Korean J Gastroenterol.
1999 Nov;34(5):660-666.
Roles of Small Intestinal Transit Time in the Pathogenesis of Cholesterol Gallstones
Abstract
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BACKGROUND/AIMS: Gallbladder motility and small intestinal transit govern the cycling frequency of bile salts and their hepatic secretion rate. Therefore, the impaired gallbladder motility and the delayed intestinal transit contribute to the formation of cholesterol gallstone by impeding the enterohepatic circulation of bile salts and causing gallbladder stasis. Patients with gallstone have multiple abnormalities in the lipid composition and physical chemistry of their gallbladder bile, which are associated with an increased proportion of deoxycholate (DCA). Namely, this increase of DCA seems to be a consequence of prolonged intestinal transit. We assessed whether prolonged intestinal transit might potentiate gallstone formation by impeding enterohepatic circulation of bile acids.
METHODS
Thirty-two nonobese and normolipidemic subjects (15 control subjects and 17 patients with cholesterol stones) were studied. Taurine-conjugated ursodeoxycholate (T-UDCA, 500 mg) was orally administered in the fasting state and plasma specimens were obtained successively every 30 minutes for 6 hours. The plasma profile of bile acids was analyzed by high-performance liquid chromatography (HPLC). We determined the time for the first appearance of orally administered T-UDCA in the plasma, reflecting small intestinal transit time.
RESULTS
Small intestinal transit was delayed in the patients with cholesterol gallstones (control, 128+/-7.5 minutes vs. Patients, 247+/-15.1 minutes; p<0.001).
CONCLUSIONS
Prolonged small intestinal transit may contribute to the formation of cholesterol gallstone.
