Horm Metab Res 2003; 35(8): 479-485
DOI: 10.1055/s-2003-41805
Original Clinical
© Georg Thieme Verlag Stuttgart · New York

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

H.  Nawawi1 , N.  S.  Osman1 , K.  Yusoff2 , B.  A.  K.  Khalid2
  • 1Chemical Pathology Unit, Department of Pathology
  • 2Department of Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia
Further Information

Publication History

Received 14 January 2003

Accepted after revision 19 March 2003

Publication Date:
02 September 2003 (online)

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.

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Assoc Prof. Dr. H. M. Nawawi

Chemical Pathology Unit · Department of Pathology · Faculty of Medicine · Universiti Kebangsaan Malaysia

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