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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The pharmacologic approach to the prevention of preeclampsia: from antiplatelet, antithrombosis and antioxidant therapy to anticonvulsants
From Alternative Medicine Review, 9/1/05 by J. Bar

The pharmacologic approach to the prevention of preeclampsia: from antiplatelet, antithrombosis and antioxidant therapy to anticonvulsants. Bar J, Ben-Haroush A, Feldberg D, Hod M. Curr Med Chem Cardiovasc Hematol Agents 2005;3:181-185.

Preeclampsia has been suggested to be a two-stage disorder of an alteration in placental perfusion (stage 1) leading to generalized vascular endothelial damage (stage 2). Because the mechanism linking the two stages remains unclear, effective primary prevention is still impossible. However, advances made in our understanding of the pathophysiology of preeclampsia have paved the way for secondary and tertiary prevention approaches. Platelets are known to be activated in early pregnancy. They also play a pivotal role in the process of inflammation, as demonstrated by the finding that CD40 ligand is shed from activated platelets to directly initiate inflammation of the vessel wall. According to the Cochrane Library Update summarizing data from over 30,000 women, secondary prevention with antiplatelet drugs is associated with a 19% decrease in the risk of preeclampsia. Additional randomized controlled trials are needed to establish the association between preeclampsia and thrombophilia. The effect of the antithrombotic agent heparin on pregnancy outcome in preeclampsia and its potential preventive action in high-risk patients need to be elucidated. One of the several hypotheses of the pathogenesis of preeclampsia focuses on the oxidative stress caused by the imbalance in prooxidant and antioxidant forces. Preliminary findings on vitamin E and vitamin C supplementation in preeclamptic women are encouraging, and suggest a rationale for larger clinical trials. Although there is currently no explanation for the positive effect of magnesium sulfate on eclamptic seizures, studies have provided enough evidence to encourage its worldwide use as the primary anticonvulsant of choice in the tertiary prevention of maternal and perinatal death in severe preeclampsia/ eclampsia. In conclusion, secondary and tertiary prevention of preeclampsia is possible when targeted at reducing maternal and neonatal morbidity and mortality.

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