Changes in plasma levels of fat-derived hormones adiponectin, leptin, resistin and visfatin in patients with rheumatoid arthritis

Background: Rheumatoid arthritis is a chronic autoimmune inflammatory condition characterised by polyarthritis and severe change in body mass and neuroendocrine environment. Objectives: To investigate plasma levels of adipocytokines (leptin, adiponectin, visfatin and resistin) in patients with rheum...

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Published in:Annals of the rheumatic diseases Vol. 65; no. 9; pp. 1198 - 1201
Main Authors: Otero, M, Lago, R, Gomez, R, Lago, F, Dieguez, C, Gómez-Reino, J J, Gualillo, O
Format: Journal Article
Language:English
Published: London BMJ Publishing Group Ltd and European League Against Rheumatism 01-09-2006
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Summary:Background: Rheumatoid arthritis is a chronic autoimmune inflammatory condition characterised by polyarthritis and severe change in body mass and neuroendocrine environment. Objectives: To investigate plasma levels of adipocytokines (leptin, adiponectin, visfatin and resistin) in patients with rheumatoid arthritis and to compare them with levels in healthy controls. Methods: Adiponectin, resistin, visfatin and leptin concentrations were measured in 31 patients with rheumatoid arthritis and 18 healthy controls by using specific enzyme-linked immunosorbent assays. Results: Patients with rheumatoid arthritis showed considerably higher plasma levels of leptin, adiponectin and visfatin than healthy controls. No marked difference was observed in resistin levels between patients and controls. Conclusion: A marked increase in plasma levels of leptin, adiponectin and visfatin was noted in patients with rheumatoid arthritis, whereas resistin levels were similar to those observed in healthy controls. Coordinated roles for adiponectin, leptin and visfatin are suggested in the modulation of the inflammatory environment in patients with rheumatoid arthritis, whereas the lack of modulation in resistin levels is predictive of an irrelevant role for this peptide, suggesting that resistin level is probably not one of the main signals associated with the pathogenesis of this disease.
Bibliography:PMID:16414972
Correspondence to:
 O Gualillo
 Research Laboratory 4, Santiago University Clinical Hospital, Research Area, Travesía Choupana sin numero, 15705 Santiago de Compostela, Spain; gualillo@usc.es
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Copyright © 2006 BMJ Publishing Group Ltd & European League Against Rheumatism
ISSN:0003-4967
1468-2060
DOI:10.1136/ard.2005.046540