Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovitis and damage of bone and cartilage. The major goals of therapy in RA are to relieve pain, swelling of joints; improve joint function; stop joint damage, and prevent disability and disease - related morbidity. The past decade has seen a major transformation in the treatment of RA in terms of approach and choice of drugs. The previous therapeutic approach, termed the therapeutic pyramid, generally involved initial conservative management with non - steroidal anti - inflammatory drugs (NSAIDs) for several years; disease - modifying antirheumatic drugs (DMARDs) were withheld until clear evidence of erosions was seen. DMARDs were then added individually in slow succession as the disease progressed. This form of treatment has been supplanted by early initiation of DMARDs and combination DMARD therapy in patients with the potential for progressive disease. The idea of early intervention with DMARDs has been validated in several randomised trials. This paradigm shift partly resulted from unsatisfactory outcomes with the pyramid approach, and an increased awareness of the cost, lost productivity, morbidity, and decreased life expectancy associated with RA. These findings are the consequences of progressive disease, and have provided the impetus for development of more effective therapies to prevent joint destruction and maintain functional status. The continuing elucidation of pathophysiological pathways relevant in RA, coupled with advanced in biotechnology, offer substantial hopes for the development of potent and specific pharmacotherapy for RA.
References
1. Hochberg MC. What have we learned from the large outcomes trials of COX-2 selective inhibitors? The rheumatologist's perspective. Clin Exp Rheumatol. 2001. 19:6 Suppl 25. S15–S22.
2. Bijlsma JW, Van Everdingen AA, Huisman M, De Nijs RN, Jacobs JW. Glucocorticoids in rheumatoid arthritis: effects on erosions and bone. Ann N Y Acad Sci. 2002. 966:82–90.
3. Conaghan PG, Brooks P. Disease - modifying antirheumatic drugs, including methotrexate, gold, sulfasalazine, antimalarials, and D - penicillamine. Curr Opin Rheumatol. 1996. 8:176–182.
![crossref](/image/icon/bnr_ref_cross.gif)
![crossref](/image/icon/bnr_ref_cross.gif)
4. Breedveld FC, Dijkmans BAC. Differential therapy in early and late stages of rheumatoid arthritis. Curr Opin Rheumatol. 1996. 8:226–229.
![crossref](/image/icon/bnr_ref_cross.gif)
![crossref](/image/icon/bnr_ref_cross.gif)
6. Weinblatt ME, Kaplan H, Germain BF, Block S, Solomon SD, Gall E, et al. Methotrexate in rheumatoid arthritis; a five year prospective multicenter study. Arthritis Rheum. 1994. 37:1492–1498.
![crossref](/image/icon/bnr_ref_cross.gif)
![crossref](/image/icon/bnr_ref_cross.gif)
7. Sharp JT, Strand V, Leung H, Hurley F, Loew-Fiedrich I. Treatment with leflunomide slows radiographic progression of rheumatoid arthritis. Arthritis Rheum. 2000. 43:495–505.
![crossref](/image/icon/bnr_ref_cross.gif)
![crossref](/image/icon/bnr_ref_cross.gif)
8. Pisetsky DS, St Clair EW. Progress in the treatment of rheumatoid arthritis. JAMA. 2001. 286:2787–2790.
![crossref](/image/icon/bnr_ref_cross.gif)
![crossref](/image/icon/bnr_ref_cross.gif)
9. Marra CA, Esdaile JM, Guh D, Fisher JH, Chalmers A, Anis AH. The effectiveness and toxicity of cyclosporin A in rheumatoid arthritis: longitudinal analysis of a population-based registry. Arthritis Rheum. 2001. 45:240–245.
![crossref](/image/icon/bnr_ref_cross.gif)
![crossref](/image/icon/bnr_ref_cross.gif)
10. Criscione LG, St Clair EW. Tumor necrosis factor - alpha antagonists for the treatment of rheumatic diseases. Curr Opin Rheumatol. 2002. 14:204–211.
![crossref](/image/icon/bnr_ref_cross.gif)
![crossref](/image/icon/bnr_ref_cross.gif)