Faecal bile acids and neutral sterols of cholesterol origin were decreased in patients with chronic liver disease, while urinary bile acids were constantly, but never greatly, increased. Thus, production of cholesterol and its conversion to bile acids was decreased in these patients. Faecal fat was only slightly increased, even in cases with a very low bile salt output, but it was negatively correlated with faecal bile acids. The reduced capacity of these patients to synthesize bile acids was shown by the fact that cholestyramine treatment, although it decreased urinary bile acids, increased faecal bile acids only slightly. The resin constantly increased faecal neutral sterols, while the increase of faecal fat was insignificant. Thus, the absorption of fats, as compared with that of sterols, was less strongly reduced by interruption of the enterohepatic circulation of bile salts. In one cirrhotic patient markedly increased faecal bile acids apparently caused cholerrhoeic diarrhoea, which was easily controlled with cholestyramine. The latter consistently increased elimination of cholesterol in cirrhotic patients, but serum cholesterol was not consistently decreased, and in these patients, in contrast to the control subjects, it was difficult to detect changes in cholesterol synthesis with the acetate-mevalonate test and serum methyl sterols.
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