Author(s): Roberts JM, Lain KY
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Abstract Pre-eclampsia is more than pregnancy induced hypertension. The emerging view described in this presentation is that pre-eclampsia is secondary to the interactions of reduced placental perfusion with diverse maternal factors that alter endothelial function. The maternal contribution is from factors that antedate pregnancy and are influenced by the usual metabolic adaptations of pregnancy. The endothelium and other targets for the effects of these interactions are more sensitive to insults during pregnancy because of activation of the inflammatory cascade as a normal part of pregnancy. At least part of the response to reduced placental perfusion may be a fetal adaptive response to attempt to overcome the reduced delivery of nutrients. A reasonable convergence point for the interaction is at the level of oxidative stress. This hypothesis has both encouraging and discouraging corollaries. The diversity of maternal factors argues that there will be no single gene to explain the disorder and no single 'magic bullet' to treat the disorder. However, it is encouraging that the recognition of maternal predisposition to the disorder directs therapy to prevent pre-eclampsia at a specific target in subsets of women. Finally, the suggestion that some of the maternal alterations are due to fetal adaptive responses encourages careful choices of agents and meticulous infant follow up in well planned clinical trials. Copyright 2002 Elsevier Science Ltd. All rights reserved.
This article was published in Placenta
and referenced in Journal of Blood Disorders & Transfusion