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HAEMODYNAMIC CONTRIBUTIONS TO THE PATHOGENESIS OF PREECLAMPSIA AND ECLAMPSIA

Published online by Cambridge University Press:  01 February 2008

IRA M BERNSTEIN*
Affiliation:
Department of Obstetrics and Gynecology and Reproductive Sciences
MARILYN J CIPOLLA
Affiliation:
Department of Obstetrics and Gynecology and Reproductive Sciences Department of Neurology, University of Vermont College of Medicine.
*
Address for correspondence: Ira M. Bernstein MD, Professor and Vice-Chair for Obstetrics, Director of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Smith 407, Fletcher Allen Health Care, 111 Colchester Avenue, Burlington, Vermont 05401-1435 University of Vermont College of Medicine

Extract

Current hypotheses regarding the origins of preeclampsia have focused on the “Two stage model”. This model suggests that the primary steps in the pathophysiologic sequence of preeclampsia are initiated by abnormal placentation including the classic finding of abnormal trophoblast invasion of maternal decidual spiral arteries. The second stage of the sequence includes the elaboration of a single or multiple substances from these disordered placentas which contribute to the generalized maternal systemic illness, eventually manifesting as endothelial injury, hypertension and proteinuria. Recent studies have focused on the role of pro and anti-angiogenic peptides as potential placentally derived aetiologic agents in this pathophysiologic sequence, although other placental products have been highlighted in recent research. Despite the fact that this modeling of preeclampsia has widespread support significant limitations to this hypothesis can be identified.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2008

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