title: Effects of cerivastatin sodium, a new HMG-CoA reductase inhibitor, on biliary lipid metabolism in patients with hypercholesterolemia.
abstract: The use of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors has become common in the treatment of hypercholesterolemia. The present uncontrolled study was undertaken to determine the effect of cerivastatin sodium (BAY w 6228), a new HMG-CoA reductase inhibitor, on biliary lipid levels in patients with hypercholesterolemia. Twenty-one hypercholesterolemic patients (World Health Organization type IIa = 16 patients; type IIb = 5 patients) received placebo during a 4- to 6-week observation period, after which they received cerivastatin sodium 0.2 mg/d for 12 weeks. Fasting blood samples were drawn for the measurement of serum lipid levels early in the morning before the start of treatment and once a month for each of the 12 weeks of cerivastatin sodium treatment. Gallbladder bile samples were aspirated with a duodenal tube by cerulein stimulation to assess bile lithogenicity. Serum total cholesterol levels decreased markedly after 12 weeks. However, no significant difference was found in the molar percentage composition of biliary lipids (e.g., cholesterol, phospholipids, and total bile acids) or in individual biliary bile acids. Consequently, no significant change in bile cholesterol saturation index was found. The index values before and after 12 weeks of treatment were 0.81 +/- 0.38 and 0.80 +/- 0.47, respectively, whereas when patients were grouped by type of hypercholesterolemia, there was a tendency toward decreased lithogenicity in patients with type IIb but not type IIa hypercholesterolemia. We concluded that cerivastatin sodium was an effective cholesterol-lowering drug that did not appear to worsen biliary lipid metabolism and that may decrease lithogenicity in patients with type IIb hypercholesterolemia.
authors.affiliation: First Department of Internal Medicine, Hiroshima University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Tazuma
authors.forename: G
authors.initials: G
authors.lastname: Yamashita
authors.forename: H
authors.initials: H
authors.lastname: Ochi
authors.forename: H
authors.initials: H
authors.lastname: Miura
authors.forename: T
authors.initials: T
authors.lastname: Kajihara
authors.forename: Y
authors.initials: Y
authors.lastname: Hattori
authors.forename: H
authors.initials: H
authors.lastname: Miyake
authors.forename: T
authors.initials: T
authors.lastname: Nishioka
authors.forename: H
authors.initials: H
authors.lastname: Hyogo
authors.forename: Y
authors.initials: Y
authors.lastname: Sunami
authors.forename: S
authors.initials: S
authors.lastname: Yasumiba
authors.forename: G
authors.initials: G
authors.lastname: Kajiyama
mesh_terms: D000328:Adult; D000368:Aged; D001646:Bile / Q000187:drug effects / Q000378:metabolism*; D001647:Bile Acids and Salts / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D004032:Diet; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000188:drug therapy* / Q000378:metabolism; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010713:Phosphatidylcholines / Q000378:metabolism; D011725:Pyridines / Q000627:therapeutic use*; D014280:Triglycerides / Q000097:blood
chemical_list: D001647:Bile Acids and Salts; D005227:Fatty Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D008055:Lipids; D010713:Phosphatidylcholines; D011725:Pyridines; D014280:Triglycerides; D002784:Cholesterol; C086276:cerivastatin