[The role of endothelium in the pathogenesis of pregnancy-induced hypertension]

Jerzy Heimrath, Andrzej Czekański, Agnieszka Krawczenko, Danuta Duś
Postȩpy Higieny i Medycyny Doświadczalnej 2007, 61: 48-57
Pregnancy-induced hypertension (PIH) is the major cause of maternal and perinatal morbidity. However, the mechanisms responsible for PIH pathogenesis have not yet been fully elucidated. The known risk factors of PIH development are: multiple pregnancy, masculine sex of fetus, very young age of women (below 18 years), advanced age (above 40 years), and obesity of the pregnant woman. In this article an attempt is made to summarize recent knowledge of the pathogenesis of PIH and, particularly, the postulated link between placental ischemia and microvascular dysfunction. The initiating event in PIH has been implicated to be reduced uteroplacental perfusion as a result of abnormal extravillous cytotrophoblast invasion. Focal ischemia and hypoxia, deportation of hypoxemic trophoblast cells, and abnormal expression of various placental biological molecules, particularly the cytokines, are thought to lead to widespread activation/dysfunction of the maternal vascular endothelium. The increased expression of adhesion molecules on activated endothelium intensifies the inflammation process and causes further endothelial injury. The quantitative importance of the various endothelial and humoral factors in mediating PIH symptoms is still unclear. Some of the factors that activate and damage endothelial cells may be of prognostic significance; however, more intensive research should be performed for a precise description of their predictive value.

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