Effects of hypolipidemic treatment on serum markers of vascular inflammation in dyslipidemic men.
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.
Hernández
Cristina
C
Endocrinology Division, Hospital General Vall d'Hebron, Barcelona, Spain.
Lecube
Albert
A
Barberá
Gloria
G
Chacón
Pilar
P
Lima
Joan
J
Simó
Rafael
R
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
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