Biliary Tract Studies

Juniper, Kerrison; Burson, E. Napier

doi:10.1016/s0016-5085(57)80130-9

Cited by 98 publications

(3 citation statements)

References 72 publications

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“…Light brown to black concretions, measuring less than 2 mm in diameter, were found among the fine brown-yellow precipitate. On light microscopic inspection, the precipitate was similar in appearance to the calcium bilirubinate crystals described by Juniper and Burson (18). The black stones, when crushed, were shown to consist of an opaque golden yellow mateial which had the same appearance as the pigment stones presented in Table 2.…”

Section: Effects Of Cholesterol Feeding On Bilesupporting

confidence: 69%

Pigment Gallstone Formation in the Cholesterol–Fed Guinea Pig

et al. 1985

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Female Hartley guinea pigs fed a 0.5% cholesterol-supplemented diet were found to form pigmented gallstones after 6 weeks (17/23) and 12 weeks (11/11), while only 2 of 44 animals fed a trace cholesterol diet formed gallstones over a comparable period. The light brown stones consisted primarily of aggregates of fine granular crystals, morphologically similar to calcium bilirubinate crystals. The stones were soluble in 0.1 N sodium hydroxide and were found to contain a substance which co-migrated with unconjugated bilirubin during thin-layer chromatography. Despite hypercholesterolemia (202 +/- 34 vs. 59 +/- 22 mg per dl in controls, p less than 0.05) and fatty infiltration of the liver, cholesterol-fed animals had a lithogenic index of only 0.22 +/- 0.04 in gallbladder bile as compared to a lithogenic index of 0.02 +/- 0.01 in animals fed the trace cholesterol diet. Accordingly, no cholesterol monohydrate crystals were found in any animals. Hematocrits among cholesterol-fed animals (47.6 +/- 1.2%) were lower than those of controls (54.8 +/- 1.3%, p less than 0.05) probably as a result of the cholesterol-induced hemolytic anemia which has been reported by others in this species. Fasting gallbladder volume was greater in cholesterol-fed animals (2.4 +/- 0.18 ml) than in controls (1.7 +/- 0.11, p less than 0.0025), and a comparable increase in gallbladder dry tissue mass was found. There was no evidence of biliary obstruction, however, and the gallbladder contractile response to octapeptide cholecystokinin was comparable in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Effects Of Cholesterol Feeding On Bilesupporting

confidence: 69%

Pigment Gallstone Formation in the Cholesterol–Fed Guinea Pig

et al. 1985

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“…Fresh samples of gallbladder bile were examined for crystals by direct microscopy. Cholesterol monohydrate crystals were identified by their birefringence and typical notched rhomboidal shape as described by Juniper and Burson (18). Unspun samples of bile were analyzed for total bile salts by the hydroxysteroid dehydrogenase method of Talalay (19) as modified by Admirand and Small (20).…”

Section: Methodsmentioning

confidence: 99%

Effects of dietary fish oil on biliary phospholipids and prostaglandin synthesis in the cholesterol‐fed pairie dog

Booker

Scott

Morte

1990

Lipids

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Cholesterol gallstone formation in the prairie dog is accompanied by an increase in the percentage of biliary phospholipids containing arachidonic acid, and an increase in gallbladder prostaglandin (PG) synthesis, but the pathogenetic significance of these changes is unclear. Dietary supplementation with eicosapentaenoic acid (EPA), an omega-3 fatty acid which is commonly found in fish oil, decreases prostaglandin synthesis in some tissues by replacing arachidonic acid, and by competitively inhibiting prostaglandin synthesis. We studied the effect of dietary fish oil on gallbladder PG synthesis, and the relative abundance of various molecular species of phosphatidylcholines and phosphatidylethanolamines in bile and gallbladder epithelium in the cholesterol-fed prairie dog. Prairie dogs were maintained for 4 weeks on one of four diets: i) control, ii) cholesterol-supplemented (0.34%), iii) menhaden oil (50 g/kg chow), or iv) cholesterol plus menhaden oil. Supplementation with menhaden oil resulted in a replacement of arachidonic and linoleic acids with EPA and docosahexaenoic acids in the phospholipids of bile and gallbladder mucosa. In cholesterol-fed animals, supplementation with menhaden oil prevented increased gallbladder PG synthesis. Menhaden oil also reduced the incidence of cholesterol monohydrate crystals among cholesterol-fed animals (9/20 with cholesterol plus menhaden oil vs 21/22 with cholesterol alone), but the improvement could not clearly be attributed to decreased PG synthesis since supplementation with menhaden oil also increased the total phospholipid concentration in bile, and decreased the degree of cholesterol saturation. These results demonstrate that dietary supplementation with omega-3 fatty acids significantly influences biliary phospholipids, and decreases the incidence of cholesterol monohydrate crystal formation in this animal model.

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“…34 – 40 This microscopic finding provided an imaging basis for clinical diagnosis of gallbladder cholesterol gallstone disease before modern gallbladder imaging techniques such as ultrasonography, x-ray film, and computed tomography (CT) were available. 28 , 29 , 41 – 48 Classical plate-like birefringent rhomboids were often detected in duodenal aspirates of patients with cholesterol gallstone disease although investigators also found some other forms of solid cholesterol crystals, i.e. , in the form of needle-like or arc-like crystals, thin plates with irregular margins, or agglomerates.…”

Section: Etymology Of Biliary Sludge and Microlithiasismentioning

confidence: 99%

Similarities and differences between biliary sludge and microlithiasis: Their clinical and pathophysiological significances

et al. 2018

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The terms biliary sludge and cholesterol microlithiasis (hereafter referred to as microlithiasis) were originated from different diagnostic techniques and may represent different stages of cholesterol gallstone disease. Although the pathogenesis of biliary sludge and microlithiasis may be similar, microlithiasis could be preceded by biliary sludge, followed by persistent precipitation and aggregation of solid cholesterol crystals, and eventually, gallstone formation. Many clinical conditions are clearly associated with the formation of biliary sludge and microlithiasis, including total parenteral nutrition, rapid weight loss, pregnancy, organ transplantation, administration of certain medications, and a variety of acute and chronic illnesses. Numerous studies have demonstrated complete resolution of biliary sludge in approximately 40% of patients, a cyclic pattern of disappearing and reappearing in about 40%, and progression to gallstones in nearly 20%. Although only a minority of patients with ultrasonographic demonstration of biliary sludge develop gallstones, it is still a matter of controversy whether microlithiasis could eventually evolve to cholesterol gallstones. Biliary sludge and microlithiasis are asymptomatic in the vast majority of patients; however, they can cause biliary colic, acute cholecystitis, and acute pancreatitis. Biliary sludge and microlithiasis are most often diagnosed ultrasonographically and bile microscopy is considered the gold standard for their diagnosis. Specific measures to prevent the development of biliary sludge are not practical or cost-effective in the general population. Laparoscopic cholecystectomy offers the most definitive therapy on biliary sludge. Endoscopic sphincterotomy or surgical intervention is effective for microlithiasis-induced pancreatitis. Ursodeoxycholic acid can effectively prevent the recurrence of solid cholesterol crystals and significantly reduce the risk of recurrent pancreatitis.

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Biliary Tract Studies

Cited by 98 publications

References 72 publications

Pigment Gallstone Formation in the Cholesterol–Fed Guinea Pig

Pigment Gallstone Formation in the Cholesterol–Fed Guinea Pig

Effects of dietary fish oil on biliary phospholipids and prostaglandin synthesis in the cholesterol‐fed pairie dog

Similarities and differences between biliary sludge and microlithiasis: Their clinical and pathophysiological significances

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