Haram K, Bjørge L, Guttu K
Kvinneklinikken, Haukeland Sykehus.
Tidsskr Nor Laegeforen. 2000 May 10;120(12):1426-31.
Preeclampsia is a progressive, multisystem disorder characterised by hypertension and proteinuria. A body of evidence suggest a genetic basis; it is generally accepted that the underlying pathological processes are in the placenta.
This article is a review of the pathophysiology of preeclampsia based on literature mainly obtained through PubMed and Medline searches.
A poorly perfused placenta, secondary to defective placental invasion of the spiral arteries, may lead to hypoxia and insufficient perfusion and cause release of cytokines which damage endothelial cells and cause dysfunction. Women with preeclampsia have markedly elevated concentrations of triglyceride-rich lipoproteins. Lipid peroxidation also causes endothelial dysfunction and thus contributes to preeclampsia. Placenta is one source of the lipid peroxides. Antioxidant deficiency is also a predisposing factor. Hyperhomocysteinaemia, protein S and protein C deficiency, and activated protein C resistance appear to be involved in the pathophysiology of severe preeclampsia and early onset preeclampsia.
The new information about mechanisms for development of preeclampsia gives a basis for new treatment modalities.
子痫前期是一种以高血压和蛋白尿为特征的进行性多系统疾病。大量证据表明其存在遗传基础；普遍认为潜在的病理过程发生在胎盘。
本文是一篇基于主要通过PubMed和Medline检索获得的文献对子痫前期病理生理学的综述。
由于螺旋动脉胎盘侵入缺陷导致胎盘灌注不良，可能会导致缺氧和灌注不足，并引起细胞因子释放，从而损害内皮细胞并导致功能障碍。子痫前期女性富含甘油三酯的脂蛋白浓度显著升高。脂质过氧化也会导致内皮功能障碍，进而促使子痫前期的发生。胎盘是脂质过氧化物的来源之一。抗氧化剂缺乏也是一个易感因素。高同型半胱氨酸血症、蛋白S和蛋白C缺乏以及活化蛋白C抵抗似乎参与了重度子痫前期和早发型子痫前期的病理生理过程。
关于子痫前期发病机制的新信息为新的治疗方式提供了依据。
