title: Joint effects of HMG-CoA reductase inhibitors and eicosapentaenoic acids on serum lipid profile and plasma fatty acid concentrations in patients with hyperlipidemia.
abstract: HMG-CoA reductase inhibitors reduce serum total cholesterol concentrations and the risk of coronary heart disease in patients with hypercholesterolemia. Recently, it has been reported that patients with combined hyperlipidemia are also at risk of coronary heart disease. However, HMG-CoA reductase inhibitor therapy alone does not sufficiently reduce serum triglyceride concentrations. Epidemiological and clinical evidence has shown that fish oil can lower plasma lipid levels, especially triglycerides. Consequently, we investigated the effects of the combination of HMG-CoA reductase inhibitors and eicosapentaenoic acid, a major component of fish oil, on hyperlipidemia. We administered 900-1,800 mg/day of the ethyl ester of eicosapentaenoic acid to patients with hyperlipidemia who had been treated with HMG-CoA reductase inhibitors for 30 +/- 6 months (means +/- SE). Serum total cholesterol and triglyceride concentrations were significantly decreased 3 months after the administration of eicosapentaenoic acid (from 5.63 +/- 0.23 mmol/l to 5.02 +/- 0.20 mmol/l, P < 0.05; from 2.07 +/- 0.41 mmol/l to 1.08 +/- 0.17 mmol/l, P < 0.01, respectively). Serum high-density lipoprotein-cholesterol concentrations were significantly increased after the treatment (from 1.23 +/- 0.12 mmol/l to 1.34 +/- 0.13 mmol/l, P < 0.05). Plasma eicosapentaenoic acid concentrations and the ratio to arachidonic acid in plasma were also significantly increased 3 months after the treatment (from 101.9 +/- 8.1 mg/l to 181.8 +/- 23.9 mg/l, P < 0.001; from 0.640 +/- 0.075 to 1.211 +/- 0.170, P < 0.001, respectively). These results suggested that the combination therapy of HMG-CoA reductase inhibitors and eicosapentaenoic acid was effective for patients with hyperlipidemia.
authors.affiliation: First Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Hamazaki
authors.forename: M
authors.initials: M
authors.lastname: Ohta
authors.forename: K
authors.initials: K
authors.lastname: Okuda
authors.forename: M
authors.initials: M
authors.lastname: Urakaze
authors.forename: S
authors.initials: S
authors.lastname: Sawazaki
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
authors.forename: A
authors.initials: A
authors.lastname: Satoh
authors.forename: R
authors.initials: R
authors.lastname: Temaru
authors.forename: Y
authors.initials: Y
authors.lastname: Ishikura
authors.forename: M
authors.initials: M
authors.lastname: Takata
authors.forename: M
authors.initials: M
authors.lastname: Kishida
authors.forename: M
authors.initials: M
authors.lastname: Kobayashi
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001053:Apolipoproteins / Q000097:blood*; D016718:Arachidonic Acid / Q000097:blood; D002784:Cholesterol; D008076:Cholesterol, HDL / Q000097:blood; D015118:Eicosapentaenoic Acid / Q000008:administration & dosage*; D005227:Fatty Acids / Q000097:blood*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy*; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D014280:Triglycerides / Q000097:blood*
chemical_list: D001053:Apolipoproteins; D008076:Cholesterol, HDL; D005227:Fatty Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008074:Lipoproteins; D014280:Triglycerides; C112017:remnant-like particle cholesterol; D016718:Arachidonic Acid; D002784:Cholesterol; D015118:Eicosapentaenoic Acid