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Clinical and epidemiological research
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Association between leptin, adiponectin and resistin and long-term progression of hand osteoarthritis
  1. Erlangga Yusuf1,
  2. Andreea Ioan-Facsinay1,
  3. Jessica Bijsterbosch1,
  4. Inge Klein-Wieringa1,
  5. Joanneke Kwekkeboom1,
  6. P Eline Slagboom2,
  7. Tom WJ Huizinga1,
  8. Margreet Kloppenburg1
  1. 1Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands
  2. 2Department of Molecular Epidemiology, Leiden University Medical Center, Leiden, The Netherlands
  1. Correspondence to Erlangga Yusuf, Department of Rheumatology, Leiden University Medical Center, Room C1-46, Postbus 9600, 2300 RC Leiden, The Netherlands; angga.yusuf{at}gmail.com

Abstract

Objective To investigate the association between baseline serum adipokines levels—leptin, adiponectin and resistin—and long-term progression of hand osteoarthritis (HOA).

Methods Baseline and 6-year radiographs of 164 patients (mean age 60 years, 81% women) with HOA (defined as a Kellgren and Lawrence score ≥2 in at least two hand joints) were assessed for joint space narrowing (JSN) in 32 hand joints using the Osteoarthritis Research Society International atlas. Progression was defined as a change in the sum of the JSN score above the smallest detectable change of 2, reflecting change above measurement error. Serum adipokines were measured at baseline and patients were categorised by adipokine tertiles. RRs (and 95% CI) of HOA progression for patients in the second and third tertiles were calculated relative to the first tertile, using generalised estimating equations. Adjustments were made for age, sex and body mass index.

Results Patients in the two highest tertiles of adiponectin had a decreased risk of 70% (RR=0.3 (0.2 to 0.7)) for HOA progression in comparison with patients in the lowest tertile. Leptin and resistin levels were not associated with progression.

Conclusion Adiponectin levels are associated with progression of HOA, suggesting that adiponectin may be involved in the pathophysiology of OA.

https://doi.org/10.1136/ard.2010.146282

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    Footnotes

    • Funding This study was financially supported by TI-Pharma, Pfizer (Groton, CT, USA), Centre for Medical Systems Biology (CMSB) within the framework of the Netherlands Genomics Initiative (NGI) and the Dutch Arthritis Association. However, they did not contribute to study design, data collection, data analysis and writing of the manuscript. Publication was not contingent on the approval of the sponsors.

    • Competing interests None.

    • Ethics approval This study was conducted with the approval of the medical ethical commission Leiden University Medical Center.

    • Provenance and peer review Not commissioned; externally peer reviewed.