Secondary hypertriglyceridaemia in patients with parenchymal liver disease.
Hypertriglyceridaemia occurring in patients with liver disease has been 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 fifty patients with acute hepatitis, twenty patients with chronic active or persistent hepatitis and fifty 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, hypertriglyceridaemia disappeared with a concomitant increase of H-TGL and LPL. It is concluded that impaired triglyceride metabolism in liver disease is at least partly caused by diminished plasma hepatic TGL activity.
D000293:Adolescent; D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D008049:Lipase / Q000097:blood; D008071:Lipoprotein Lipase / Q000097:blood; D008107:Liver Diseases / Q000097:blood* / Q000201:enzymology; D008297:Male; D008875:Middle Aged; D014280:Triglycerides / Q000097:blood*
D014280:Triglycerides; D008049:Lipase; D008071:Lipoprotein Lipase