van Beck E, Peeters L L
Department of Obstetrics and Gynecology, University Hospital Maastricht, The Netherlands.
Obstet Gynecol Surv. 1998 Apr;53(4):233-9. doi: 10.1097/00006254-199804000-00021.
The objective of this review was to provide a comprehensive and practical concept on the pathogenesis of preeclampsia on the basis of the currently available scientific evidence. A MEDLINE search was performed of English-language articles published between 1966 and 1997, supplemented with references cited in relevant research articles. Using our data sources, we developed a scheme describing the sequence of events between implantation and the time of manifest clinical disease characterized by generalized endothelial cell dysfunction. A yet unidentified toxic circulating factor released by the ischemic placenta, is held responsible for the impaired endothelial cell function. Particularly, epidemiological studies point to a concept in which immune maladaptation to the fetal allograft plays a key role in causing defective placentation leading to placental ischaemia. The incidence of preeclampsia in sisters and daughters of women who had had preeclampsia is raised. Disease states with vascular involvement, like chronic hypertension and diabetes mellites, are associated with an increased risk for preeclampsia. Recently subclinical abnormalities in hemostasis, metabolism and volume homeostasis have been described in patients with a history of preeclampsia. Placental ischemia secondary to defective placentation, a prerequisite for the development of preeclampsia, has a multifactorial origin consisting of three major components: immune maladaptation, genetic predisposition, and vascular mediated factors. Probably, a summation of these factors will determine whether a pregnant woman is to develop the syndrome. The recently described subclinical abnormalities in hemostasis, metabolism, and vascular function in patients with a history of preeclampsia might give the clinician the opportunity to reduce the recurrence risk by pharmacotherapeutic intervention.
本综述的目的是基于当前可得的科学证据，就子痫前期的发病机制提供一个全面且实用的概念。我们对1966年至1997年间发表的英文文章进行了MEDLINE检索，并补充了相关研究文章中引用的参考文献。利用我们的数据来源，我们制定了一个方案，描述了从着床到以全身内皮细胞功能障碍为特征的明显临床疾病发生之间的一系列事件。一种尚未明确的由缺血胎盘释放的循环毒性因子，被认为是导致内皮细胞功能受损的原因。特别是，流行病学研究指向一种概念，即对胎儿移植物的免疫适应不良在导致胎盘形成缺陷进而导致胎盘缺血中起关键作用。子痫前期患者的姐妹和女儿患子痫前期的几率会升高。伴有血管受累的疾病状态，如慢性高血压和糖尿病，与子痫前期风险增加相关。最近，有子痫前期病史的患者出现了止血、代谢和容量稳态方面的亚临床异常。胎盘形成缺陷继发的胎盘缺血是子痫前期发生的一个先决条件，其起源是多因素的，包括三个主要因素：免疫适应不良、遗传易感性和血管介导因素。这些因素的综合作用可能会决定一名孕妇是否会患上该综合征。最近描述的有子痫前期病史的患者在止血、代谢和血管功能方面的亚临床异常，可能会为临床医生提供通过药物治疗干预降低复发风险的机会。
