Evaluating The Levels Of Total Protein And Lipid Profile In Pre-Eclamptic Patients.
INTRODUCTION
Hypertensive disorders of pregnancy such as pre-eclampsia (PE) and pregnancy-induced hypertension (PIH) are a major cause of maternal morbidity (Magee et al., 2014). 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).
Pre-eclampsia is a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine (Eiland et al., 2012). This condition begins after 20weeks of pregnancy (Al-Jameil et al., 2014).
In 2013, the American College of Obstetricians and Gynecologists defined this blood pressure as high, when it is greater than 140mmHg systolic or 90mmHg diastolic at two separate times, more than four hours apart in a woman after 20weeks of pregnancy.
Pre-eclampsia can present as late as 4-6 weeks postpartum. Postpartum pre-eclampsia is the occurrence of hypertension and proteinuria after delivery.
Hypertension is a common but not universal finding in postpartum pre-eclampsia, proteinuria may occur less often than in pre-eclampsia during pregnancy (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).
A major consequence of this sequence of events is generalized endothelial dysfunction (Eiland et al., 2012; Young et al., 2010).
This disorder is mediated by placental products that reach the maternal circulation and 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 (Airoldi and Weinstein, 2007).
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