[Pathogenesis of alcohol-induced hyperlipidemia: case report of hypertriglyceridemia over 10,000 mg%].

A 53-year old woman developed excessive hypertriglyceridemia (greater than 10,000 mg/dl) with features of toxic liver damage after prolonged ethanol ingestion. Lipoprotein-lipase-activity was not decreased, apolipoprotein-C-II analysis, as shown by gel-electrophoresis, revealed a regular pattern. Treatment with parenteral nutrition and abstinence of ethanol resulted in a complete normalization of plasma triglycerides after transient remnant-hyperlipidemia. Decrease of triglycerides was accompanied by declining liver enzyme activities. As suggested by unimpaired activity of lipolysis, the extent of hypertriglyceridemia may be explained by a reversible receptor mediated defect of hepatic catabolism, aggravated by hepatic overproduction of triglyceride-rich-particles. Although receptor dysfunction is not yet understood, the transient appearance of remnant particles may be a helpful criteria in diagnosis of ethanol induced hypertriglyceridemia.