Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8996925 | Medical Hypotheses | 2005 | 8 Pages |
Abstract
Endothelial cell dysfunction is a key feature of the pathogenesis of pre-eclampsia. The cause of the endothelial cell injury is probably multifactorial, but poor placenta perfusion plays a major role. In pre-eclampsia, characteristic pathological lesions in the placenta are fibrin deposits, acute atherosis and thrombosis. The similarity between the lesions of pre-eclampsia and atherosclerosis has led to speculations of a common pathophysiological pathway. An abnormal lipid profile is known to be strongly associated with atherosclerotic cardiovascular disease and has a direct effect on endothelial function. Abnormal lipid metabolism seems important in the pathogenesis of pre-eclampsia too. An elevated plasma lipoprotein (a) concentration is a known risk factor for atherosclerotic cardiovascular disease. In this paper, we discuss three hypotheses about the mechanisms by which lipoprotein (a) may be associated with pre-eclampsia:
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Authors
G.T.R. Manten, Ytje Y. van der Hoek, J. Marko Sikkema, Hieronymus A.M. Voorbij, Ton M. Hameeteman, Gerard H.A. Visser, Arie Franx,