Secondary hypertriglyceridaemia in patients with parenchymal liver disease

Abstract

Hypertriglyceridemia occurring in patients with liver disease was studied by measuring hepatic triglyceride lipase (H-TGL) and plasma lipoprotein lipase (LPL) by selective precipitation of H-TGL with specific antibodies. Lipid analysis, determination of lecithin-cholesterol-acyltransferase (LCAT) activity and liver function tests were performed in parallel in 50 patients with acute hepatitis, 20 patients with chronic active or persistent hepatitis and 50 with cirrhosis of the liver. Total post-heparin lipolytic activity (PHLA) decreased with the severity of liver dysfunction. This decrease was due to low H-TGL and only to some degree to low LPL activity. With improvement over several weeks of hospitalization, hypertriglyceridemia disappeared with a concomitant increase of H-TGL and LPL. Impaired triglyceride metabolism in liver disease is at least partly caused by diminished plasma hepatic TGL activity.