Clofibrate and Gallstones

Cooper, Jane; Geizerová, H; Oliver, M.F.

doi:10.1016/s0140-6736(75)91845-0

Cited by 62 publications

(15 citation statements)

References 2 publications

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“…Similar findings have appeared for clofibrate, a drug used in the treatment of hyperlipidemia [270][271][272]. Both drugs share an ability to increase the concentration of cholesterol in the bile.…”

Section: Gallstonessupporting

confidence: 76%

Drug-induced gastrointestinal disease

Hyson

Burrell

Toffler

1977

Gastrointest Radiol

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The gastrointestinal tract is a common target for adverse drug reactions. The resultant changes are often nonspecific (e.g., mucosal ulceration, intestinal infarction, motility disturbance) and in many cases no radiographically detectable lesion may occur. A comprehensive review of the reported drug-induced disorders of the digestive organs is herein presented and their radiographic manifestations are described.

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Section: Gallstonessupporting

confidence: 76%

Drug-induced gastrointestinal disease

Hyson

Burrell

Toffler

1977

Gastrointest Radiol

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“…However, it was more effective in decreasing VLDL than LDL, and its use had been associated with significant increases in gallstones (15) and other diseases of the gastrointestinal tract. Later studies would show that the drug, although having a favorable effect on cardiac events, actually increased overall mortality (16).…”

Section: How Did the Candidate Drugs Look?mentioning

confidence: 99%

Thematic review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy, part IV: The 1984 Coronary Primary Prevention Trial ends it—almost

Steinberg

2006

Journal of Lipid Research

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“…11 However, despite their profound TG lowering capacity, fibrates have been shown to increase the risk of cholelithiasis [12][13][14] by increasing biliary cholesterol saturation. 15 As the risk of cholelithiasis is already increased in HTG, 3 4 treatment with fibrates could enhance the risk of cholelithiasis and subsequently pancreatitis even further.…”

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confidence: 99%

Gall bladder dysmotility: a risk factor for gall stone formation in hypertriglyceridaemia and reversal on triglyceride lowering therapy by bezafibrate and fish oil

Jonkers

Smelt²,

Ledeboer³

et al. 2003

Gut

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Background and aim: The aim of this study was to unravel the mechanisms responsible for the increased risk of gall stone disease in hypertriglyceridaemia (HTG) and to compare the effects of triglyceride lowering therapy by bezafibrate and fish oil on determinants of cholelithiasis (biliary lipid composition and gall bladder motility) in HTG patients. Patients and methods: Gall bladder motility (ultrasonography) was studied postprandially and during infusion of cholecystokinin (CCK). Determinants of cholelithiasis and serum lipids were compared between nine HTG patients and 10 age, sex, and body mass index matched normolipidaemic controls. The effects of bezafibrate and fish oil in HTG patients were studied in a randomised cross over trial. Results: HTG patients showed 14-fold higher serum triglyceride (TG) levels than controls. Biliary lipid composition, fasting gall bladder volumes, and CCK levels did not differ between HTG patients and controls. Gall bladder emptying was reduced in HTG patients compared with controls during CCK infusion (−22%) as well as in response to a meal (−37%; both p<0.001). Postprandial CCK levels were significantly higher in HTG patients. Both bezafibrate and fish oil reduced serum TG levels (−68% and −51% v baseline, respectively; both p<0.01). Fasting CCK levels were not affected whereas CCK induced gall bladder emptying increased during bezafibrate (+29%; p<0.001) and tended to increase on fish oil therapy (+13%; p=0.07). Postprandial gall bladder motility improved on bezafibrate and fish oil (+47 and +25% v baseline, respectively; both p<0.02) at least partly due to increased gall bladder sensitivity to CCK (both p<0.05 v baseline). Bezafibrate but not fish oil increased the molar ratio of cholesterol to bile acids (+40%; p<0.05) but no effects on cholesterol saturation index were seen with either treatment. Conclusions: We suggest that impaired gall bladder motility occurs in HTG patients due to decreased sensitivity to CCK, which may add to the enhanced risk of gall stone disease in HTG patients. Triglyceride lowering therapy by both fish oil and bezafibrate improve gall bladder dysmotility without adversely affecting biliary cholesterol saturation.

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Clofibrate and Gallstones

Cited by 62 publications

References 2 publications

Drug-induced gastrointestinal disease

Drug-induced gastrointestinal disease

Thematic review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy, part IV: The 1984 Coronary Primary Prevention Trial ends it—almost

Gall bladder dysmotility: a risk factor for gall stone formation in hypertriglyceridaemia and reversal on triglyceride lowering therapy by bezafibrate and fish oil

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