High levels of two proteins in the blood of pregnant women appear to indicate the subsequent development of preeclampsia, a life-threatening complication of pregnancy, report a team of researchers from the National Institutes of Health and Beth Israel Deaconess Medical Center. The proteins, which interfere with the growth and function of blood vessels, also signal the development of high blood pressure during pregnancy.
The findings appear in the September 7 New England Journal of Medicine.
"This finding appears to be an important step in developing a cure for preeclampsia," said Elias A. Zerhouni, M.D., Director of the National Institutes of Health. "It may also provide the basis for predicting whether or not a woman will develop the disorder."
Preeclampsia is a leading cause of maternal death and often occurs without warning. The condition results in high blood pressure and protein in the urine. Preeclampsia may begin with mild symptoms, then progress to severe preeclampsia and to eclampsia--dangerously high blood pressure and convulsions--which may result in disability or death. When preeclampsia is not severe, the high blood pressure it causes can usually be treated in the short term. The only cure for preeclampsia is delivery of the baby. The condition is estimated to complicate from 3 to 5 percent of all pregnancies.
When preeclampsia occurs late in a pregnancy, the baby can be delivered with relatively few ill effects. However, if preeclampsia occurs early in pregnancy, delivery of the baby would result in premature birth, which increases the risk of death, and for such lifelong complications as blindness, cerebral palsy, and learning disabilities. In such instances, physicians are forced to weigh the mother's risk of severe disease or eclampsia against the consequences of preterm birth for the baby.
In the current study, the researchers present strong evidence that an imbalance of two proteins
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Contact: Robert Bock
bockr@mail.nih.gov
301-496-5133
NIH/National Institute of Child Health and Human Development
6-Sep-2006