Abstract
Material and method: This was a cross-sectional (case-control) study conducted to evaluate the role of oxidative stress and dyslipidemia as indicators of pathogenesis and risks of preeclampsia in pregnant Sudanese women attending Wad-Medani Obstetrics and Gynecology Teaching Hospital.
Result and conclusion: pregnant with increase in BMI have a higher chance of developing PE. Low level of high-density lipoprotein cholesterol and high level of low-density lipoprotein cholesterol define that dyslipidemia increasing the risk of PE, Decreased levels of NO and TAC might reflect the oxidative stress and likely contribute to the pathophysiological mechanisms of PE.
Keywords: preeclampsia; oxidative stress; total antioxidant capacity; nitric oxide; dyslipidemia.
1. Introduction
Pregnancy is one of the most important periods in the life of a woman, a family and a society (Whitehouse et al., 2012). The success of pregnancy is a result of ongoing interactions between the placenta and the maternal immune and cardiovascular systems (James et al., 2010).
Pregnancy is a transient condition, but when it is complicated by preeclampsia (PE) it has lasting 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, excessive thrombin generation, 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).
During healthy pregnancy, there is an elevation in oxygen demand along with an increase in the production of reactive oxygen species (ROS) to carry out signaling for physiological processes in pregnancy, such as oocyte maturation, ovarian steroidogenesis, ovulation, implantation, blastocyst formation, luteolysis and luteal maintenance (Emet et al., 2013). Preeclamptic women can present associated endothelial dysfunction, dyslipidemia and aggravated systemic production of free radicals (Wild et al., 2016).
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). Prevalence of preeclampsia has increased by up to 30% over the last decade (Leffert, 2015).
The exact cause of PE remains uncertain, therefore PE is still a disease of theories (Adu-Bonsaffoh et al., 2015). But although the cause remains largely unknown, 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. This in turn leads to the second, symptomatic stage, where in 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). At the cellular level, preeclampsia associated with the release of free radicals by the placenta and therefore generation of oxidative stress. Placenta-borne oxidative and stresses are even sometimes considered as the major molecular determinants of the maternal disease (Aouache et al., 2018).