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Upon completion of the chapter, the reader will be able to:

  1. Identify risk factors for developing adult rheumatoid arthritis (RA) or juvenile idiopathic arthritis (JIA).

  2. Describe the pathophysiology of RA, with emphasis on the specific immunologic components.

  3. Discuss the comorbidities associated with RA.

  4. Recognize the typical clinical presentation of RA or JIA.

  5. Create treatment goals for a patient with RA or JIA.

  6. Compare the available pharmacotherapeutic options, selecting the most appropriate regimen for a given patient.

  7. Propose a patient education plan that includes nonpharmacologic and pharmacologic treatment measures.

  8. Formulate a monitoring plan to evaluate the safety and efficacy of a therapeutic regimen designed for an individual patient with RA or JIA.




Rheumatoid arthritis (RA) is a complex systemic inflammatory condition manifesting initially as symmetric swollen and tender joints of the hands and/or feet. Some patients may experience mild articular disease, whereas others may present with aggressive disease and/or extraarticular manifestations. The systemic inflammation of RA leads to joint destruction, disability, and premature death. Juvenile idiopathic arthritis (JIA) is the most common form of arthritis in children.




RA has a prevalence of 0.5% to 1%.1,2 Patients with RA have a 50% increased risk of premature death and a decreased life expectancy of 3 to 10 years compared with individuals without RA.3 The underlying causes of increased mortality are unclear. RA arises from an immunologic reaction, perhaps in response to a genetic or infectious antigen. Risk factors associated with the development of RA include the following:


  • Female gender (3:1 females to males)

  • Increasing age (peak onset 35–50 years of age)

  • Current tobacco smoking.4 Tobacco users are more likely to have extraarticular manifestations and to experience treatment nonresponsiveness. This risk is reduced when a patient has remained tobacco-free for at least 10 years.

  • Family history of RA. Genetic studies demonstrate a strong correlation between RA and the presence of major histocompatibility complex class II human leukocyte antigens (HLA), specifically HLA-DR1 and HLA-DR4.5,6 HLA is a molecule associated with the presentation of antigens to T lymphocytes.

  • Emerging evidence suggests that stress may influence RA onset and disease activity. It appears that individual major stressful life events do not play a significant role. Instead, chronic presence of minor stressors (daily hassles, work and relationship stress, financial pressures) may affect the immune response and RA disease activity.7

  • The prevalence of JIA is approximately 1 in 1000 children.8 There are no known risk factors for JIA.




The characteristics of a synovium affected by RA are: (a) the presence of a thickened, inflamed membrane lining called pannus; (b) development of new blood vessels; and (c) influx of inflammatory cells in the synovial fluid, predominantly T lymphocytes. The pathogenesis of RA is driven by T lymphocytes, but the ...

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