title: Effects of pravastatin and atorvastatin on HDL cholesterol and glucose metabolism in patients with dyslipidemia and glucose intolerance: the PRAT study.
abstract: OBJECTIVE
  While statins have the property of increasing high-density lipoprotein cholesterol (HDL-C) in addition to lowering low-density lipoprotein cholesterol (LDL-C), a potential adverse effect on glucose metabolism has raised a concern over statin therapy. In a comparative trial, we investigated the effects of low-dose pravastatin and atorvastatin on HDL-C and glucose metabolism in patients with elevated LDL-C levels and glucose intolerance.
  
  
  METHODS
  Eligible patients were men aged ≥20 years or postmenopausal women who had LDL-C ≥140 mg/dL, HDL-C <80 mg/dL, and triglycerides <500 mg/dL and who had glucose intolerance. The patients were randomly allocated to either pravastatin (10 mg/day) or atorvastatin (10 mg/day) treatment for 12 months in an unblinded fashion. The percent changes from the baseline were compared between the treatments.
  
  
  RESULTS
  Of 202 patients who were randomized to either of the two treatments, 195 patients started the study medication, and 187 patients underwent the follow-up measurements at 6 or 12 months (pravastatin, n= 93; atorvastatin, n= 94). HDL-C increased by 4.3% (p= 0.03) in the pravastatin group and by 5.8% (p=0.0005) in the atorvastatin group and showed no between-group difference (p= 0.38). LDL-C decreased substantially in both groups (pravastatin, 21.5%; atorvastatin, 35.5%), and the decrease was much greater in the atorvastain group (p<0.0001). HbA1c slightly increased in both groups, but showed no measurable difference in the increase between the two treatments (p=0.30).
  
  
  CONCLUSIONS
  Pravastatin and atorvastatin of 10 mg per day each increased HDL-C by almost the same extent. These two statins did not show a differential effect on glucose metabolism.
authors.affiliation: International University of Health and Welfare, Graduate School of Pharmaceutical Medicine, Fukuoka, Japan. jsas@nifty.com
authors.forename: Jun
authors.initials: J
authors.lastname: Sasaki
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Otonari
authors.forename: Yasufumi
authors.initials: Y
authors.lastname: Uchida
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Ikeda
authors.forename: Sadatoshi
authors.initials: S
authors.lastname: Biro
authors.forename: Suminori
authors.initials: S
authors.lastname: Kono
mesh_terms: D000328:Adult; D000069059:Atorvastatin; D001786:Blood Glucose / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood*; D050171:Dyslipidemias / Q000097:blood*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D018149:Glucose Intolerance / Q000097:blood*; D006538:Heptanoic Acids / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D017698:Postmenopause; D017035:Pravastatin / Q000008:administration & dosage / Q000494:pharmacology*; D011758:Pyrroles / Q000008:administration & dosage / Q000494:pharmacology*; D055815:Young Adult
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D000069059:Atorvastatin; D005947:Glucose; D017035:Pravastatin