Background Adipokines have inflammatory and immunomodulatory properties that may contribute to erosive joint damage. The association of serum adipokine levels with progression of radiographic joint damage in patients with rheumatoid arthritis (RA) was prospectively explored.
Methods Patients with RA underwent serum adipokine assessment (adiponectin, resistin, leptin) at three timepoints and hand/feet x-rays, scored using the Sharp-van der Heijde Score (SHS), at baseline and the third study visit, separated by an average of 39±4 months. The associations of baseline and average adipokine levels with change in SHS were explored, adjusting for pertinent confounders.
Results Of the 152 patients studied, 85 (56%) showed an increase in SHS (defined as >0 SHS units). Among the adipokines studied, only adiponectin was significantly associated with radiographic progression, with average adiponectin levels more strongly associated than baseline levels. After adjusting for average C reactive protein and baseline SHS, patients in the highest quartile of average adiponectin had a SHS progression rate more than double the lowest quartile (1.00 vs 0.48 units/year; p=0.008). Similarly, those in the highest quartile of adiponectin had a more than fivefold greater odds of any radiographic progression compared with the lowest quartile (OR 5.75; p=0.002). The magnitude of the association of average adiponectin levels with radiographic progression was greater in women, those with body mass index <30 kg/m2 and those receiving baseline biological disease-modifying antirheumatic drugs.
Conclusions These prospective data provide evidence of temporality and dose-response in the relationship between circulating adiponectin and erosive joint destruction in RA, and highlight subgroups of patients at highest risk for adiponectin-associated radiographic progression.
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Funding This work is supported by grant numbers AR050026-01 (JMB) and 1K23AR054112-01 to JTG from the National Institutes of Health, National Institute of Arthritis and Musculoskeletal and Skin Diseases; a Clinical Investigator Fellowship Award from the Research and Education Foundation of the American College of Rheumatology to JTG; and the Johns Hopkins Bayview Medical Center General Clinical Research Center (grant number M01RR02719).
Competing interests None.
Ethics approval This study was conducted with the approval of the Johns Hopkins University.
Provenance and peer review Not commissioned; externally peer reviewed.
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