Abnormal levels of two molecules found in the blood appear to predict the development of preeclampsia, a life-threatening complication of pregnancy, according to a study by researchers at the National Institute of Child Health and Human Development of the National Institutes of Health and the Beth Israel Deaconess Medical Center, Harvard Medical School, Boston. The findings will appear in the February 12 issue of The New England Journal of Medicine but are scheduled for early release on the Journal's Web site at www.nejm.org, to coincide with a presentation at the Society for Maternal-Fetal Medicine Annual Meeting.

When compared to women who did not have preeclampsia, women who later developed the condition had elevated blood levels of a substance known as soluble fms-like tyrosine kinase 1 (sFlt-1), before their preeclampsia occurred. Conversely, beginning early in their pregnancies, these women had lower levels of a substance known as placental growth factor (PlGF) in the blood than did women who did not develop preeclampsia.

Women who developed preeclampsia also had lower levels of another substance, vascular endothelial growth factor (VEGF). The researchers were unable to use VEGF levels to predict the development of preeclampsia; however, VEGF appears to be important for the healthy functioning of blood vessels, and the researchers theorize that the lack of VEGF as well as PlGF contributes to the health problems resulting from preeclampsia.

Preeclampsia can occur suddenly, without warning. Usually, a pregnant woman with preeclampsia develops dangerously high blood pressure and begins excreting protein in the urine. In some cases, the condition may progress to eclampsia, a series of potentially fatal seizures. Although the high blood pressure and seizures can be treated, the only cure for preeclampsia is delivery of the baby. According to the study authors, preeclampsia affects about 5 percen
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Contact: Bob Bock
bockr@mail.nih.gov
301-496-5134
NIH/National Institute of Child Health and Human Development
5-Feb-2004

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