Biologic Response Modifiers

نویسنده

Richard J. Misischia

چکیده

Despite remarkable advances in therapy, rheumatoid arthritis (RA) still results in significant morbidity, mortality, and disability [1]. In addition to symmetrical joint swelling of the feet and hands, large joints such as the shoulders, hips, knees, and cervical spine can be affected. RA also may affect the pulmonary, cardiovascular, and ocular systems. Rheumatoid factor is present in up to 80% of RApatients, and the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level are usually elevated in the presence of active disease. Joint erosions, joint space narrowing, and periarticular osteopenia are radiographic hallmarks of the disease. Erosions can occur as early as 3 months after onset of RA. The etiology of RA is unknown and until recently, therapy has not targeted specific disease pathways. Past treatment options for RA have included nonsteroidal anti-inflammatory agents and corticosteroids, especially for acute phases of the disease. Disease-modifying antirheumatic drugs (DMARDs), such as methotrexate, have improved the long-term prognosis of RA and its symptoms and have been the mainstay of treatment for many years. Methotrexate inhibits synthesis of both RNA and DNA and stimulates the release of adenosine, an important mediator of inflammation [2]. Despite general efficacy, many patients have a suboptimal response to methotrexate and require further intervention, such as the addition of a second DMARD, which may increase risk of toxicity. Better understanding of the immune system, especially the role of cytokines in the inflammatory process, has led to more focused treatment, particularly the use of biologic response modifiers. In the past 3 years, 2 biological agents, infliximab and etanercept, have been approved for treatment of refractory RA. Biological agents are monoclonal antibodies or recombinant forms of the naturally occurring inhibitory molecules directed against specific cellular or molecular targets [3]. Both of these agents target tumor necrosis factor alpha (TNF-α) and, in effect, neutralize its role in the inflammatory process.

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