Rheumatology Advance Access originally published online on May 29, 2008
Rheumatology 2008 47(7):1082-1087; doi:10.1093/rheumatology/ken187
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Resistin in serum is associated with higher levels of IL-1Ra in post-menopausal women with rheumatoid arthritis
Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.
Correspondence to: H. Forsblad d’Elia, Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at Göteborg University, Guldhedsgatan 10, S-413 46 Göteborg, Sweden. E-mail: helena.forsblad{at}vgregion.se
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Abstract |
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Objectives. The aim of this study was to investigate associations between serum levels of resistin, an adipokine and markers of inflammation, bone metabolism, plasma lipids and kidney function in post-menopausal RA patients and to evaluate if HRT during 2 yrs affected resistin levels.
Methods. Eighty-eight women were randomly allocated to receive HRT, vitamin D3 and calcium or vitamin D3 and calcium alone. Serum levels of resistin, IL-1β, IL-1 receptor antagonist (IL-1Ra), IL-6, IL-6 soluble receptor, TNF-
were measured by ELISA, markers of bone metabolism, carboxyterminal cross-linked telopeptide of type I collagen (ICTP) and carboxyterminal propeptide of type I procollagen by RIA, ESR, CRP, Hb, creatinine and lipids by standard laboratory techniques, BMD and total lean mass (TLM) by DXA and joint destruction by Larsen score. Resistin was also measured in 42 healthy control women.
Results. There was no difference in resistin concentration between patients and healthy controls. Resistin was significantly correlated with IL-1Ra, CRP, TNF-, ICTP, glucocorticosteroids and Larsen score and inversely with BMD, hip and with TLM. In multiple regression analysis, IL-1Ra, TLM and use of corticosteroids remained determinants of resistin. Patients treated with HRT displayed significant increase in resistin compared with controls in the first but not the second year.
Conclusions. Resistin was associated with increased inflammation, particularly by the acute-phase reactant IL-1Ra antagonizing IL-1β, joint destruction, glucocorticosteroids and with reduced BMD and TLM. These findings suggest resistin being a significant mediator in the inflammatory process in RA. Further studies examining the mechanisms behind the relation between resistin and IL-1Ra are encouraged. HRT does not seem to have important long-term effect on resistin.
KEY WORDS: Rheumatoid arthritis, Resistin, Hormone replacement therapy, Oestrogen, Oestradiol, Cytokines, Interleukin-1Ra, Glucocorticosteroids, Bone mineral density, Total lean mass
Submitted 30 January 2008;
revised version accepted 10 April 2008.
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