title: Effects of hypolipidemic treatment on serum markers of vascular inflammation in dyslipidemic men.
abstract: BACKGROUND
  The purpose of our study was to assess the effect of hypolipidemiant drugs on serum markers of vascular inflammation (E-Selectin, VCAM-1 and MCP-1) in dyslipidemic men without cardiovascular disease.
  
  
  METHODS
  84 dyslipidemic men were consecutively recruited from the Lipid Unit of a tertiary hospital. The patients were placed on statins (n=44) or fibrates (n=22), depending on the lipid profile, for 4 months. In the control group (n=18), a hypolipidemiant diet alone was indicated.
  
  
  RESULTS
  Baseline levels of VCAM-1 and MCP-1 were not correlated with the lipid profile. By contrast, baseline E-Selectin levels correlated directly with glucose and triglyceride levels, and negatively with HDL-C. In multiple regression analysis, HDL-C and glucose concentrations independently influenced E-selectin levels. After treatment, we observed a significant decrease of E-Selectin levels in patients treated with statins, and the changes in E-Selectin levels were inversely associated with HDL-C variations. We did not observe any changes in VCAM-1 levels after the treatment regime we used. Regarding MCP-1, a significant increase was detected in the patients receiving fibrates. In addition, the percentage increment of MCP-1 was higher in patients treated with gemfibrozil than in patients who received bezafibrate.
  
  
  CONCLUSIONS
  We observed a reduction in E-Selectin levels after statin therapy. This finding was associated with increased HDL-C. Fibrates, especially gemfibrozil, increased MCP-1 concentrations. This deleterious effect was unrelated to changes in lipid profile, and may help explain why fibrates have less impact than statins in reducing cardiovascular disease.
authors.affiliation: Endocrinology Division, Hospital General Vall d'Hebron, Barcelona, Spain.
authors.forename: Cristina
authors.initials: C
authors.lastname: Hernández
authors.forename: Albert
authors.initials: A
authors.lastname: Lecube
authors.forename: Gloria
authors.initials: G
authors.lastname: Barberá
authors.forename: Pilar
authors.initials: P
authors.lastname: Chacón
authors.forename: Joan
authors.initials: J
authors.lastname: Lima
authors.forename: Rafael
authors.initials: R
authors.lastname: Simó
mesh_terms: D000328:Adult; D001629:Bezafibrate / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood; D019040:E-Selectin / Q000097:blood; D015248:Gemfibrozil / Q000627:therapeutic use; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood* / Q000188:drug therapy*; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000188:drug therapy; D006953:Hyperlipoproteinemia Type IV / Q000097:blood / Q000188:drug therapy; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000097:blood*; D008148:Lovastatin / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D019821:Simvastatin / Q000627:therapeutic use; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015415:Biomarkers; D018932:Chemokine CCL2; D019040:E-Selectin; D000960:Hypolipidemic Agents; D018836:Inflammation Mediators; D019010:Vascular Cell Adhesion Molecule-1; D008148:Lovastatin; D019821:Simvastatin; D015248:Gemfibrozil; D001629:Bezafibrate