MATERNAL SERUM LIPIDS IN EGYPTIAN PATIENTS WITH PREECLAMPSIA

Abstract

Preeclampsia is an important cause of fetal and maternal morbidity and mortality worldwide. It complicates about 3% of pregnancies. It occurs during second and third trimester of pregnancy. It is characterized by blood pressure of ≥140/90 mm Hg or rise in systolic blood pressure of more than 30 mmHg or diastolic blood pressure of more than 15 mmHg after 20 weeks of gestation, in conjugation with proteinuria ≥300 mg/24 hours or greater or equal to +1 or 30 mg/dl by dipstick response. Preeclampsia can result in eclampsia when convulsions develop or manifest as the hemolysis, elevated liver enzymes and low platelet count (HELLP) syndrome. Both eclampsia and HELLP syndrome are known to be associated with severe complications such as cerebral hemorrhage, renal insufficiency, lung oedema and liver hemorrhages. The pathophysiology of preeclampsia likely involves both maternal and fetal/placental factors. Abnormalities in the development of placental vasculature early in pregnancy may result in relative placental underperfusion/ hypoxia/ischemia, which then leads to release of antiangiogenic factors into the maternal circulation that alter maternal systemic endothelial function and cause hypertension and other manifestations of the disease. Women with preeclampsia 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. These microscopic lesions are similar to atherosclerosis found outside pregnancy. Lipid deposits are also seen in the glomeruli of preeclamptic patients, a finding known as glomerular endotheliosis.