A new study by researchers at Beth Israel Deaconess Medical Center (BIDMC), in collaboration with a research team from The Hospital for Sick Children, Toronto, has confirmed //the previous findings that elevated levels of the sFlt1 placental protein leads to the onset of preeclampsia and also a second protein which, in combination with sFlt1, puts preeclampsic patient to a severe condition.
These new findings, reported in the June 4, 2006 on-line issue of Nature Medicine, provide another critical piece of information about this puzzling disease, which complicates five percent of all pregnancies worldwide and is a major cause of maternal and fetal mortality, particularly in developing nations.
‘Preeclampsia typically develops in the third trimester of pregnancy and is characterized by high blood pressure, edema and protein in the urine,’ explains the study’s senior author S. Ananth Karumanchi, MD, a nephrologist in the cat BIDMC and Assistant Professor of Medicine, Obstetrics and Gynecology at Harvard Medical School.
Three years ago, Karumanchi and his colleagues demonstrated that the placenta plays a central role in the course of these events, and that elevated levels of a placental protein called sFlt1 (soluble fms-like tyrosine kinase) are key to the onset of the disease.
However, for unknown reasons, a subset of preeclampsia patients will go on to experience severe preeclampsia – a group of dramatically escalated symptoms characterized by a sudden, massive rise in blood pressure, which can lead to the onset of seizures, as well as the development of fetal growth restriction and the HELLP syndrome. HELLP, which stands for hemolysis, elevated liver enzymes and low platelets, indicates that the mother’s liver and blood-clotting systems are not functioning properly, and the health of both mother and infant are in serious danger.
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