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Ruppin DC, Murphy GM, Dowling RH. Gall stone disease without gall stones--bile acid and bile lipid metabolism after complete gall stone dissolution. Gut. 1986;27(5):559-66doi: 10.1136/gut.27.5.559.
Ruppin, D. C., Murphy, G. M., & Dowling, R. H. (1986). Gall stone disease without gall stones--bile acid and bile lipid metabolism after complete gall stone dissolution. Gut, 27(5), 559-66. https://doi.org/10.1136/gut.27.5.559
Ruppin, D C, et al. "Gall stone disease without gall stones--bile acid and bile lipid metabolism after complete gall stone dissolution." Gut vol. 27,5 (1986): 559-66. doi: https://doi.org/10.1136/gut.27.5.559
Ruppin DC, Murphy GM, Dowling RH. Gall stone disease without gall stones--bile acid and bile lipid metabolism after complete gall stone dissolution. Gut. 1986 May;27(5):559-66. doi: 10.1136/gut.27.5.559. PMID: 3699565; PMCID: PMC1433487.
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Gut. 1986 May;27(5):559-66. doi: 10.1136/gut.27.5.559.

Gall stone disease without gall stones--bile acid and bile lipid metabolism after complete gall stone dissolution.

Gut

D C Ruppin, G M Murphy, R H Dowling

PMID: 3699565 PMCID: PMC1433487 DOI: 10.1136/gut.27.5.559
Free PMC Article

Abstract

Although bile acid and bile lipid metabolism have been studied in established cholelithiasis, little is known about them in patients destined to develop gall stones, but in whom the stones have not yet appeared (prestone gall stone disease). After confirmed complete gall stone dissolution and withdrawal of treatment, gall stones recur frequently. Before the stones reappear, these patients have 'poststone gall stone disease'. In 13 such patients we confirmed complete gall stone dissolution with two normal cholecystograms and in 11 of the 13 by normal ultrasonography, measured bile acid and bile lipid composition in fasting duodenal bile, bile acid synthesis from marker corrected three day faecal bile acid excretion, bile acid pool size using an abbreviated isotope dilution technique, 'steady-state' bile lipid secretion using a duodenal amino acid perfusion system and then calculated the enterohepatic cycling frequency of the bile acid pool and the relationship between pool size and body weight. The results confirm that after withdrawal of treatment the biliary cholesterol saturation index reverts to levels (1.6 +/- SEM 0.4) comparable with those before dissolution therapy first began (1.6 +/- 0.2; NS). The mean bile acid pool size in the 13 patients of 4.4 +/- 0.5 mmol was comparable with that in untreated gall stone patients. Pool size was significantly smaller in the nine non-obese patients (3.5 +/- 0.3), than in the four obese (6.0 +/- 0.8; p less than 0.05). It also correlated significantly with body weight (r = 0.72) and with %IBW (r = 0.79). The coefficients of variation for biliary bile acid, phospholipid and cholesterol secretion were high, but the mean hourly secretion rates were of the same order as those seen in untreated gall stone patients studied with the amino acid duodenal perfusion stimulus. These results provide a baseline for assessing the response to postdissolution treatment and may indicate metabolic events leading to gall stone formation.

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