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Ann Rheum Dis 2009;68:1316-1321 doi:10.1136/ard.2007.086728
  • Clinical and epidemiological research

Sustained changes in lipid profile and macrophage migration inhibitory factor levels after anti-tumour necrosis factor therapy in rheumatoid arthritis

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  1. C A Wijbrandts1,
  2. S I van Leuven2,
  3. H D Boom1,
  4. D M Gerlag1,
  5. E G S Stroes2,
  6. J J P Kastelein2,
  7. P P Tak1
  1. 1
    Department of Clinical Immunology and Rheumatology, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands
  2. 2
    Department of Vascular Medicine, Academic Medical Center/University of Amsterdam, Amsterdam, The Netherlands
  1. Professor P P Tak, Division of Clinical Immunology and Rheumatology, Academic Medical Center/University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands; P.P.Tak{at}amc.uva.nl
  • Accepted 3 August 2008
  • Published Online First 22 August 2008

Abstract

Background: Macrophage migration inhibitory factor (MIF) has recently emerged as an important cytokine possibly linking rheumatoid arthritis (RA) and atherogenesis. Because atherogenesis is accelerated in RA this study was conducted to investigate whether anti-tumour necrosis factor (TNF) therapy could lead to sustained downregulation of systemic MIF levels and improvement in lipid profiles.

Methods: Fifty RA patients with active disease (disease activity score in 28 joints (DAS28) ≥3.2), who started adalimumab therapy at 40 mg every other week, were included. At baseline, weeks 16 and 52 serum levels of MIF and lipids were assessed. In addition, the DAS28 and serum C-reactive protein (CRP) levels and erythrocyte sedimentation rate (ESR) were determined.

Results: After 16 weeks of adalimumab therapy, both DAS28 and MIF levels were significantly decreased (p<0.001 and p = 0.020, respectively). This was sustained up to week 52 (p<0.001 and p = 0.012, respectively). CRP levels and ESR were significantly reduced after 16 and 52 weeks of adalimumab therapy (p<0.001). High-density lipoprotein cholesterol levels increased at week 16 (p<0.001), but returned to baseline at week 52. Apolipoprotein (apo) A-I levels increased at week 16 (p<0.001) and remained stable (p = 0.005). This resulted in an improved apo B/A-I ratio.

Conclusions: The results underline the sustained downregulation of MIF as a potential new mechanism by which anti-TNF therapy might reduce vascular inflammation, and as such perhaps cardiovascular morbidity in RA patients. This hypothesis is supported by an improved apo B/A-I ratio as well as reduced CRP levels in these patients.

Footnotes

  • Competing interests: PPT is a member of the advisory board of Abbott and has received honoraria for lectures. The study sponsors had no involvement in the study design, the collection, analysis and interpretation of the data, writing the report, or the decision to submit the paper for publication.

  • Funding: This study was supported by Abbott Laboratories.

  • Ethics approval: Approval for this study was obtained from the institutional ethics review committee at the Academic Medical Center/University of Amsterdam.

  • Patient consent: Obtained.

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