von Dadelszen Peter, Magee Laura A
Department of Obstetrics and Gynaecology, Children's and Women's Health Centre of British Columbia and University of British Columbia, Vancouver, British Columbia, Canada.
Acta Obstet Gynecol Scand. 2002 Jul;81(7):642-8.
Preeclampsia/eclampsia remains an important cause of maternal and perinatal morbidity and mortality. Its origins lie in a mismatch between fetoplacental demands and the ability of the uteroplacental arteries to supply those demands, a situation that also arises in normotensive intrauterine growth restriction (the fetal syndrome of preeclampsia in isolation). Why is there this differential response to the same underlying pathology? This review summarises the evidence surrounding a potential trigger for the differential response, namely infection. This builds on the inflammatory model of preeclampsia for which there is increasing support. The evidence for an infectious trigger is principally indirect, linking the similarities between acute atherosis in preeclampsia and atherosclerosis, the increased likelihood of developing cardiovascular disease later in life following a preeclampsia pregnancy, and the association between chronic infection and atherogenesis. Also reviewed is the human and animal model evidence for an infectious trigger for preeclampsia. Perhaps preeclampsia truly is the 'toxemia' of pregnancy.
子痫前期/子痫仍然是孕产妇和围产儿发病及死亡的重要原因。其根源在于胎儿-胎盘需求与子宫胎盘动脉满足这些需求的能力之间不匹配，这种情况在正常血压的胎儿生长受限（孤立的子痫前期胎儿综合征）中也会出现。为什么对相同的潜在病理状况会有这种不同的反应呢？本综述总结了围绕这种不同反应潜在触发因素（即感染）的证据。这是基于子痫前期炎症模型展开的，该模型得到了越来越多的支持。感染触发因素的证据主要是间接的，包括子痫前期急性动脉粥样硬化与动脉粥样硬化之间的相似性、子痫前期妊娠后晚年患心血管疾病可能性增加，以及慢性感染与动脉粥样硬化形成之间的关联。还综述了子痫前期感染触发因素的人体和动物模型证据。也许子痫前期真的是妊娠的“毒血症”。
