Extract

Preeclampsia is a multisystem disorder specific to pregnant women. It remains one of the most important causes of maternal and fetal mortality and morbidity in developed countries (1). Although the pathogenesis of this condition is not fully understood, it is now widely accepted that vascular endothelial cell dysfunction is the final common pathway responsible for the maternal syndrome (2)(3). The underlying pathological changes that lead to the endothelial cell dysfunction remain incompletely understood, but poor placentation has been proposed as a major contributory factor (2)(4)(5). As a result of incomplete or failure of trophoblastic invasion of the spiral arteries, placental ischemia results, leading to the release of one or more factors that are responsible for the damage of the maternal vascular endothelium (5)(6). The normal process of trophoblastic invasion is complete by 20 weeks of gestation. Hence, the initiating placental pathology should exist prior to this stage of pregnancy, long before the onset of the clinical syndrome. Therefore, it might be possible to develop new plasma/serum biochemical markers for identifying subjects at increased risk of developing preeclampsia.

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