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FRI0082 Effect of hydroxychloroquine therapy on cartilage injury in rheumatoid arthritis
  1. HB Lindsley,
  2. D Eyre,
  3. L Atley,
  4. DD Smith
  1. Internal Medicine, University of Kansas Medical Center, Kansas City, USA

Abstract

Background Better methods for assessing articular injury are needed to monitor efficacy of disease-modifying therapy in rheumatoid arthritis (RA).

Objectives The purpose of this study was to measure serum levels of cross-linked peptides from the C-telopeptide of type II collagen (col2CTx) during treatment of patients with RA.

Methods Serial serum samples were taken from a previous clinical trial1 in which 213 subjects with active RA received a loading dose of hydroxychloroquine 400, 800 or 1200 mg/d for six weeks, then 400 mg/d for up to Week 24. They also received naproxen 1000 mg/d. From 213 subjects in the original trial, 152 paired sera were available for study; col2CTx levels were measured at Weeks 0 and 24, using an ELISA that measures a breakdown product of human cartilage. These levels were compared with tender (TJC) and swollen (SJC) joint counts, and the erythrocyte sedimentation rate (ESR).

Results Median (± SEM) col2CTx levels decreased by 10% (p = 0.006, Wilcoxon signed ranks) by 24 weeks. Clinical variables decreased much more dramatically by 24 weeks; the TJC declined by 67% (p = 0.000), and the SJC, by 56% (p = 0.000). The ESR declined by 33% (p = 0.000) during this same period. Thus, the magnitude in reduction of circulating col2CTx was less than TJC, SJC and ESR but did show significant improvement.

Abstract FRI0082 Table 1

Conclusion This limited improvement in col2CTX may be due to a lag in suppression of structural damage to cartilage. Since joint radiographs typically require a year or more to show a reduction in joint destruction, the measurement of col2CTx may give an earlier indication of reduction in injury to cartilage. Further clinical studies need to be done in patients treated with more intensive antirheumatic therapy and over longer time periods.

Reference

  1. Furst DE, et al. Arthritis Rheum. 1999;42(2):357–65

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