Pathophysiology of preeclampsia

Abstract

Preeclampsia is a complex clinical syndrome, with hypertension representing but one manifestation. Pathogenetically important events in the development of preeclampsia include incomplete trophoblastic invasion of the maternal spiral arteries, poor trophoblastic perfusion, elaboration of a putative endothelial cell toxin, and endothelial cell injury with resulting activation of coagulation, impairment of vasodepressor function, and altered endothelial permeability. These changes lead to the clinical signs and symptoms, which occur relatively late in the course of preeclampsia. The primary immunologic, genetic, and biochemical basis of preeclampsia remains speculative.