Pregnancy-induced hypertension (PIH) is the most frequent complication in pregnancy after the 20th week of gestation. This form of hypertension is classified as preeclampsia (PE) and gestational hypertension (GH). The latter is defined as the acute development of hypertension in a woman whose blood pressure (BP) was normal in the early stages of pregnancy and who subsequently developed persistent elevation of BP to at least 140/90 mmHg. Both GH and concomitant 24 hours Proteinuria (0.3 gm/L or more) in the absence of urinary tract infection is defined as PE (Ronald et al., 2007). The condition of PE is the main cause of maternal and perinatal mortality (Buchbinder et al., 2002). Preeclampsia develops in 4–5% of human pregnancies. It is characterized by an elevated blood pressure and Proteinuria and develops after 20 weeks of gestational age. PE can result in eclampsia when convulsions develop or manifest as the hemolysis, elevated liver enzymes and low platelet count (HELLP) syndrome. (Van Wijk et al., 2000). Several etiologies have been implicated in the development of preeclampsia. Endothelial dysfunction or inappropriate endothelial cell activation are the most common clinical manifestations in preeclampsia, including enhanced endothelial-cell permeability and platelet aggregation (Wang et al., 2004). Endothelial dysfunction is accompanied by elevated levels of inflammatory markers such as CRP (Teran et al., 2001). C-reactive protein (CRP) is an objective and sensitive index of overall inflammatory activity in the body (Kluft and Maat, 2002). There had been a growing interest in the role of inflammation as a key factor of endothelial dysfunction. A generalized activation of circulating leukocytes, characteristic of inflammation, has been found during preeclampsia (Redman et al., 1999).