Choline has been recommended for the treatment of hepatic diseases, especially those of nutritional origin, and for the prevention of arteriosclerosis. Little is known of its fate after oral or intravenous administration. A recent Spanish report (1) that patients with liver diseases and dogs with experimental hepatic damage excrete in the urine considerably more than normal of a substance precipitated by Reinecke salt (and considered as choline by the authors) after large doses of choline given orally, suggested that the utilization of choline might be altered in hepatobiliary disease. In addition, studies with radiophosphorous (2) indicate a reduced rate of phospholipid formation in the presence of hepatocellular damage and an increased rate in biliary obstruction, suggesting that less choline might appear in the urine than normal in obstructive jaundice and more than normal in liver cell damage.To test these hypotheses and to investigate the fate of choline after its oral adrministration 1 ) the identity of the reineckate precipitated from the urine was determined, and 2) the influence upon its excretion of physiologic conditions as well as hepatobiliary diseases was studied. MATERIALFour normal subj ects and 22 patients with various hepatobiliary diseases were given on separate occasions single doses of choline bicarbonate3 equivalent to 2-8 grams of choline base (230-920 mg. choline N). Their diets were not controlled. Urine samples, collected at various intervals, were preserved with 25 ml. of concentrated hydrochloric acid (diluted with equal parts of water) per liter of urine.
Previous investigations ( 1 ) have demonstrated that in normal persons approximately 60 per cent of choline salts fed in a single dose is transformed by intestinal bacteria to trimethylamine (TMA), which is excreted in the urine mainly as the oxide. In chronic liver diseases, considerably less of the ingested choline appears in the urine as total trimethylamines (TTMA). This difference was considered as evidence of an altered action of the intestinal bacteria in these diseases ( 1 ). The concept of the intestinal formation of urinary trimethylamines, based in part upon the reduction of TTMA excretion following administration of antimicrobial agents, was confirmed by the observation (2) that choline as such appears in the urine after intravenous administration of choline, but the basal excretion of urinary TTMA is not altered significantly. The concept of altered choline utilization by intestinal bacteria in liver diseases, as reflected by reduced transformation of choline to TMA, required further elaboration. This was partly carried out in animal experiments (3), but in addition it was necessary to perform a series of clinical studies to clarify the results of human and animal investigations reported previously. Studies of the physiologic processes included the following: (a) whether choline bound in the form of phospholipids is transformed to TMA to the same degree as are choline salts, (b) investigation into the site and completeness of intestinal transformation of choline, and (c) determination of the effects of aureomycin upon the transformation of large amounts of choline.
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