Pre-eclampsia is diagnosed when a pregnant woman develops high blood pressure (two separate readings taken at least 6 hours apart of 140/90 or more) and 300 mg of protein in a 24 hour urine sample (proteinuria). Swelling or edema(especially in the hands and face)was originally considered an important sign for a diagnoses of pre-eclampsia, but in current medical practice only hypertension and proteinuria are necessary for a diagnoses.

Some women develop high blood pressure without the proteinuria, this is called Gestational Hypertension or, Pregnancy Induced Hypertension (PIH). Both Preeclampsia and PIH are very serious conditions and require careful monitoring of mother and baby.

Appearance

Pre-eclampsia is much more common in the first pregnancy (3-5% of births) and usually becomes evident in the third trimester (and virtually always after the 20th week of pregnancy). It is also more common in women who have preexisting hypertension, diabetes,renal disease, and family history of pre-eclampsia. It is also more common in women with a multiple gestation (twins, triplets and more).

Pre-eclampsia may also occur in the immediate post-partum period or up to 6-8 weeks post-partum. This is referred to as "post partum pre-eclampsia".

Causes

Pre-eclampsia is thought to be caused by inflammatory mediators secreted by the placenta and acting on the vascular endothelium. If severe, it progresses to fulminant pre-eclampsia, with headaches and visual disturbances, and further to HELLP syndrome and eclampsia. These are life-threatening conditions for both the developing fetus and the mother.

Pathogenesis

There are many theories on the pathogenesis of preeclampsia, although the exact cause is not known. Most involve abnormal development of the placenta, which leads to a distressed placenta that secretes factors into the maternal blood. These factors damage the maternal blood vessels, leading to high blood pressure and protein in the urine. In normal placenta the decidual spiral arteries are invaded by extravillous trophoblasts which makes the arteies eventually open into trophoblastic cavities called lacunae (though they are initially kept plugged by the trophoblasts). The invading trophoblasts replace some of the smooth muscles and endothelium of these arteries near the implantation site. This is supposed to help the spiral arteries to widen into thin and funnel like near their opening into the lacunae. This establishes a high capacity and low resistance circulation. The maternal blood in the lacunar network bath the chorionic villi lined by syncytiotrophoblast, supplying oxygen and nutrients to, and removing metabolic wastes from, the fetal circulation which is not in direct contact with the maternal blood. In case of preeclampsia the spiral arteries are insufficiently invaded by trophoblasts. They remain narrow and the smooth mucle layer (tunica media) around the arteries become hyperplastic. This leads to insufficient maternal perfusion of the placenta in preeclampsia. One of the factors, released into blood from the placenta, that has been speculated (by Karumanchi et al) to be a mediator of the "toxemia", is a soluble splice variant isoform of the VEGF receptor 1 (sFlt 1).

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Proteins may predict preeclampsia - Pregnancy alert
From Science News, 2/14/04 by E. Francisco

Blood concentrations of two proteins that affect blood vessel growth appear to foretell preeclampsia, the baffling pregnancy condition that can threaten the lives of both a woman and her unborn baby. The findings from two new studies may lead scientists to develop screening tests and treatments for the disease.

Preeclampsia strikes about 5 percent of pregnancies in the United States. In these cases, during the second half of a pregnancy, women develop high blood pressure and excess protein in their urine. The condition can escalate to eclampsia, which includes potentially fatal seizures. Preeclampsia can be moderated, but the only known cure is delivery of the baby and removal of the placenta.

"If we could predict the development of preeclampsia, we could offer treatment before it becomes a serious problem," says Duane Alexander, director of the National Institute of Child Health and Human Development (NICHD) in Bethesda, Md.

Both new studies examined pregnant women's blood concentrations of placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt1). In a normal pregnancy, PIGF promotes growth of placental blood vessels, whereas sFlt1 keeps that growth in check and halts it late in the third trimester.

In one study, researchers led by NICHD epidemiologist Richard J. Levine examined blood samples that had been archived pregnancies of 120 women eventually diagnosed with preeclampsia and 120 women without the disease. The work is reported in the Feb. 12 New England Journal of Medicine.

Beginning 13 to 16 weeks into pregnancy, women who developed preeclampsia had significantly lower PlGF concentrations than the other women did. In contrast, blood concentrations of sFlt1 were similar for the two groups until the third trimester. Then, more of the women who developed the disease showed a spike in sFlt1 concentrations.

"It appears that early on, the differences in PlGF are apparent, whereas later on, differences in sFlt1 are more apparent" says Ravi Thadhani, a nephrologist at Massachusetts General Hospital in Boston and a coauthor of the study.

Thadhani and Levine also participated in the second study, which reviewed concentrations of the two proteins during only the first trimester of pregnancy. The study included blood samples from 40 women who developed preeclampsia, 80 women who had high blood pressure or bore small babies but didn't develop preeclampsia, and 80 women who completed normal pregnancies.

The findings were consistent with those of the first study and, in addition, suggested that PlGF and sFlt1 readings can selectively predict preeclampsia, setting the disease apart from other pregnancy problems that lead to high blood pressure or low birth weight. The findings appear in the February Journal of Clinical Endocrinology and Metabolism.

"This is exciting work that marks a new chapter in our efforts to understand and conquer a very bad and continually understudied disease" says nephrologist Marshall D. Lindheimer of the University of Chicago.

"If sFlt1 and PlGF are good markers, we can design a test for women at high risk for preeclampsia," says Levine. For preeclampsia treatments, he adds, "I believe that in the future, we will have people try to develop molecules that would block sFlt1."

However, Levine calls the new papers "just a start" toward fully understanding what causes preeclampsia.

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