Division of Basic Medical Sciences, St George's University of London, London, UK.
J Pathol. 2010 Aug;221(4):363-78. doi: 10.1002/path.2719.
The success of pregnancy is a result of countless ongoing interactions between the placenta and the maternal immune and cardiovascular systems. Pre-eclampsia is a serious pregnancy complication that arises from multiple potential aberrations in these systems. The pathophysiology of pre-eclampsia is established in the first trimester of pregnancy, when a range of deficiencies in placentation affect the key process of spiral artery remodelling. As pregnancy progresses to the third trimester, inadequate spiral artery remodelling along with multiple haemodynamic, placental and maternal factors converge to activate the maternal immune and cardiovascular systems, events which may in part result from increased shedding of placental debris. As we understand more about the pathophysiology of pre-eclampsia, it is becoming clear that the development of early- and late-onset pre-eclampsia, as well as intrauterine growth restriction (IUGR), does not necessarily arise from the same underlying pathology.
妊娠的成功是胎盘与母体免疫和心血管系统之间无数持续相互作用的结果。子痫前期是一种严重的妊娠并发症,源于这些系统中多种潜在的异常。子痫前期的病理生理学在妊娠的前三个月就已确立,此时胎盘形成的一系列缺陷会影响关键的螺旋动脉重塑过程。随着妊娠进入第三个三个月,螺旋动脉重塑不足以及多种血液动力学、胎盘和母体因素汇聚在一起激活母体的免疫和心血管系统,这些事件可能部分是由于胎盘碎片的脱落增加所致。随着我们对子痫前期病理生理学的了解越来越多,很明显,早发型和晚发型子痫前期以及宫内生长受限(IUGR)的发展不一定源于相同的潜在病理。