ABSTRACT
Pre-eclampsia has remained a significant public health threat in both developed and developing countries contributing to maternal and perinatal morbidity and mortality globally (Shah et al.,2009; Magee et al., 2014). It is a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine (proteinuria), which begins after 20 weeks of pregnancy ((Eiland et al., 2012; Al-Jameil et al., 2014). Blood pressure is said to be high, when it is greater than 140mmHg systolic or 90mmHg diastolic measured at two separate times, more than four hours apart in a woman after 20 weeks of pregnancy (American College of Obstetricians and Gynecologists, 2013). Pre-eclampsia can present as late as 4-6 weeks postpartum. Postpartum pre-eclampsia is the occurrence of hypertension and proteinuria after delivery. Though hypertension is common, it is however, not a universal finding in postpartum pre-eclampsia with proteinuria occurring less often (Mattlys et al., 2004). Despite being one of the leading causes of the maternal morbidity and mortality, the aetiology and pathogenesis of pre-eclampsia remain to be elucidated. It has been termed the ‘‘disease of theories’’ because of the multiple hypotheses that have been proposed to explain its occurrence(Solomon and Seely, 2004).There is strong evidence that a major cause predisposing a susceptible woman to pre-eclampsia is an abnormally implanted placenta(Al-Jameil et al., 2014; Steegers et al., 2010). The abnormal implantation may stem from the maternal immune system’s response to the placenta, specifically a lack of established immunological tolerance in pregnancy which trigger endothelial dysfunction, thereby evoking cardiovascular diseases such as vasospasm, increased endothelial permeability and activation of thrombogenic mechanisms, and leading to the early events of atherosclerosis (Eiland et al., 2012; Young et al., 2010). Several other factors including genetic, immune, vascular and oxidative stress are also implicated in the pathogenesis of pre-eclampsia (Eiland et al., 2012; Young et al., 2010). Women with pre-eclampsia present arterial lesions at the uteroplacental implantation site. These morphological lesions are usually observed in cases of acute atherosclerosis, and are characterized by areas with fibrinoid necrosis surrounded by lipid-laden macrophages (Ross, 2010). Lipid deposits are also seen in the glomeruli of pre-eclamptic patients, a finding known as glomerular endotheliosis (Airoldi and Weinstein, 2007).
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