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1. Introduction
Pregnancy is important period in the life of a woman (Whitehouse et al., 2012). When pregnancy complicated by preeclampsia (PE) it effects on both the mother and the fetus (Leeman and Fontaine, 2008). PE is a pregnancy multisystem disorder characterized by hypertension (?140/90mmHg), proteinuria (?300mg/24hrs or ?1+dipstick) with or without edema, that appear after 20 weeks of gestation in a previously normotensive non-proteinuric pregnant women (Ghulmiyyah and Sibai, 2012).
PE found uniquely in the pregnant patient and one that has puzzled scientists for years and one of the ”great obstetrical syndromes”(Lin et al., 2015), is characterized by systemic inflammation, endothelial cell dysfunction, an anti-angiogenic state and is often associated with multiple organ involvement (Soto et al., 2012). However, PE is fundamentally a placental disease which manifests itself, in most cases, by involvement of the vascular (i.e. hypertension) and renal systems (i.e. proteinuria) (Ogge et al., 2011).
PE is one of the most common complications of human pregnancy with an overall incidence 2-12% (Rajaee et al., 2015) and the syndrome results in more than 63,000 maternal deaths worldwide annually, 75% are experienced in a mild form, and 25% in a severe form (Duhig and Shennan, 2015). PE is still a serious threat, mainly in underdeveloped countries where its incidence and mortality rates are higher , and the
prevalence increased by up to 30% over the last decade (Leffert, 2015).
PE is not the result of a one causative factor or pathophysiological pathway, but rather a complex entity with multiple etiological components contributing to its development and progression (Cubro et al., 2018).
PE is still a disease of theories as the exact cause remains uncertain (Adu-Bonsaffoh et al., 2015). The pathogenesis is thought to occur in two main phases, the first stage is asymptomatic, characterized by abnormal placental development during the first trimester resulting in placental insufficiency and the release of excessive amounts of placental materials into the maternal circulation. In the second symptomatic stage, the pregnant woman develops characteristic hypertension, renal impairment, and proteinuria and is at risk for the hemolysis, elevated liver enzymes and low platelet account (HELLP) syndrome, eclampsia, and other end organ damage (Steegers et al., 2010).