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Fecal bile salt excretion was studied in healthy volunteers, patients with regional ileitis, and patients with ileal resection. 10 muc of carboxyl-(14)C-cholic acid was given orally. Stools and urine were collected daily for 5-10 days, the bile salts extracted, and the radioactivity assayed. Urinary excretion was negligible. All patients with ileal resection excreted bile salts in the feces significantly faster than controls, and five of the six excreted 50% of the radioactivity within 24 hr. Their mean intestinal transit time was 5.6 hr compared to 26 hr for the controls. Two of the three patients with regional ileitis excreted bile salts almost as rapidly as patients with ileal resection. Vitamin B(12) absorption was also defective in those patients, but the intestinal transit time was not decreased. To study the effect of rapid intestinal transit on bile salt excretion, four of the control subjects were given orally 1200 ml of 10% mannitol for 7 days, and the labeled cholic acid excretion rate was again studied. The mean intestinal transit time was markedly shortened, mild steatorrhea developed, and the fecal bile salt excretion rate increased slightly. It is concluded that ileal resection and ileal disease are major factors and rapid intestinal transit is a minor factor in causing excessive fecal bile salt loss. The relevance of bile salt wastage to lipid malabsorption is unknown because of insufficient information about compensatory jejunal absorption, maximum rate of hepatic bile salt synthesis, and the minimum necessary intraluminal concentration of conjugated bile salt.
Meihoff et al. (Thu,) studied this question.