Goals: lessen pain, reduce inflammation, improve/maintain function, prevent long-term joint damage, control of systemic involvement. Increasing trend to treat RA more aggressively earlier in disease course (Fig. 167-1).

• Pt education on disease, joint protection
• Physical and occupational therapy-strengthen periarticular muscles, consider assistive devices.
• Aspirin or NSAIDs.
• Intraarticular glucocorticoids.
• Systemic glucocorticoids.
• Disease-modifying antirheumatic drugs (DMARDs)-e.g., methotrexate; IM gold compounds; hydroxychloroquine; sulfasalazine; d-penicillamine. Each agent has individual toxicities-pt education and monitoring required. Have been used in combination but with increased toxicity.
• Biologic therapy-TNF modulatory agents (etanercept, infliximab, adalimumab) effective at controlling RA in many pts and can slow the rate of progression of radiographic joint damage and decrease disability; carries potential for serious infection and individual toxicities. IL-1 receptor antagonist (anakinra) can improve the signs and symptoms of RA. Rituximab, a chimeric antibody directed to CD20 that depletes mature B cells, has been approved for RA patients who have failed anti-TNF therapy. Abatacept (CTLA4-Ig)-inhibits T cell activation, can be given with or without methotrexate, and is usually given in those who have failed or have contraindications to anti-TNF therapy.
• Immunosuppressive therapy-e.g., azathioprine, leflunomide, cyclosporine, and cyclophosphamide. Generally reserved for pts who have failed DMARDs and biologics.
• Surgery-may be considered for severe functional impairment due to deformity.

Figure 167-1
Algorithm for the medical management of rheumatoid arthritis. Coxib, COX-2 inhibitors; DMARD, disease-modifying anti-rheumatic drug; CCP, cyclic citrullinated polypeptide; MTX, methotrexate; SSA, sulfasalazine; TNF, tumor necrosis factor.

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