title: Effects of fluvastatin on biliary lipids in subjects with an elevated cholesterol saturation index.
abstract: OBJECTIVE
  3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors have been suggested as agents to reduce the biliary cholesterol saturation index (CSI) in duodenal bile and therefore might be supportive in primary or secondary prevention of gallstones. However, the efficiency of the therapy seems to depend on both the HMG-CoA reductase inhibitor used and the study population selected.
  
  
  METHODS
  We therefore investigated the effect of a high-dose application of fluvastatin on biliary lipid composition in 21 subjects exhibiting mild hypercholesterolaemia and a history of current gallstones or cholecystectomy due to gallstone disease. Subjects were treated either with 40 mg fluvastatin twice per day over a 3-month period (n = 14) or with placebo (n = 7). Bile samples were aspirated during endoscopy after intravenous ceruletid stimulation before and after therapy.
  
  
  RESULTS
  Both groups were comparable in CSI (mean +/- SD) at baseline (1.78 +/- 0.2 placebo vs. 1.97 +/- 0.4 verum). CSI significantly decreased in the verum group to 1.45 +/- 0.4 (P = 0.003) mainly due to increased phospholipid levels, whereas no difference was observed in the placebo group (1.85 +/- 0.7, n.s.). In addition, the verum group exhibited a significant reduction of hydrophobic deoxycholic acid, which has been reported to induce cholesterol crystal precipitation, and an increase of hydrophilic cholic acid.
  
  
  CONCLUSIONS
  Fluvastatin might decrease the risk of cholesterol gallstone formation in patients with elevated biliary CSI during long-term treatment by reduction of biliary cholesterol saturation and percentage change in deoxycholic acid content.
authors.affiliation: Universitätsklinikum Regensburg, Institut für Klinische Chemie und Blutbank, Franz-Josef-Strauss-Allee 11, D-93053 Regensburg, Germany. mustafa.porsch-oezcueruemez@klinik.uni-regensburg.de
authors.forename: M
authors.initials: M
authors.lastname: Porsch-Ozçürümez
authors.forename: P D
authors.initials: PD
authors.lastname: Hardt
authors.forename: H
authors.initials: H
authors.lastname: Schnell-Kretschmer
authors.forename: K
authors.initials: K
authors.lastname: von Bergmann
authors.forename: C
authors.initials: C
authors.lastname: Darui
authors.forename: J
authors.initials: J
authors.lastname: Nonhoff
authors.forename: C
authors.initials: C
authors.lastname: Abletshauser
authors.forename: H U
authors.initials: HU
authors.lastname: Klör
mesh_terms: D000368:Aged; D001647:Bile Acids and Salts / Q000097:blood / Q000378:metabolism*; D002769:Cholelithiasis / Q000517:prevention & control; D004311:Double-Blind Method; D005229:Fatty Acids, Monounsaturated / Q000627:therapeutic use*; D005260:Female; D000077340:Fluvastatin; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000188:drug therapy*; D007211:Indoles / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged
chemical_list: D001647:Bile Acids and Salts; D005229:Fatty Acids, Monounsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D000077340:Fluvastatin