Department of Microbiology, Faculty of Medicine, Health Sciences Centre, Kuwait University, Safat, Kuwait.
Med Princ Pract. 2013;22 Suppl 1(Suppl 1):8-19. doi: 10.1159/000354200. Epub 2013 Aug 15.
Preeclampsia (PE) is an important, common, and dangerous complication of pregnancy; it causes maternal and perinatal illness and is responsible for a high proportion of maternal and infant deaths. PE is associated with increased blood pressure and proteinuria, with a whole host of other potentially serious complications in the mother and fetus. The maternal syndrome in PE is primarily that of generalized dysfunction of the maternal endothelium, and this generalized endothelial dysfunction appears to be part of an exaggerated systemic inflammatory response that involves maternal leukocytes and proinflammatory cytokines. This review examines evidence that points to a significant role for the maternal immune system; inadequate trophoblast invasion of spiral arteries initiates ischemia and hypoxia in the placenta, resulting in an increased release of proinflammatory cytokines in the placenta. Placental ischemia and hypoxia also cause the enhanced release of trophoblast microparticles into the maternal circulation which stimulates increased induction of proinflammatory cytokines and the activation of maternal endothelial cells. This activation results in a systemic, diffuse endothelial cell dysfunction which is the fundamental pathophysiological feature of this syndrome. Recent evidence also supports important roles for proinflammatory cytokines in hypertension, proteinuria, and edema which are characteristic features of PE.
子痫前期 (PE) 是妊娠的一种重要、常见且危险的并发症；它会导致母亲和围产儿患病，并导致很大比例的母亲和婴儿死亡。PE 与血压升高和蛋白尿有关，还会导致母亲和胎儿出现一系列其他潜在严重的并发症。PE 中的母体综合征主要是母体内皮细胞的普遍功能障碍，而这种普遍的内皮功能障碍似乎是全身性炎症反应过度的一部分，其中涉及母体白细胞和促炎细胞因子。这篇综述考察了一些证据，这些证据表明母体免疫系统起着重要作用；滋养细胞不能侵入螺旋动脉会引发胎盘的缺血和缺氧，导致胎盘释放更多的促炎细胞因子。胎盘的缺血和缺氧也会导致滋养细胞微颗粒更多地释放到母体循环中，从而刺激更多的促炎细胞因子诱导和母体内皮细胞的激活。这种激活导致全身性弥漫性内皮细胞功能障碍，这是该综合征的基本病理生理学特征。最近的证据还支持促炎细胞因子在高血压、蛋白尿和水肿中的重要作用，这些是 PE 的典型特征。
