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Research Article Free access | 10.1172/JCI115961

Disorders of bile acid metabolism in cholesterol gallstone disease.

F Berr, E Pratschke, S Fischer, and G Paumgartner

Department of Medicine II, Klinikum Grosshadern, University of Munich, Federal Republic of Germany.

Find articles by Berr, F. in: PubMed | Google Scholar

Department of Medicine II, Klinikum Grosshadern, University of Munich, Federal Republic of Germany.

Find articles by Pratschke, E. in: PubMed | Google Scholar

Department of Medicine II, Klinikum Grosshadern, University of Munich, Federal Republic of Germany.

Find articles by Fischer, S. in: PubMed | Google Scholar

Department of Medicine II, Klinikum Grosshadern, University of Munich, Federal Republic of Germany.

Find articles by Paumgartner, G. in: PubMed | Google Scholar

Published September 1, 1992 - More info

Published in Volume 90, Issue 3 on September 1, 1992
J Clin Invest. 1992;90(3):859–868. https://doi.org/10.1172/JCI115961.
© 1992 The American Society for Clinical Investigation
Published September 1, 1992 - Version history
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Abstract

The aim of the study was to evaluate the metabolism of individual bile acids in patients with cholesterol gallstone disease. Therefore, we determined pool size and turnover of deoxycholic (DCA), cholic (CA), and chenodeoxycholic acid (CDCA) in 23 female gallstone patients classified according to their gallbladder function and in 15 healthy female controls. Gallstone patients had normal hepatic bile acid synthesis, but, depending on gallbladder function, differed with respect to turnover and size of the bile acid pools: Patients with well-emptying gallbladder (group A, n = 9) had enhanced turnover and reduced pools of CA (-46%; P less than 0.01 vs. controls) and CDCA (-24%; P less than 0.05), but normal input and size of the DCA pool. With reduced gallbladder emptying (less than 50% of volume; group B, n = 6), turnover and pools of CA, CDCA, and DCA were similar as in controls. Patients with loss of gallbladder reservoir (group C, n = 8) had increased input (+100%; P less than 0.01) and pool size of DCA (+45%; P = 0.07) caused by rapid conversion of CA to DCA, while the pools of CA (-71%; P less than 0.001 vs. controls) and CDCA (-36%; P less than 0.05) were reduced by enhanced turnover. Thus, in patients with cholesterol gallstones, the pools of primary bile acids are diminished, unless gallbladder emptying is reduced. Furthermore, in a subgroup of gallstone patients, who had completely lost gallbladder function, the CA pool is largely replaced by DCA owing to rapid transfer of CA to the DCA pool. This probably contributes to supersaturation of bile with cholesterol.

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