Gallbladder motility in cholesterol gallstone disease

Festi, Davide; Frabboni, R.; Bazzoli, Franco; Sangermano, A; Ronchi, M; Rossi, L; Parini, Paolo; Orsini, M.; Primerano, A.M.; Mazzella, Giuseppe; Aldini, Rita; Roda, Enrico

doi:10.1016/0016-5085(90)90487-l

Cited by 114 publications

(15 citation statements)

References 29 publications

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“…This could be caused by enhanced emptying of the gallbladder, or by hastened transit (34) or decreased fractional absorption of bile acids in the small intestine. Emptying of the gallbladder is normal or reduced, but not enhanced, in gallstone patients (35,36); reduced emptying ofthe gallbladder is associated with slower fractional turnover and larger pool size of bile acids in healthy subjects (34) as well as in gallstone patients (37) (Fig. 2, group B).…”

Section: Discussionmentioning

confidence: 98%

Disorders of bile acid metabolism in cholesterol gallstone disease.

Berr

Pratschke²,

Fischer³

et al. 1992

J. Clin. Invest.

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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 < 0.01 vs. controls) and CDCA (-24%; P < 0.05), but normal input and size of the DCA pool. With reduced gallbladder emptying (< 50% of volume; group B, n = 6), turnover and pools of CA, CDCA, and DCA were similar as in controls. Patients with loss ofgallbladder reservoir (group C, n = 8) had increased input (+100%; P < 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 < 0.001 vs. controls) and CDCA (-36%; P < 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. (J. Clin. Invest. 1992. 90:859-868.) Key words: bile acid metabolism * cholesterol gallstone disease * deoxycholic acid -gallbladder emptying . cholesterol saturation of bile IntroductionIn most nonobese patients with cholesterol gallstones, the pools of cholic acid (CA)' and chenodeoxycholic (CDCA) are reduced ( 1-6), and deoxycholic acid (DCA) is often increased in bile (7). Both changes could contribute to supersaturation of bile with cholesterol ( 1, 7, 1. Abbreviations used in this paper: CA, cholic acid; CCK, cholecystokinin; CDCA, chenodeoxycholic acid; DCA, deoxycholic acid; FTR, fractional turnover rate. circulation (9), the increase ofDCA by raising biliary secretion of cholesterol ( 10).The small pools ofCA and CDCA may be caused by a small gallbladder reservoir ( 1 1), by enhanced turnover (2, 5), or by inhibition of bile acid synthesis by an oversensitive feedback mechanism ( 1 2) or by elevated levels of DCA ( 13,14). An increased fraction ofDCA in bile could be caused by high input and large pool size of DCA. CA is nearly completely 7a-dehydroxylated to DCA by anaerobic bacteria in the colon (7,15,16), but only 30-40% of this DCA is absorbed from the intestine ( 17 ). The DCA pool could be expanded by increased input of DCA owing to increased synthesis ofthe precursor CA or to an increased fraction of CA transferred to the DCA pool.It is still unclear which of the above factors account(s) for the reduction in CA and CDCA pool size and which for an increase in biliary DCA. ...

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Section: Discussionmentioning

confidence: 98%

Disorders of bile acid metabolism in cholesterol gallstone disease.

Berr

Pratschke²,

Fischer³

et al. 1992

J. Clin. Invest.

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“…2,11,12 A reduction in gallbladder motility might play an important role in the pathogenesis of cholesterol gallstones by favoring the precipitation of cholesterol crystals, especially in obese individuals, who are known to have a greater biliary secretion of cholesterol. 13 In general, obese individuals have a greater fasting gallbladder volume than do nonobese people.…”

Section: Discussionmentioning

confidence: 99%

“…[9][10][11] In this study, we used cholecystosonography to evaluate gallbladder volumes and ejection fractions (EFs) in obese women without gallstones and aimed to determine any statistical relationships with obesity-related factors (BMI, waist and hip circumferences, body fat percentage, body fat weight, and serum lipid levels).…”

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confidence: 99%

Sonographic evaluation of gallbladder volume and ejection fraction in obese women without gallstones

Sari

Balcı

Çoban

et al. 2003

J of Clinical Ultrasound

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“…Abnormalities in gallbladder emptying and delayed enterohepatic circulation of bile acids, associated with elevated cholesterol saturation of bile as observed in cholesterol gallstone patients, may contribute to gallstone formation [21, 22, 23]. In addition, changes in gastroduodenal motility have been demonstrated in cholecystectomy patients compared with normal subjects.…”

Section: Introductionmentioning

confidence: 99%

Effects of Intraduodenal Bile on Interdigestive Gastrointestinal and Gallbladder Motility in Healthy Subjects

Luiking¹,

Kloppers²,

Roelofs³

et al. 2001

Digestion

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Background/Aims: The enterohepatic circulation of bile acids is related to normal inter-digestive gastrointestinal motility, with the gut peptide motilin also being involved. This study aimed to investigate the effect of intraduodenal artificial bile infusion on antroduodenal and gallbladder motility so as to further elucidate the controlling factors. Methods: Twelve fasting, healthy male volunteers received artificial bile (80 mol% bile acids; 15 mol% phospholipids; 5 mol% cholesterol) or placebo (saline) intraduodenally for 10 min starting 30 min after the end of phase III, according to a double-blind, randomised, cross-over design. Antroduodenal motility, gallbladder volumes, and plasma motilin levels were measured. All values are means ± SEM. Results: The interval between infusion and the subsequent phase III, as well as the origin of this phase III were not significantly different between bile and saline. Antral pressure waves were significantly more frequent during and immediately after bile infusion compared with saline infusion (p < 0.05). The duration of phase I following infusion was significantly longer after bile (24.8 ± 3.7 min) than after saline infusion (13.1 ± 1.7 min; p < 0.05). The mean gallbladder volume tended to increase in the hours following bile infusion, but to decrease after saline infusion (p = 0.06). Plasma motilin increased after bile and saline infusion in an almost identical way. Conclusion: This study provides no clear evidence for a role of intraduodenal artificial bile (i.e. its main constituents) in the regulation of migrating motor complex cycling or feedback inhibition of inter-digestive gallbladder emptying.

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Gallbladder motility in cholesterol gallstone disease

Cited by 114 publications

References 29 publications

Disorders of bile acid metabolism in cholesterol gallstone disease.

Disorders of bile acid metabolism in cholesterol gallstone disease.

Sonographic evaluation of gallbladder volume and ejection fraction in obese women without gallstones

Effects of Intraduodenal Bile on Interdigestive Gastrointestinal and Gallbladder Motility in Healthy Subjects

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