Brief overview of treatmant of RA from Medscape

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Rheumatoid Arthritis: Beyond Joint Inflammation to Treat Nonarticular Symptoms CME/CEBelow are some key learning points to help reinforce the educational impact of this activity:

Rheumatoid arthritis (RA) is a chronic immune-mediated joint disease that primarily targets the synovial membrane and is the most common form of inflammatory arthritis.

RA also presents with non-joint-related features, including extra-articular (eg, vasculitis, aortitis, scleritis, and fibrosis) or systemic (atherosclerosis, osteoporosis, fever, anorexia, and weight loss) manifestations that can significantly and negatively affect quality of life. Although this distinction is artificial, it can be useful when assessing therapy and prognosis.

The goal of RA management is to recognize and treat patients early to prevent or control joint damage, prevent loss of function, and reduce pain. Pharmacologic therapy, such as nonsteroidal anti-inflammatory drugs and glucocorticosteroids, can alleviate symptoms but joint damage may progress.

Evidence shows that progression can be limited or arrested by nonbiologic and biologic disease-modifying antirheumatic drugs (DMARDs). Commonly used nonbiologic DMARDs include methotrexate, hydroxychloroquine, sulfasalazine, and leflunomide. Currently, US Food and Drug Administration (FDA)-approved biologic DMARDs include the antitumor necrosis factor (anti-TNF) agents, etanercept, infliximab, and abatacept; rituximab, a B-cell-depleting agent; and abatacept, a costimulation modulator.

Few well-controlled trials have addressed the effects of currently available therapeutic agents for the prevention and/or treatment of extra-articular or systemic manifestations of RA.

Although FDA-approved agents have improved outcomes for many patients, some patients do not respond or suboptimally respond to treatment; some may even discontinue treatment because of complications, such as serious infections and treatment side effects.

Several new agents are in clinical development, and those in late-stage development include certolizumab, a TNF inhibitor; tocilizumab, an interleukin [iL]-6 receptor antagonist; and golimumab, a fully human anti-TNF-alpha monoclonal antibody.Regards,

Helen Fosam, PhD

S. Firestein, MD

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