ABSTRACT

Introduction Plasma lipid and lipoprotein concentrations are determined by many different environmental and genetic factors. Physiological alterations in maternal lipoprotein metabolism due to estrogen occur during gestation and result in increased plasma concentrations in late term. Maternal hypertriglyceridemia is a characteristic feature during pregnancy, but the exact mechanism remains in doubt.1 Estrogen concentrations gradually increase during normal pregnancy and during late gestation induce hypertriglyceridemia by increasing the hepatic production and decreasing the peripheral clearance of plasma triglyceride-rich lipoproteins (TRLs).2 Marked hypertriglyceridemia can develop in the late gestation of pregnancy as a consequence of mutations in genes, such as lipoprotein lipase (LPL) or apolipoprotein E (APOE) or other causes such as diabetes mellitus, alcohol abuse, use of beta-blockers or excessive weight gain.3,4

Although rarely encountered, severe hypertriglyceridemia may result in the potentially life-threatening complication of acute pancreatitis.5