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Ann Rheum Dis 2009;68:1197-1200 doi:10.1136/ard.2008.096057
  • Clinical and epidemiological research

Effects of infliximab therapy on biological markers of synovium activity and cartilage breakdown in patients with rheumatoid arthritis

  1. H Marotte1,
  2. E Gineyts2,
  3. P Miossec1,
  4. P D Delmas2
  1. 1
    Hospices Civils de Lyon-bioMérieux Research Unit on Rheumatoid Arthritis, Hospital Edouard Herriot, Lyon, France
  2. 2
    INSERM Research Unit 831 and University Lyon-1, Lyon, France
  1. Dr H Marotte, Clinical Immunology Unit, Departments of Immunology and Rheumatology and Hospices Civils de Lyon-bioMérieux Research Unit on Rheumatoid Arthritis, Hôpital Edouard Herriot, Pavillon F, 69437 Lyon Cedex 03, France; hubert.marotte{at}laposte.net
  • Accepted 3 August 2008
  • Published Online First 19 August 2008

Abstract

Background: Defining the remission criteria of rheumatoid arthritis (RA) remains a critical issue. Markers of synovium activity, urinary glucosyl-galactosyl-pyridinoline (Glc-Gal-PYD) and of cartilage destruction, urinary C-terminal crosslinking telopeptide of type II collagen (CTX-II) have been shown to reflect disease activity and joint damage progression in RA.

Methods: The prospective study cohort comprised 66 RA patients treated with infliximab and methotrexate and 76 healthy controls. Measurements of urinary Glc-Gal-PYD and CTX-II were performed at baseline and at 1 year of infliximab therapy.

Results: At baseline, urinary Glc-Gal-PYD and CTX-II levels were increased in patients with RA and correlated with modified Sharp scores and progression of joint damage. Patients with more progressive joint destruction had higher Glc-Gly-PYD and CTX-II baseline levels.

Conclusion: These markers reflected bone erosion evolution and might be useful for treatment monitoring and evaluation of RA. Markers remained high even in clinical responders after infliximab, suggesting persistence of synovitis.

Footnotes

  • Competing interests: None.

  • Ethics approval: Ethics approval was obtained.

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