High blood pressure, fluid retention, and excess protein in the urine all signal the onset of preeclampsia, a condition that affects one in 20 women during the third trimester of pregnancy. While a cause for concern in all cases—about 200,000 women suffer from preeclampsia in the US each year, and it is a leading cause of premature births—only those women who experience large and sudden increases in blood pressure face the threat of severe complications for themselves and their fetuses.
Researchers already knew that changes in the concentrations of two proteins—placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFit1)—keyed the onset of milder forms of preeclampsia but did not seem to cause the life-threatening levels of high blood pressure seen in severe cases. Their new study in The New England Journal of Medicine names a third factor, soluble endoglin, that seems to kick preeclampsia into overdrive. This protein, which the researchers found in high concentrations in the placentas of women with severe preeclampsia, normally helps maintain the blood vessels, but when it sloughs off the blood vessel walls and combines with sFit1, it actually weakens them.
The study reports that soluble endoglin levels begin to increase markedly two to three months before the onset of preeclampsia and that this increase is usually accompanied by an increased ratio of sFit1 to PlGF. This forewarning should enable researchers to develop a diagnostic test that will allow healthcare providers to counter a major cause of maternal and fetal mortality worldwide.
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