oxidative stress, angiogenesis and function imbalance, immune disorder, inflammation, maternal cardiovascular dysfunction are important components of the pathogenesis of preeclampsia. This review introduces the research progress on the pathogenesis of preeclampsia from these aspects in an effort to understand the occurrence and development of preeclampsia, provide help for early diagnosis and intervention, and improve the maternal and fetal outcomes.

Key words: Pre-eclampsia, Inflammation, Placenta, Vascular remodeling, Pathogenesis