(Circulation. 2000;101:2335.)
© 2000 American Heart Association, Inc.
Editorials |
From Magee-Womens Research Institute, and the Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Pittsburgh, Pa.
Correspondence to James M. Roberts, MD, Magee-Womens Research Institute, 204 Craft Ave, Suite 610, Pittsburgh, PA 15213. E-mail rsijmr@mail.magee.edu
Key Words: Editorials pregnancy angiotensin receptors hypertension
Preeclampsia is a pregnancy-specific disorder that presents major health problems for mothers and their babies. It is a major cause of maternal mortality, especially in developing countries, where it may account for 80% of maternal deaths.1 Even in developed countries, perinatal mortality is increased 5-fold. The last figure is especially tragic. Many of these infant deaths are secondary to iatrogenic prematurity, because the management remains as it has for the last 100 years (early delivery to terminate the process). Understandably, preeclampsia has been a major target of research to improve pregnancy outcome, yet it remains an enigmatic "disease of theories." Nonetheless, in the last 10 years, an approach to understanding the disorder that addresses features other than simply the accompanying hypertension has rapidly accelerated understanding.2 In this issue of Circulation, Dechend and colleagues3 present another in their fascinating series of observations demonstrating that preeclamptic women manifest agonistic antibodies to angiotensin-1 (AT1) receptors. They demonstrate that these antibodies have the capability to activate the production of tissue factor by vascular smooth muscle cells in vitro. How does this observation fit into emerging concepts of the pathogenesis of preeclampsia?
Eclampsia was described nearly 2000 years ago as seizures
occurring during pregnancy that abated with delivery. It was not until
the turn of this century that it was recognized that increased blood
pressure and proteinuria accompanied, and in most cases preceded,
eclampsia, hence "preeclampsia."4 With this
recognition, it was rapidly evident that these signs, even
unaccompanied by seizures, signaled a disorder
This article has been cited by other articles:
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R. Dechend, P. Gratze, G. Wallukat, E. Shagdarsuren, R. Plehm, J.-H. Brasen, A. Fiebeler, W. Schneider, S. Caluwaerts, L. Vercruysse, et al. Agonistic Autoantibodies to the AT1 Receptor in a Transgenic Rat Model of Preeclampsia Hypertension, April 1, 2005; 45(4): 742 - 746. [Abstract] [Full Text] [PDF] |
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R. Dechend, C. Viedt, D. N. Muller, B. Ugele, R. P. Brandes, G. Wallukat, J.-K. Park, J. Janke, P. Barta, J. Theuer, et al. AT1 Receptor Agonistic Antibodies From Preeclamptic Patients Stimulate NADPH Oxidase Circulation, April 1, 2003; 107(12): 1632 - 1639. [Abstract] [Full Text] [PDF] |
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