Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Common duct gallstones are mainly of the brown pigment type, which are usually attributed to bacterial factors. Bacterial beta-glucuronidase most probably plays a role in the pathogenesis in many but not all patients. The role of other bacterial factors is more undecided. The aims of this study were to investigate a possible association between lipopolysaccharides (LPS) and choledocholithiasis, and to examine the interrelationship to beta-glucuronidase. Common duct bile obtained at endoscopic retrograde cholangiography in 86 patients was assayed for LPS by a limulus amebocyte lysate test, and beta-glucuronidase activity at pH 7.0 was measured. We found that both elevated concentration of LPS and the presence of juxtapapillary duodenal diverticula were associated with common duct stones (p < 0.01, both). Patients who had their common duct stones removed recently had a lower LPS concentration and a lower activity of beta-glucuronidase than those who had a stone in situ (p < 0.01, both), but still higher LPS concentration than those without choledocholithiasis at all (p < 0.01). In multiple logistic regression analysis, elevated LPS was the significant predictor of common duct stones (p < 0.01), and not confounding with neither beta-glucuronidase nor juxtapapillary diverticula. We conclude that gram-negative bacteria convey bacterial factors associated with choledocholithiasis, by mechanisms independent of, and additional to beta-glucuronidase.
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PMID:Lipopolysaccharides and beta-glucuronidase activity in choledochal bile in relation to choledocholithiasis. 938 34

Bacteria are traditionally accorded a greater role in pigment gallstone formation in Eastern populations. Stone color is thought to predict the presence of bacteria; that is, black stones (Western predominant) are supposedly sterile and brown stones (Eastern predominant) contain bacteria. We previously reported that, regardless of appearance, most pigment gallstones contain bacteria. This study examined, in a large Western population (370 patients), the incidence, appearance, and chemical composition of pigment stones, and the characteristics of gallstone bacteria. One hundred eighty-six pigment stones were obtained aseptically. Bacteria were detected by means of scanning electron microscopy and gallstone culture. Chemical composition was determined by infrared spectroscopy. Bacteria were tested for slime and beta-glucuronidase production. Seventy-three percent of pigment stones contained bacteria. Choledocholithiasis was associated with gallstone bacteria. Ca-bilirubinate was present in all pigment stones. Ca-palmitate was characteristic of infected stones, and more than 75% Ca-carbonate was characteristic of sterile stones. Neither chemical composition nor stone appearance predicted the presence of bacteria. Ninety-five percent and 67% of infected pigment stones contained bacteria that produced slime and beta-glucuronidase, respectively. Most pigment stones contained bacteria that produced beta-glucuronidase, slime, and phospholipase, factors that facilitate stone formation. Thus bacteria have a major role in Western pigment gallstone formation. Furthermore, gallstone color did not predict composition or bacterial presence.
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PMID:Pathogenesis of pigment gallstones in Western societies: the central role of bacteria. 1250 29

Juxtapapillary duodenal diverticula (JPD) are observed in around 10-20% of patients undergoing endoscopic retrograde cholangiopancreatography (ERCP). They are acquired extraluminal outpouchings of the duodenal wall through 'locus minoris resistance' and their incidence increases with age. They have been studied mainly with regard to their association with pancreatobiliary disease. Choledocholithiasis is considered to be strongly associated with JPD, but the role of JPD in the development of cholecystolithiasis and pancreatitis is still disputable. Since JPD are located in the vicinity of the papilla of Vater, they not only cause mechanical compression of the bile duct but also induce dysfunction of the sphincter of Oddi. They are considered to lead to bile stasis and to allow reflux from the duodenum into the bile duct, which results in an ascending infection of beta-glucuronidase-producing bacteria. The ERCP procedure can be hampered by JPD, although recent papers have reported no difference in the successful cannulation rate or complications between patients with JPD and those without JPD. Disorders caused by JPD are amenable to appropriate therapy, e.g. endoscopic sphincterotomy and surgical intervention.
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PMID:Juxtapapillary duodenal diverticula and pancreatobiliary disease. 2055 52