title: Pravastatin compared to bezafibrate in the treatment of dyslipidemia in insulin-treated patients with type 2 diabetes mellitus.
abstract: BACKGROUND
  Both HMG-CoA reductase inhibitors and fibric acid derivates are used for the treatment of dyslipidemia in Type 2 diabetes patients. The aim of this study was to compare the lipid lowering effect of 40 mg pravastatin, a HMG-CoA reductase inhibitor, and 400 mg bezafibrate, a fibric acid derivate, on serum lipids, lipoproteins and lipoprotein composition in 45 (22 men and 23 women) dyslipidemic, insulin-treated Type 2 diabetes patients.
  
  
  METHODS
  The study used a double-blind, cross-over design.
  
  
  RESULTS
  Pravastatin treatment was more effective in reducing total cholesterol, LDL-cholesterol, LDL-triglycerides, LDL-ApoB and LDL/HDL-cholesterol ratio (all p<0.001 between groups) and total/HDL-cholesterol and ApoA1/LDL-ApoB ratios (both p<0.01) and always induced a decrease in LDL-cholesterol concentrations and LDL/HDL-cholesterol ratio irrespective of baseline triglyceride concentration. Bezafibrate was more effective in increasing HDL-cholesterol (p<0.01 between groups), ApoA1 lipoprotein and decreasing triglycerides (both p<0.001 between groups) but induced an increase in LDL-cholesterol concentration particularly in patients with baseline triglyceride concentrations exceeding 2.0 mmol/l. With bezafibrate treatment the LDL-cholesterol/LDL-ApoB ratio showed a tendency to rise, suggesting a change in the LDL particle composition to a less small and dense form, while pravastatin treatment induced a decrease in this ratio suggesting a change in the LDL particle to a more dense form. With pravastatin treatment a small rise in HbA(1c) was observed.
  
  
  CONCLUSIONS
  Pravastatin treatment is superior in lowering cholesterol-enriched lipoprotein subpopulations and improving cardiovascular risk factors. Bezafibrate is more effective in raising HDL-cholesterol and alters LDL particle composition to a more favorable form.
authors.affiliation: Department of internal medicine Ziekenhuis Amstelveen, Amstelveen, The Netherlands. rustemeijer@wxs.nl
authors.forename: C
authors.initials: C
authors.lastname: Rustemeijer
authors.forename: J A
authors.initials: JA
authors.lastname: Schouten
authors.forename: H J
authors.initials: HJ
authors.lastname: Voerman
authors.forename: H E
authors.initials: HE
authors.lastname: Hensgens
authors.forename: A J
authors.initials: AJ
authors.lastname: Donker
authors.forename: R J
authors.initials: RJ
authors.lastname: Heine
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D001629:Bezafibrate / Q000627:therapeutic use*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications* / Q000188:drug therapy*; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use*; D014280:Triglycerides / Q000097:blood
chemical_list: D000924:Anticholesteremic Agents; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D000960:Hypolipidemic Agents; D007328:Insulin; D014280:Triglycerides; D002784:Cholesterol; D017035:Pravastatin; D001629:Bezafibrate