Abstract
Pre-eclampsia is a pregnancy-specific disorder that has a worldwide prevalence of 5–8%. It is one of the main causes of maternal and perinatal morbidity and mortality globally and accounts for 50 000–60 00 deaths annually, with a predominance in the low- and middle-income countries. It is a multisystemic disorder however its aetiology, pathogenesis and pathophysiology are poorly understood. Recently it has been postulated that it is a two-stage disease with an imbalance between angiogenic and anti-antigenic factors. This review covers the latest thoughts on the pathogenesis and pathology of pre-eclampsia. The central hypothesis is that pre-eclampsia results from defective spiral artery remodelling, leading to cellular ischaemia in the placenta, which in turn results in an imbalance between anti-angiogenic and pro-angiogenic factors. This imbalance in favour of anti-angiogenic factors leads to widespread endothelial dysfunction, affecting all the maternal organ systems. In addition, there is foetal growth restriction (FGR). The exact aetiology remains elusive.
Highlights
Role of the placenta in normal pregnanciesPlacentation and trophoblast invasion of the maternal tissue involves two processes, firstly vascularisation to establish a foeto-placental vascular network, and secondly, invasion of the maternal spiral arteries by the cytotrophoblasts or endovascular trophoblasts (EVTs).[13] At the time of implantation, trophoblastic cells differentiate into cytotrophoblasts and syncytiotrophoblasts
Pre-eclampsia is a pregnancy-specific disorder that has a worldwide prevalence of 5–8%
The central hypothesis is that pre-eclampsia results from defective spiral artery remodelling, leading to cellular ischaemia in the placenta, which in turn results in an imbalance between anti-angiogenic and pro-angiogenic factors
Summary
Placentation and trophoblast invasion of the maternal tissue involves two processes, firstly vascularisation to establish a foeto-placental vascular network, and secondly, invasion of the maternal spiral arteries by the cytotrophoblasts or endovascular trophoblasts (EVTs).[13] At the time of implantation, trophoblastic cells differentiate into cytotrophoblasts and syncytiotrophoblasts. The cytotrophoblasts form the extravillous trophoblasts (EVT), which invade the decidual and junctional zone myometrial segments, the inner third of the myometrium and the spiral arteries. The migration of trophoblasts into the spiral arteries is influenced by a number of factors such as cytokines, growth factors, oxygen tension, and the local cellular environment, for example immune cells such as macrophages and decidual/ uterine natural killer (dNK) cells.[17] The dNK cells are thought to play an important role in regulating placentation but the exact mechanism of action is still unclear.[18]
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