Abstract

Objective: To examine the hypothesis that hepatic bile acid sulphation may be specifically impaired in the cholestatic liver disease, primary biliary cirrhosis (PBC), conceiveably leading to ongoing hepatocyte destruction by retained unconjugated and conjugated hydrophobic bile acids and, conversely, to examine whether sulphation may be induced in PBC to dispose of bile acids retained due to cholestasis. Methods: Under optimum substrate conditions and using butanol extraction, hepatic bile acid sulphotransferase (BAST) activity (pmol bile acid sulphate/mg protein/min) was measured by separately incubating six bile acid substrates with liver cytosol from liver biopsy material obtained from 22 patients with PBC, 17 patients with chronic parenchymal liver diseases, 12 of whom had alcoholic liver disease, and nine normal controls

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