Treatment of rheumatoid arthritisBMJ 2006; 332 doi: https://doi.org/10.1136/bmj.332.7534.152 (Published 19 January 2006) Cite this as: BMJ 2006;332:152
- Paul Emery (email@example.com), arc professor of rheumatology
- Academic Unit of Musculoskeletal Disease, Leeds Teaching Hospitals NHS Trust, Chapel Allerton Hospital, Leeds LS7 4SA
- Accepted 20 December 2005
Rheumatoid arthritis is a systemic disease that affects the synovial joints. It is a persistent chronic disease that spreads from joint to joint and affects about 0.5% of people worldwide. Not that long ago it was believed that antirheumatic therapy made little, if any, difference to the long term outcome of the disease.1 It was thought to be difficult to see patients appropriately early enough in the disease's progression, that an accurate diagnosis was not possible, and that therapies were ineffective. All this has now changed and this review examines these changes.
Sources and selection criteria
I obtained references from Medline, my personal archives, and the proceedings of the last two major international meetings—the European League against Rheumatism, Vienna and the American College of Rheumatology, San Diego. Search terms used were “inflammatory arthritis”, “rheumatoid arthritis”, “early rheumatoid arthritis”, “therapy”, “biologics”, “biologicals”, “anti-TNF therapy”, “DMARDS”, and “NSAIDs”.
Conventional management of rheumatoid arthritis
The standard treatment of patients with rheumatoid arthritis has included non-steroidal anti-inflammatory drugs. Although these drugs improve symptoms and signs, they do little to alter the structural progression and long term disability associated with rheumatoid arthritis. In the past, further therapy using disease modifying antirheumatic drugs was only prescribed when there was radiographic evidence of erosions (holes in bones). Disease modifying antirheumatic drugs were thought to reduce the damage shown on radiographs (disease modification), but although objective evidence for this effect was hard to obtain, proof has now been unequivocally shown. Disease modifying antirheumatic drugs are thought to act by direct or indirect inhibition of cytokines, unlike non-steroidal anti-inflammatory drugs, which act mainly by inhibiting cyclooxygenase and thereby reducing the production of inflammatory prostaglandins (inhibiting symptoms but not influencing structural damage).