title: Reduction in serum levels of adhesion molecules, interleukin-6 and C-reactive protein following short-term low-dose atorvastatin treatment in patients with non-familial hypercholesterolemia.
abstract: Hypercholesterolemia causes endothelial dysfunction, an early feature of atherosclerosis, leading to increased production of adhesion molecules and cytokines. The aim of this study was to investigate the effects of three months of treatment with low dose atorvastatin on serum levels of adhesion molecules, interleukin-6 (IL-6) and highly sensitive C-reactive protein (hs-CRP) in patients with non-familial hypercholesterolemia. Fifty-five patients with non-familial hypercholesterolemia were randomized to treatment with atorvastatin 10 mg/day or placebo for 3 months. Soluble intercellular adhesion molecules-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, IL-6 and hs-CRP levels were measured to assess the inflammatory activity of the endothelium. There was a significant reduction in ICAM-1 at 2 weeks (p<0.0001) with further reduction at 3 months (p<0.0001). At 3 months, there were significant reductions in VCAM-1 (p<0.02), IL-6 (p<0.0001) and hs-CRP (p<0.01), but an increase in E-selectin levels (p<0.002). Treatment with statin was an independent determinant of change in ICAM-1 (p<0.05) and IL-6 levels (p<0.05) after correcting for anthropometric indices, blood pressure and lipid profile. Low-dose atorvastatin treatment leads to reduction in proinflammatory markers of endothelial function, suggesting an attenuation of endothelial activation and improvement in endothelial function, independent of lipid lowering. This may lead to a reduction in the progression of atherosclerosis.
authors.affiliation: Chemical Pathology Unit, Department of Pathology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Cheras, Kuala Lumpur, Malaysia. hapizah@mail.hukm.ukm.my
authors.forename: H
authors.initials: H
authors.lastname: Nawawi
authors.forename: N S
authors.initials: NS
authors.lastname: Osman
authors.forename: K
authors.initials: K
authors.lastname: Yusoff
authors.forename: B A K
authors.initials: BA
authors.lastname: Khalid
mesh_terms: D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D019040:E-Selectin / Q000378:metabolism; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006937:Hypercholesterolemia / Q000097:blood* / Q000188:drug therapy*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011758:Pyrroles / Q000008:administration & dosage*; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*; D000093242:Interleukin-6 Inhibitors
chemical_list: D000069059:Atorvastatin; D002097:C-Reactive Protein; D019040:E-Selectin; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018799:Intercellular Adhesion Molecule-1; D015850:Interleukin-6; D008055:Lipids; D011758:Pyrroles; D019010:Vascular Cell Adhesion Molecule-1; D000093242:Interleukin-6 Inhibitors