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Abstract
Pre-eclampsia is a multisystem disorder specific to pregnant women. It remains one of the most important causes of maternal and fetal mortality and morbidity worldwide (Lam et al., 2005).
Although the pathogenesis of this condition is not fully understood, it is now widely accepted that vascular endothelial cell dysfunction is the final common pathway responsible for the maternal syndrome. The underlying pathological changes that lead to endothelial dysfunction remain incompletely understood, but poor placentation has been proposed as a major factor (Maynard et al., 2005).
A number of circulating placenta-produced factors have been implicated in causing the endothelial dysfunction and the clinical phenotype characteristic of pre-eclampsia (Dimitrakova et al., 2004). Bdolah et al. (2005) reported that excess secretion of a naturally occurring anti-angiogenic molecule of placental origin referred to as soluble Fms-like tyrosine kinase 1 (sFlt-1) may contribute to the pathogenesis of pre-eclampsia. Soluble Flt-1 acts by antagonizing two angiogenic molecules, vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) which are not only important in angiogenesis, but also in maintaining the endothelial health. So abnormalities in these angiogenic factors lead to abnormal placentation and the accompanying hypoxia which in turn, results in more sFlt-1 production (Baumwell and Kaurmanchi, 2007).