Are pigmented gall stones caused by a "metabolic" liver defect?

Tritapepe, R; Padova, C. Di; Rovagnati, P

doi:10.1136/bmj.280.6217.832

Cited by 11 publications

(8 citation statements)

References 2 publications

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“…In addition to an altered composition and/or flow rate of bile brought about by vagotomy or gastrectomy [11,15,16,18,19], damaged liver function may give rise to a condition that makes the bile more lithogenic [12,13]. As perioperative hepatic dysfunction was much more common in patients with GSs compared with GS-free patients, we consider this complication very important in the process of GS development.…”

Section: Discussionmentioning

confidence: 99%

“…When these results are combined, we can assume that, in the early postoperative period, a considerable amount of bile re mains even after the maximal evacuation of the GB. Bile stasis in the GB has long been postulated to facilitate GS formation [3,5,6,9], More recently, an increased inci dence of GB sludge has been reported in patients main tained on long-term intravenous hyperalimentation that could be attributed to a lithogenic change of bile and/or bile stasis due to an altered GB motor function [24,38,39], Further, a possibility for this sludge to evolve into several kinds of GSs, especially into a pigment variety, has been suggested [12,13]. The identification of GSs in 82% of our patients within 5 years after the surgery is in agreement with a relatively short incubation time of 7 months to 5 years [6,19,40,41 ].…”

Section: Discussionmentioning

confidence: 99%

“…With this background, the incidence and incubation period of GS formation were analyzed in patients gastrectomized for cancer. The gallbladder (GB) motor function was studied for its presumed relation to GS formation [3][4][5][6][7][8][9][10][11] and other clinical conditions associated with the lithogenesis [12,13] were traced.…”

Section: Introductionmentioning

confidence: 99%

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Increased Risk of Gallstones following Curative Gastrectomy for Cancer

et al. 1989

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The incidence of gallstones in patients who had undergone radical gastrectomy for cure of gastric cancer was 4–8 times higher than in the general population. At least two factors seem to be involved in this high incidence: one is complete vagotomy which is inevitable in gastrectomy with lymph node dissection, and the other perioperative hepatic dysfunction. One fourth of these patients with gallstones required cholecystectomy with or without T-tube drainage. The high incidence of gallstones and a rather difficult cholecystectomy we experienced forced us to perform prophylactic cholecystectomy in these gastric cancer patients diagnosed with: cirrhosis or hepatitis; hemophilia or other hematologic disorders, and the cancer lesion involving the aborad part of the stomach.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Increased Risk of Gallstones following Curative Gastrectomy for Cancer

et al. 1989

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“…Since a considerable body of evidence in dicates unconjugated bilirubin as the major factor in pigment stone development [3,26,27], we hypothesize that alcohol may con tribute to the pathogenesis of pigment chole lithiasis by increasing this form of biliary pig ment. Our present results are consistent with the reported predominance of pigment gall stones in alcoholics [21,23].…”

Section: Discussionmentioning

confidence: 99%

“…As the intermittent or persistent biliary secretion of increased amounts of unconju gated bilirubin has been associated with the pathogenesis of pigment gallstones [3,21,26]. the data obtained in the rabbit prompted us to speculate that alcohol could be a risk factor for pigment stone development.…”

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confidence: 99%

Effect of Ethanol on Biliary Unconjugated Bilirubin and Its Implication in Pigment Gallstone Pathogenesis in Humans

Padova¹,

Tritapepe

Rovagnati³

et al. 1982

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Though some epidemiological investigations support the association between pigment gallstone formation and chronic alcoholism with cirrhosis, little attention has been paid to the influence of alcohol itself on biliary bilirubin secretion, so that the pathogenesis of pigment cholelithiasis in alcoholics is hitherto unknown. On different days we intravenously administered ethanol (0.7 g/kg body weight), diluted with 500 ml of saline, or saline alone to 6 non-obese patients with an indwelling T tube and reestablished enterohepatic bile circulation. At the time of the investigation bile cultures were negative for aerobic and anaerobic bacteria. Ethanol significantly increased biliary unconjugated bilirubin in respect to control values. The phenomenon reached a maximum 2 h after alcohol infusion when the value of unconjugated bilirubin averaged 2.37 ± 0.30% of total bilirubin in contrast to 0.65 ± 0.14% in control conditions (p < 0.01), and subsided 6 h after the end of ethanol infusion. Since increased amounts of biliary unconjugated bilirubin predispose to pigment stone formation, it can be speculated that alcohol contributes to pigment cholelithiasis pathogenesis by enhancing the biliary concentrations of this form of pigment.

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Acute ethanol administration increases biliary concentrations of total and unconjugated bilirubin in rabbits

et al. 1981

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Epidemiological investigations have revealed that alcoholic cirrhosis is associated with a high frequency of pigment gallstones, but only scanty information is available on the effects of ethanol on biliary secretion of bilirubin. We have injected intravenously 1.0 and 1.5 g/kg body wt of ethanol into six cholecystectomized rabbits and a common bile duct fistula. Experiments were performed ten days after surgery and a stream-splitting apparatus was interposed in the circuit in order to withdraw continuously biliary samples without interruption of enterohepatic bile circulation. Analysis of hourly data showed that both ethanol doses significantly increase the biliary concentration of total bilirubin, without affecting bile flow and lipid composition. Alcohol also promoted the efflux of unconjugated bilirubin into bile. The maximum effect occurred within the first 5 hr following alcohol administration. Thereafter the bile returned to normal. Since excessive concentrations of biliary unconjugated bilirubin favor pigment gallstone development, it can be speculated that alcohol acts as a risk factor for pigment lithiasis by enhancing the biliary levels of this form of pigment.

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Are pigmented gall stones caused by a "metabolic" liver defect?

Cited by 11 publications

References 2 publications

Increased Risk of Gallstones following Curative Gastrectomy for Cancer

Increased Risk of Gallstones following Curative Gastrectomy for Cancer

Effect of Ethanol on Biliary Unconjugated Bilirubin and Its Implication in Pigment Gallstone Pathogenesis in Humans

Acute ethanol administration increases biliary concentrations of total and unconjugated bilirubin in rabbits

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