Disease relevance of Cholelithiasis

• In a search for a way to distinguish cholesterol gallstones from pigment gallstones by oral cholecystography, we evaluated 56 patients with surgically confirmed cholelithiasis [1].
• In 14 patients with cystic fibrosis who had stopped taking pancreatic enzymes for one week molar percentage of lipid composition accounted for by cholesterol (mean +/- S.E., 16.3 +/- 2.9) and saturation index (2.0 +/- 0.3) were comparable to values of the cholelithiasis group and higher (P less than 0.01) than those of controls [2].
• In view of the reported excess prevalence of atherosclerosis and cholelithiasis in diabetes, we investigated several aspects of cholesterol metabolism under metabolic ward conditions in six Pima Indians with maturity-onset diabetes mellitus [3].
• CONCLUSIONS: In patients with cholelithiasis who present with biliary colic, a single 75-mg intramuscular dose of diclofenac can provide satisfactory pain relief and decrease substantially the rate of progression to acute cholecystitis [4].
• A multidrug resistance 3 gene mutation causing cholelithiasis, cholestasis of pregnancy, and adulthood biliary cirrhosis [5].

Psychiatry related information on Cholelithiasis

• In the search for an animal model of genetic determinants of cholesterol cholelithiasis, we found strain, gender and individual differences in mice [6].

High impact information on Cholelithiasis

• Targeted disruption of the murine cholecystokinin-1 receptor promotes intestinal cholesterol absorption and susceptibility to cholesterol cholelithiasis [7].
• CONCLUSIONS: Our findings suggest a primary role of the nuclear bile salt receptor FXR and the canalicular cholesterol transporter ABCG5/ABCG8 in the genetic susceptibility and pathogenesis of cholesterol cholelithiasis in these strains of inbred mice [8].
• ABCB4 gene mutation-associated cholelithiasis in adults [9].
• METHODS: Mice of both sexes were examined for gallstone weight and evaluated according to a scoring system for the physical chemistry of cholelithiasis during feeding of a lithogenic diet [8].
• Cholesterol gallstones were present in all groups at the end of each period; aspirin did not alter the incidence of cholelithiasis [10].

Chemical compound and disease context of Cholelithiasis

• In the 26 patients with symptomatic cholelithiasis or common-duct stones, crystals were not seen in the bile of the seven patients with pigment stones but were present in the bile of all 19 patients with cholesterol stones [11].
• Chenodeoxycholic acid is an important drug for the treatment of cholesterol cholelithiasis in man [12].
• Three of the 6 stone-forming patients underwent cholecystectomy because of complications secondary to cholelithiasis after a mean 43-day course of parenteral nutrition [13].
• Despite this risk and ample experimental evidence demonstrating that estrogen increases bile lithogenicity, no relationship between estrogen use and cholelithiasis was observed [14].
• No evidence for a direct role of deoxycholate in the pathogenesis of cholesterol cholelithiasis was obtained in these studies [15].

Biological context of Cholelithiasis

• Genetic epidemiology of cholesterol cholelithiasis among Chilean Hispanics, Amerindians, and Maoris [16].
• Kinetics of cholesterol and bile acids in patients with cholesterol cholelithiasis [17].
• In this study, we characterized ABCB4 gene mutations in a series of patients with symptomatic cholelithiasis to determine the genetic basis and the clinical phenotype of ABCB4 gene mutation-associated cholelithiasis [9].
• This study was designed to examine the oxidative stress changes during pigment gallstone formation and to investigate whether melatonin (MLT) could act as a chemopreventive agent for cholelithiasis in a guinea pig model [18].
• C57L/J (gallstone-susceptible) and AKR/J (gallstone-resistant) mice have been utilized for quantitative trait loci (QTL) analysis to identify the Lith 1 locus for cholelithiasis [19].

Anatomical context of Cholelithiasis

• The effect on biliary lipid and bile acid composition was assessed during the development of gallbladder nonfunction in 5 subjects with asymptomatic cholesterol cholelithiasis [20].
• Hypersecretion of mucus glycoprotein by the gallbladder epithelium in experimental cholelithiasis [21].
• The ground squirrel fulfills all criteria required to be regarded as an excellent animal model and is well suited for continued study into the role of the epithelial cell during cholesterol cholelithiasis [22].
• The similarities of pathologic findings in gallstone pancreatitis and common bile duct obstruction emphasize the role of choledocholithiasis in the pathogenesis of pancreatitis associated with cholelithiasis [23].
• Alpha-asarone is a hypolipidaemic agent obtained from Guatteria gaumeri, a medical plant used in Mexico to treat hypercholesteraemia and cholelithiasis. alpha-Asarone has been shown to be hepatocarcinogenic and mutagenic in a human lymphocyte assay, a murine bone marrow cell assay and in an unscheduled DNA synthesis assay [24].

Gene context of Cholelithiasis

• Characterization of the pathophysiologic roles of Lith3 and the new biliary mucin gene Glycam1 might provide insights into primary defects of human cholelithiasis and lead to new therapeutic strategies for prestone intervention [25].
• Hence, mouse gallbladder K8/K18/K19 expression is induced in response to cholelithiasis injury [26].
• In contrast, the Cpe (fat) mutation enhanced the prevalence of cholelithiasis markedly when compared with the background strain [27].
• MATERIALS AND METHODS: Surgical liver biopsies were obtained from 11 patients with untreated cholesterol cholelithiasis and nine gallstone-free subjects; mRNA levels of cholesterol 7alpha-hydroxylase (CYP7A1) and related nuclear receptors and coactivators were assayed by quantitative real-time RT-PCR [28].
• The bilirubin levels for the cholelithiasis patients with the homozygous variant-UGT1A1 gene were significantly different from the control analog (18.0+/-6.5 and 12.7+/-2.9 micromol/L, respectively; P<0.001, Student's t test) [29].

Analytical, diagnostic and therapeutic context of Cholelithiasis

• Aspirin does not inhibit cholesterol cholelithiasis in two established animal models [10].
• Recent anecdotal reports suggest that total parenteral nutrition may be associated with an increased incidence of both acalculous cholecystitis and cholelithiasis [30].
• Electron microscopy was performed to assess potential hepatotoxicity before and after 9 and 24 months of chenodeoxycholic acid (CDCA) therapy (375 or 750 mg, daily) in 103 patients with cholelithiasis [31].
• Three patients had cholelithiasis as the cause of perforation; the fourth patient had previously undergone gallstone dissolution with methyl tert-butyl ether lavage and developed bile peritonitis a few hours after removal of the catheter [32].
• Effect of castration and hormonal supplementation on cholesterol cholelithiasis in the male hamster [33].

References