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| According to the revised treatment guidelines established by the American College of Rheumatology,1 the ultimate goal in managing rheumatoid arthritis (RA) is to induce complete remission, although this occurs infrequently. Thus, in managing RA, the interim goals of treatment are to: |
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control inflammatory symptoms |
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decrease pain |
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prevent or control joint damage |
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prevent loss of function. |
The aim of treatment should be to improve functionality and health-related quality of life, in addition to relieving the signs and symptoms of RA |
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The currently available treatment options address some, but not all, of these management goals.
For example, non-steroidal anti-inflammatory drugs (NSAIDs) have analgesic and anti-inflammatory properties but do not alter the course of the disease or prevent joint destruction.1 Low-dose glucocorticoids are highly effective for relieving symptoms and may slow the rate of progression of joint damage. Despite these benefits, the use of glucocorticoids is often temporary, and their adverse effects (eg, osteoporosis, hypertension, weight gain, fluid retention) limit their long-term utility, particularly at high doses.1 Conversely, disease-modifying antirheumatic drugs (DMARDs) have the potential to reduce or prevent joint damage and to preserve joint integrity and function. Unfortunately, conventional DMARDs have several limitations.
For example, not all DMARDs:1 |
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prevent bone damage, despite apparent control of clinical symptoms |
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confer lasting benefits |
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are well tolerated. |
Some conventional DMARDs (eg, methotrexate, hydroxychloroquine, sulphasalazine) are also relatively slow acting and, in some cases, a clinical response may require several months of treatment.2 Newer biological DMARDs that block the effects of tumour necrosis factor-α (TNF-α), such as etanercept and infliximab, are now available. While these agents have been shown to reduce the clinical signs and symptoms and inhibit the progression of joint damage in patients with active RA, treatment has been associated with a high incidence of potentially serious infections (eg, tuberculosis) or sepsis.3,4
The biological therapy for use in RA — Kineret® (anakinra)—is a recombinant form of the naturally occurring IL-1Ra, and blocks the biological activity of IL-1 by competitively inhibiting the binding of IL-1 to IL-1RI.5,6 R.I.S.E. provides detailed information on the mechanism of action, efficacy and safety of Kineret® (anakinra).
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Kineret® ( anakinra) is an effective treatment for patients with RA
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References
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