ABNORMAL DUODENAL BILE COMPOSITION IN PATIENTS WITH ACALCULOUS CHRONIC CHOLECYSTITIS

Citation
A. Venkataramani et al., ABNORMAL DUODENAL BILE COMPOSITION IN PATIENTS WITH ACALCULOUS CHRONIC CHOLECYSTITIS, The American journal of gastroenterology, 93(3), 1998, pp. 434-441
Citations number
5
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
00029270
Volume
93
Issue
3
Year of publication
1998
Pages
434 - 441
Database
ISI
SICI code
0002-9270(1998)93:3<434:ADBCIP>2.0.ZU;2-5
Abstract
Objective: Our goal was to characterize biliary lipid composition in p atients with the syndrome of chronic biliary pain, absence of gallston es, and inflammation of the gallbladder mucosa (acalculous chronic cho lecystitis), Methods: Duodenal bile, obtained from 27 patients with a history of right upper quadrant pain and with negative imaging studies of the biliary tract, was analyzed enzymatically for bile acids, phos pholipids, and cholesterol, Fifteen patients were found to have inflam mation and/or fibrosis of the gallbladder at cholecystectomy, Results: The 15 patients with abnormal gallbladder histology had more dilute d uodenal bile, as indicated by a low bile acid concentration and a lowe r proportion of phospholipids (p < 0.01) when values were compared wit h those of duodenal bile samples from postmenopausal women without gal lbladder disease or from radiolucent gallstone subjects participating in the National Cooperative Gallstone Study. Cholecystectomy relieved pain in 9 of 14 patients. Conclusions: Some patients with acalculous c hronic cholecystitis have duodenal bile samples characterized by a dec reased bile acid concentration and a decreased proportion of biliary p hospholipids. The low biliary bile acid concentration may result from impaired gallbladder contraction and/or secretion by the biliary tract epithelium, The low proportion of phospholipid may result from posthe patic hydrolysis of luminal phosphatidylcholine followed by absorption of the hydrolysis products. The latter process could be caused by and /or contribute to mucosal inflammation and would also elevate the chol esterol saturation of bile, increasing the risk for cholesterol gallst one formation. (C) 1998 by Am. Cell. of Gastroenterology.