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Abstract
Pre-eclampsia (PE) is a part of a spectrum of medical conditions known as hypertensive disorders of pregnancy. It is a multisystem disorder peculiar to human pregnancy. It occurs in 4–5% of all pregnancies and remains a leading cause of maternal and neonatal mortality and morbidity.
Although various research efforts, the etiology of preeclampsia still remains unclear. The hypertension associated with preeclampsia develops during pregnancy and remits after delivery, thus implicating the placenta as the main initiator. Inadequate trophoblast invasion of uterine spiral arteries is one mechanism thought to lead to placental ischemia. The ischemic placenta elaborates a variety of factors into the maternal blood stream that contribute to the generalized endothelial dysfunction
Endothelial dysfunction is associated with an imbalance in haemostatic functions. Endothelial cells are responsible for the release of tissue plasminogen activator (t-PA) which is capable of converting plasminogen into the serine protease plasmin, an enzyme that proteolytically degrades fibrin (and fibrinogen).Endothelial cells also contribute to the release of plasminogen activator inhibitor-1 (PAI-1). This results in inhibition of the fibrinolytic system through inhibition of plasmin release which in turn amplifies the pathogenic role of fibrin deposition during severe inflammation. Multiple factors, including lipoproteins, cytokines, and inflammatory proteins can modulate the endothelial cells to produce t-PA and PAI-1.
Endothelial dysfunction is accompanied by elevated levels of inflammatory markers; such markers are much higher in women with PE than those seen in normal pregnancy.
C-reactive protein (CRP), named for its capacity to precipitate the somatic C-polysaccharide of streptococcus pneumonie, was the first acute- phase protein to be described and is a sensitive systemic marker of inflammation and tissue damage. It plays a role in eliciting the inflammatory response characteristic of preeclampsia.