Slow progression of joint damage in early rheumatoid arthritis treated with cyclosporin a
Article first published online: 12 DEC 2005
Copyright © 1996 American College of Rheumatology
Arthritis & Rheumatism
Volume 39, Issue 6, pages 1006–1015, June 1996
How to Cite
Pasero, G., Priolo, F., Marubini, E., Fantini, F., Ferraccioli, G., Magaro, M., Marcolongo, R., Oriente, P., Pipitone, V., Portioli, I., Tirri, G., Trotta, F. and Casa-Alberighi, O. D. (1996), Slow progression of joint damage in early rheumatoid arthritis treated with cyclosporin a. Arthritis & Rheumatism, 39: 1006–1015. doi: 10.1002/art.1780390618
- Issue published online: 12 DEC 2005
- Article first published online: 12 DEC 2005
- Manuscript Accepted: 23 JAN 1996
- Manuscript Received: 15 MAY 1995
- Sandoz P.F., Italy
Objective. To evaluate the ability of low-dose cyclosporin A (CsA) to control radiologic disease progression, and to assess the clinical efficacy and tolerability of CsA, compared with conventional disease-modifying antirheumatic drugs (DMARDs), in patients with early active rheumatoid arthritis (RA).
Methods. In this long-term, multicenter, prospective, open, blinded end point, randomized trial, 361 consenting patients with early (< 4 years since diagnosis) active RA were enrolled. Of the eligible patients, 167 were treated with CsA at 3 mg/kg/day, and 173 with DMARDs. The decision to use conventional antirheumatic drugs as controls was based on the fact that joint erosion could be expected to occur after 1 year regardless of the type of DMARD being used. The possibility of switching therapies in both groups was intended to keep the largest possible number of patients in the study.
Results. Blinded evaluation of hand and foot radiographs after 12 months of treatment showed that CsA led to a significant (P < 0.001) delay in the mean ± SD progression in the eroded joint count (1.3 ± 3.1 versus 2.4 ± 3.0 for the control group) and in the joint damage score (3.6 ± 8.9 versus 6.9 ± 9.1 for the control group), both measured by the Larsen-Dale method. When only the patients without erosion at baseline were considered (37 in the CsA-treated group and 54 in the control group), erosion appeared in only 10.8% of the CsA-treated patients, but in 51.8% of the controls (P = 0.00005). Low-dose CsA was as effective as traditional DMARDs in controlling clinical symptoms. Maintenance on the initially prescribed treatment regimen (“survival on treatment”) was also better at 12 months with CsA than with DMARDs (89.2% versus 77.5%; P = 0.002). The tolerability of CsA was acceptable.
Conclusion. These 12-month results suggest that low-dose CsA decreases the rate of further joint damage in previously involved joints as well as the rate of new joint involvement in previously uninvolved joints, in patients with early RA.