Placental origins of preeclampsia: challenging the current hypothesis.

Preeclampsia is a major contributor to the maternal and neonatal mortality and morbidity.1,2 It is the 2nd largest cause of maternal mortality worldwide and affects 5% to 7% of pregnant women worldwide.3,4 The precise etiopathogenesis of preeclampsia remains to be a subject of extensive research, but it is believed that it is likely to be multifactorial. Nevertheless, it is accepted that it is the presence of the placenta rather than the fetus, which is responsible for development of preeclampsia. Although the placenta plays a crucial role in the development of preeclampsia, the onset, severity, and progression is significantly affected by the maternal response to placentally derived factors and proteins. Therefore, mother and fetus should be taken into account when calculating the risk for preeclampsia. Preeclampsia is generally defined as the development of hypertension and proteinuria after 20 weeks of gestation in a previously normotensive woman,3,4 although different variations of this have been proposed by different groups and organizations. (ACOG, ISSHP, Australian college). It has also been further subdivided into mild, moderate, and severe preeclampsia as well as early and late onset preeclampsia, of which the latter is a more contemporary concept.5 It has been suggested that early (before 34 0 weeks) and late (after 34 0 weeks) onset preeclampsia have different etiologies and therefore a different clinical expression, but it is still a subject of considerable research. There are, however, some basic differences between the 2 groups: