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Secondary hypertriglyceridaemia in patients with parenchymal liver disease
Author(s) -
KLOSE G.,
WINDELBAND J.,
WEIZEL A.,
GRETEN H.
Publication year - 1977
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1977.tb01651.x
Subject(s) - medicine , lipoprotein lipase , endocrinology , triglyceride , triglyceride lipase , liver disease , cirrhosis , hypertriglyceridemia , hepatic lipase , liver function tests , cholesterol , adipose tissue
. 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 lecithincholesterol‐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.