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PubMed1970

Cholelithiasis.

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Bile Acids and Salts↗
PubMed1990

Percutaneous endoscopic treatment of cholelithiasis.

Surgical management of gallstones was first performed successfully in 1878. Over the past decade, several new treatment alternatives have evolved that challenge the supremacy of traditional surgical cholecystectomy. Two endoscopic alternatives, e.g., percutaneous cholecystolithotomy (PCCL) and laparoscopic cholecystectomy (LC) are the latest additions to the growing armamentarium. Our initial experience with PCCL and LC as compared with our traditional cholecystectomy experience shows a 57% reduction in hospital days, a 58% reduction in postoperative analgesic dose, and 50% or more reduction in disabling convalescence in favor of the endoscopic alternatives. A review of the efficacy and morbidity of traditional surgery, peroral drug chemolysis (PDC), shockwave lithotripsy plus PDC, and percutaneous transhepatic lavage with methyl terbutyl ether suggests that the endoscopic alternatives are less morbid than traditional surgery and more efficacious and perhaps less morbid than other non-invasive or minimally invasive alternatives. Both original data and a literature review are presented.

Chenodeoxycholic Acid↗
PubMed1989

Cholelithiasis in hamsters: effects of cholic acid and calcium on gallstone formation.

Dietary cholic acid (0.1%) and/or calcium (2.6% as calcium carbonate) were added to a semipurified diet containing cholesterol and ethynyl estradiol to determine whether the incidence of pigment and/or cholesterol gallstones would be changed. Male golden Syrian hamsters were fed the experimental diets for 96 days (Group 1, control; Group 3, cholic acid plus calcium) or only an average of 60 days (Group 2, 0.1% cholic acid). Animals in Group 2 became ill (weight loss, low food intake, diarrhea) possibly due to cholic acid (or deoxycholic acid) toxicity. Cholesterol gallstones and crystals were absent in all experimental groups. The incidence of pigment gallstones was: control, Group 1, 12/16; 0.1% cholic acid, Group 2, 3/13; and 0.1% cholic acid plus calcium, Group 3, 11/22. Cholic acid with or without calcium produced an elevation of both liver and plasma cholesterol: Group 2, 80.1 mg/g and 501 mg/dl; Group 3, 103.7 mg/g and 475 mg/dl vs Group 1, 65 mg/g and 209 mg/dl, respectively. The lithogenic indices of the bile were lower in Groups 2 and 3 compared to Group 1, controls, 0.45 and 0.58 vs 1.16, respectively. The extent of the portal tract pathology could not be correlated with the presence or absence of pigment gallstones or with the levels of lithocholic acid in the hamster bile. In summary, when semipurified diets were supplemented with ethynyl estradiol and cholic acid, with and without calcium supplementation, no cholesterol gallstones formed and the incidence of pigment gallstones was not altered.

Animals↗
PubMed2002

Association of cholecystokinin A receptor gene polymorphism with cholelithiasis and the molecular mechanisms of this polymorphism.

BACKGROUND: The etiology of gallstone formation is multifactorial, and genetic factors are involved. The genetic variations of cholecystokinin A receptor (CCK-AR) in patients having gallstones and the molecular mechanisms of this polymorhpism were examined. The involvement of CCK-AR in gallstone formation was confirmed using CCK-AR gene knockout mice. METHODS: CCK-AR gene expression was determined by Northern transfer analysis in gallbladders with or without gallstones. Genetic variations were determined by Southern blot and by direct sequencing. Molecular mechanisms in terms of the transcriptional activity and methylation status were examined. Finally, we investigated whether gallstone formation was enhanced in CCK-AR gene knockout mice. RESULTS: The gene expression of CCK-AR was significantly decreased in gallbladders with gallstones compared to those without gallstones. No genetic variations were detected in the coding region, but two sequence variations were detected in the promoter region in gallstone patients. However, no significant differences were found for the promoter activities of polymorphic promoter constructs. In contrast, less methylation in the promoter region was related to substantial expression of the CCK-AR gene. Gallstone formation was enhanced in CCK-AR gene knockout mice. The homozygote (GG/TT) polymorphism of the CCK-AR gene showed a significantly higher percentage of body fat. CONCLUSIONS: Deteriorating gallbladder contractions, possibly induced by alterations in the CCK-AR gene, as well as CCK-AR gene polymorphism, promoted gallstone formation.

Adenocarcinoma↗
PubMed1990

Chronic treatment with a long-acting somatostatin analogue in a patient with intestinal carcinoid tumor: occurrence of cholelithiasis.

The long-acting somatostatin analogue SMS 201-995 has been used efficaciously in the therapy of metastatic carcinoid tumor, vasoactive intestinal peptide producing islet cell carcinoma, acromegaly, and TSH secreting pituitary tumors. We report the development of a gallstone in a patient treated for 23 months with a long acting somatostatin analogue for a metastatic carcinoid tumor. Symptomatic improvement and a reduction in the urinary excretion of 5-hydroxyindoleacetic acid occurred. There was no evidence of a gallstone on ultrasound and CT scan of the abdomen prior to somatostatin therapy. A progressively enlarging, asymptomatic gallstone developed during therapy.

Carcinoid Tumor↗