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Visfatin is not associated with inflammation or metabolic syndrome in patients with severe rheumatoid arthritis undergoing anti-TNF-a therapy
M.A. Gonzalez-Gay, T.R. Vazquez-Rodriguez, M.T. Garcia-Unzueta, A. Berja, J.A. Miranda-Filloy, J.M. De Matias, C. Gonzalez-Juanatey, J. Llorca
CER459
2010 Vol.28, N°1
PI 0056, PF 0062
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PMID: 20346239 [PubMed]
Received: 16/06/2009
Accepted : 12/10/2009
In Press: 10/03/2010
Published: 15/03/2010
Abstract
OBJECTIVES:
Visfatin is an insulin-mimetic adipokine. In non-rheumatoid arthritis (RA) patients circulating levels of visfatin are correlated with the amount of visceral fat. Recent studies have disclosed an implication of visfatin in inflammation. Chronic systemic inflammation is of major importance in the development of atherosclerosis in RA. In the present study we investigated whether inflammation, obesity or metabolic syndrome are potential determinants of circulating visfatin concentrations in a group of RA patients on periodical treatment with the TNF-α blocker infliximab due to severe disease. We also assessed whether the infusion of infliximab may alter circulating visfatin concentrations in patients with severe RA.
METHODS:
We investigated 33 non-diabetic patients with RA on periodical treatment with infliximab. Serum visfatin levels were determined immediately prior to and after infliximab infusion.
RESULTS:
There was no correlation between body mass index of RA patients and baseline serum level of visfatin. Also, no significant correlations between baseline visfatin levels and the age at the time of the study or at the onset of the disease, disease duration, ESR and CRP levels, DAS28, lipids, insulin sensitivity, resistin or the cumulative prednisone dose at the time of the study were found. Visfatin levels did not change upon infliximab infusion.
CONCLUSIONS:
In RA patients on TNF-α blocker treatment, circulating visfatin levels are unrelated to disease activity, adiposity or metabolic syndrome. The beneficial effect of anti-TNF-α therapy on cardiovascular mortality in RA does not seem to be mediated by changes in serum levels of visfatin.
