Abstract
Preeclampsia (PE) is an important, common, and dangerous complication of pregnancy; it causes maternal and perinatal illness and is responsible for a high proportion of maternal and infant deaths. PE is associated with increased blood pressure and proteinuria, with a whole host of other potentially serious complications in the mother and fetus. The maternal syndrome in PE is primarily that of generalized dysfunction of the maternal endothelium, and this generalized endothelial dysfunction appears to be part of an exaggerated systemic inflammatory response that involves maternal leukocytes and proinflammatory cytokines. This review examines evidence that points to a significant role for the maternal immune system; inadequate trophoblast invasion of spiral arteries initiates ischemia and hypoxia in the placenta, resulting in an increased release of proinflammatory cytokines in the placenta. Placental ischemia and hypoxia also cause the enhanced release of trophoblast microparticles into the maternal circulation which stimulates increased induction of proinflammatory cytokines and the activation of maternal endothelial cells. This activation results in a systemic, diffuse endothelial cell dysfunction which is the fundamental pathophysiological feature of this syndrome. Recent evidence also supports important roles for proinflammatory cytokines in hypertension, proteinuria, and edema which are characteristic features of PE.