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(Ann Intern Med 2002;136:908)

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  • Autoimmune disease that causes systemic inflammatory process; clinical picture shows bilateral swelling of joints
  • Natural progression involves chronic inflammation that is generally low-grade, starts in a few joints; can eventually involve many joints; periodic inflammatory flares are very painful
    • Joint destruction begins when lymphocytes localize to synovial tissue, become activated → activate complement causing release of cytokines (inflammation) → inflammatory process attracts other immune cells to the area; ↑ synovial fluid production → T-cell & B-cell activation at the joint T-helper cells (CD4): release interferon, tumor necrosis factor (TNF), interleukin-2 (IL-2) (inflammatory mediators)
    • B cells: produce plasma cells → antibody (AB) formation; the antibodies bind to complement, causing formation of polymorphonuclear leukocytes (PMNs); PMNs release cytotoxins & cytokines; cytotoxins cause direct joint damage

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Physical Presentation

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(Best Pract Res Clin Rheumatol 2005;19:55)

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  • Morning joint stiffness → typically lasts 30–60min, may persist all day
  • Bilateral joint involvement typical → generally starts in small joints of hands & feet, knees, shoulders; may also occur in wrists & ankles

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(Arthritis Rheum 2012;64:625)

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Laboratory Findings

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(South Med J 2005;98:185; South Med J 2005;98:704)

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  • Rheumatoid factor (RF): antibody detected in approximately 2/3 RA patients; markers of inflammation (↑ C-reactive protein [CRP], erythrocyte sedimentation rate [ESR])
  • Complete blood cell count (CBC): often normochromic anemia & thrombocytosis

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RA treatment has 2 components:

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  • Symptomatic treatment (pain/inflammation/swelling): NSAIDs, corticosteroids, opiates, etc. (acetaminophen NOT appropriate → no anti-inflammatory properties)
    • Glucocorticoid therapy beneficial; risk may be substantial → no evidence ↑ vs ↓ dose; success seen with both (Arthritis Rheum 2008;59:762)
  • Disease-modifying treatment (goal of establishing remission): initiate disease-modifying anti-rheumatic drug (DMARD) within 6mo of diagnosis; assess efficacy & reevaluate/adjust therapy Q1–3mo if remission/low-disease activity not achieved (Ann Rheum Dis 2010;70:1519); treatment approach based on disease duration, activity & prognosis (Arthritis Rheum 2012;64:625)
    • EULAR Guidelines recommend treating “as soon as the diagnosis of RA is made”; American College of Rheumatology 2008 guidelines suggest treatment based on duration of disease
    • Start with methotrexate (MTX) or leflunomide (LEF) (though hydroxychloroquine [HCQ] often initial treatment in mild disease) (Ann Rheum Dis 2010;69:987)

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Table Graphic Jump Location
Table 38-1 Approach RA Treatment (Arthritis Rheum 2012;64:625)

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