Evaluation Of Total Protein And Lipid Profile In Pre-Eclamptic Patients Attending Antenatal Care
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Evaluation Of Total Protein And Lipid Profile In Pre-Eclamptic Patients Attending Antenatal Care
ABSTRACT
Pre-eclampsia remains a major public health concern in both industrialised and developing nations, contributing to maternal and neonatal morbidity and mortality worldwide (Shah et al., 2009; Magee et al., 2014).
It is a pregnancy disease characterised by the beginning of high blood pressure and, in many cases, a substantial amount of protein in the urine (proteinuria), which occurs after 20 weeks of pregnancy (Eiland et al., 2012; Al-Jameil et al., 2014).
Blood pressure is considered high when it is greater than 140mmHg systolic or 90mmHg diastolic measured at two different times more than four hours apart in a woman after 20 weeks of pregnancy (American College of Obstetricians and Gynaecologists, 2013).
Pre-eclampsia can appear as late as 4-6 weeks postpartum. Postpartum pre-eclampsia is the development of hypertension and proteinuria following birth. Though hypertension is widespread, it is not the only finding in postpartum pre-eclampsia, with proteinuria occurring less frequently (Mattlys et al., 2004).
Despite being one of the top causes of maternal morbidity and mortality, the aetiology and pathophysiology of pre-eclampsia have yet to be determined. It has been dubbed the ”disease of theories” due to the numerous hypotheses presented to explain its occurrence.
An improperly inserted placenta is a key risk factor for pre-eclampsia (Al-Jameil et al., 2014; Steegers et al., 2010). The abnormal implantation may be caused by the maternal immune system’s response to the placenta, specifically a lack of established immunological tolerance during pregnancy
which causes endothelial dysfunction, resulting in cardiovascular diseases such as vasospasm, increased endothelial permeability, and activation of thrombogenic mechanisms, as well as the onset of atherosclerosis (Eiland et al., 2012; Young et al., 2010).
Other variables involved in the pathophysiology of pre-eclampsia include genetic, immunological, vascular, and oxidative stress (Eiland et al., 2012; Young et al., 2010). Women with preeclampsia have vascular lesions at the uteroplacental implantation site.
These morphological lesions are typically seen in situations of acute atherosclerosis and are distinguished by fibrinoid necrosis surrounded by lipid-laden macrophages (Ross, 2010). Pre-eclamptic patients’ glomeruli may also include lipid deposits, a condition known as glomerular endotheliosis (Airoldi and Weinstein, 2007).
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