Treatment of RA involves an integrated approach, incorporating medications and nondrug therapies. Nonpharmacologic interventions include dietary counseling, exercise, physical therapy, smoking cessation, lipid control (to reduce the associated cardiovascular risks), and immunizations (to reduce the risk of infection linked with the use of immunosuppressive agents).
The ultimate goal of pharmacologic treatment (discussed in detail at the end of this chapter) is disease remission. Early diagnosis and treatment are imperative in preventing or delaying the long-term effects of disease progression. Mild symptoms of joint stiffness and pain can be treated with analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs), although these agents do not alter the long-term prognosis. Glucocorticoids are sometimes helpful in controlling the acute stages of inflammation; severe cases may require sustained low-dose therapy (<10 mg/day).
Disease-modifying antirheumatic drugs (DMARDs), which are divided into nonbiologic and biologic agents, have been shown to slow disease progression, reduce potential joint destruction, and maintain joint function while also limiting the need for long-term steroid use. In addition to their anti-inflammatory effect, these drugs reduce the body’s heightened autoimmune reaction. Thus, the clinician should consider screening for preexisting infectious conditions such as hepatitis B and C and tuberculosis. Among nonbiologic agents, methotrexate is generally the first-line treatment, but other options are available. Biologic agents, developed through genetic engineering, are modified proteins that can target cytokines. The largest group of currently available agents consists of anti–tumor necrosis factor (TNF)-α inhibitors. Other biologics act by blocking interleukin (IL)-1 or IL-6 receptors or in modifying T-cell or B-cell activity. One emerging group of DMARDs, which are technically small-molecule drugs as opposed to true biologic agents, targets the inhibition of the Janus kinase (JAK) enzyme involved in mediating inflammation.
Angelotti F, Parma A, Cafaro G, Capecchi R, Alunno A, Puxeddu I. One year in review 2017: pathogenesis of rheumatoid arthritis. Clin Exp Rheumatol. 2017;35(3):368–378.
Singh JA, Saag KG, Bridges SL Jr, et al; American College of Rheumatology. 2015 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res (Hoboken). 2016;68(1):1–25.
Excerpted from BCSC 2020-2021 series: Section 1 - Update on General Medicine. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.