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Gallbladder mucin, arachidonic acid, and bile lipids in patients who develop gallstones during weight reduction

Shiffman, Mitchell L., Shamburek, Robert D., Schwartz, Charles C., Sugerman, Harvey J., Kellum, John M., Moore, Edward W.·1993·Gastroenterology
DOI 10.1016/0016-5085(93)90968-i
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Abstract

Background Arachidonic acid (AA) and hydrophobic bile salts (BS) stimulate gallbladder mucin (GBM) secretion, which is thought to be an essential step in gallstone pathogenesis. The present study was performed to evaluate the relationship between AA, BS, and GBM in patients who develop gallstones following weight reduction. Methods Eleven patients who underwent gastric bypass, developed symptomatic gallstones, and then underwent cholecystectomy were evaluated. Gallbladder bile was obtained for analysis during each procedure. Matched patients who did not develop gallstones following gastric bypass served as controls. Results GBM increased in every patient who developed stones (mean increase: 5000%). The largest increase was observed soon after gastric bypass, and this declined curvilinearly with time. Gallbladder bile cholesterol was initially elevated but then rapidly declined before increasing back to pregastric bypass levels after weight loss was complete. No significant changes in phosphatidylcholine molecular species (including AA) or BS composition were observed following weight reduction. Concentrations of cholesterol, phospholipids, and changes in [AA] over time were each a linear function of [BS]. No relationship between GBM and any of these bile constituents was apparent. Conclusions These observations strongly suggest that increases in GBM, which occur with gallstone formation in humans, are not the result of alterations in biliary AA or BS composition.

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Metadata

Authors
Shiffman, M. L., Shamburek, R. D., Schwartz, C. C., Sugerman, H. J., Kellum, J. M., & Moore, E. W.
Venue
Gastroenterology
Publisher
Elsevier BV
Published
1993-10
Volume
105
Issue
4
Pages
1200-1208
ISSN
0016-5085
DOI
10.1016/0016-5085(93)90968-i
Cited by
65
References
0
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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