| Literature DB >> 12665969 |
Abstract
The etiology of rheumatoid arthritis (RA) remains unclear at present, but advances have been made in the drug therapy for RA. Recent attention has been focused on selective cyclooxygenase-2 (COX-2) inhibitors, nonsteroidal antiinflammatory drugs (NSAIDs) that inhibit a subtype of cyclooxygenase. Various clinical studies have confirmed that the selective COX-2 inhibitors cause fewer severe gastrointestinal complications, although an increased incidence of myocardial infarction was suggested. Terminal enzymes of the arachidonic acid cascade, such as membrane-associated prostaglandin E synthase, might be a target for new NSAIDs in the near future. Low-dose glucocorticoid treatment for RA has been reconsidered possibly to prevent articular destruction of RA. Special attention for glucocorticoid-induced osteoporosis by concomitant administration of bisphosphonates might be necessary. Disease-modifying antirheumatic drugs should be effective in delaying the progression of joint destruction and physical disability. Methotrexate, sulfasalazine, and leflunomide have shown such an effect. Inhibition of articular destruction was also proven by administration of the biologic agents etanercept and infliximab plus methotrexate. Tuberculosis complicated with infliximab therapy is one of the most important concerns in Japan. Agents that improve the quality of life of patients with RA are still needed.Entities:
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Year: 2003 PMID: 12665969 DOI: 10.1007/s007760300045
Source DB: PubMed Journal: J Orthop Sci ISSN: 0949-2658 Impact factor: 1.601