van Beek E, Peeters L L
Academisch Ziekenhuis, afd. Obstetrie en Gynaecologie, Maastricht.
Ned Tijdschr Geneeskd. 1997 Jul 12;141(28):1379-84.
The central factor in the pathogenesis of preeclampsia appears to be placental ischaemia which is supposed to be caused by an initial defective placentation. The impaired placental function leads to generalized endothelial cell dysfunction, which in its turn gives rise to hypertension, proteinuria, oedema, thrombocytopenia and hypoperfusion, especially of liver and kidneys. The link between placental ischaemia and endothelial dysfunction could consist of a toxic circulating 'factor X' and the multifactorial origin of the defective placentation. Impaired development of immunological tolerance may lead to an activated immune system during trophoblast invasion which then causes defective placentation. Genetic predisposition and maternal vascular pathology could be modulating factors in this process. The recent finding of latent abnormalities in haemostasis, in metabolism (giving rise to thrombophilia), and in volume homeostasis in patients with a history of preeclampsia in suggestive of an important role of these vascular mediators in the pathogenesis of preeclampsia.
子痫前期发病机制的核心因素似乎是胎盘缺血，推测其由最初的胎盘形成缺陷所致。胎盘功能受损会导致全身内皮细胞功能障碍，进而引发高血压、蛋白尿、水肿、血小板减少以及灌注不足，尤其是肝脏和肾脏的灌注不足。胎盘缺血与内皮功能障碍之间的联系可能包括一种有毒的循环“X因子”以及胎盘形成缺陷的多因素起源。免疫耐受发育受损可能导致滋养层侵入期间免疫系统激活，进而引起胎盘形成缺陷。遗传易感性和母体血管病变可能是这一过程中的调节因素。近期对子痫前期病史患者止血、代谢（导致血栓形成倾向）和容量稳态潜在异常的研究结果表明，这些血管介质在子痫前期发病机制中起着重要作用。
