Reply| Volume 177, ISSUE 1, P244, July 01, 1997

To the Editors: We are gratified by the interest in our hypothesis expressed by Kilpatrick. Certainly, the suggestions are compatible with the general hypothesis positing heterogeneity in the pathophysiologic mechanisms of preeclampsia. In addition, the observations are compatible with the more specific suggestion that maternal and fetal-placental factors might converge at the point of generating oxidative stress. Platelet activation in response to either free radical–mediated endothelial injury or more directly in the intervillous space in response to oxidative stress would fit well with the observation advanced by B||Aaodis et al. In addition, immune-mediated generation of oxidative stress could provide a nidus for free radical generation, perhaps again in the intervillous space.
Nonetheless, we feel the most important part of our hypothesis is not the specific convergence point but rather the concept that not all preeclampsia is alike. The letter Kilpatrick wrote well demonstrates the implications for research of this hypothesis. We also emphasize that we are not necessarily referring to a maternal or fetal-placental disease but rather to an interaction of fetal-placental and maternal constitutional factors.
James M. Roberts, MD, Roberta B. Ness, MD, MPH, Magee Women's Research Institute and Graduate School of Public Health, University of Pittsburgh, 130 DeSoto St., Pittsburgh, PA
6/8/82736
NO LABEL6/8/82736