RA has a different cause than OA. It is considered to be one of the autoimmune diseases with the joint damage primarily found in the synovial tissue (APS, 2002; Danter, 2009). There have been many theories as to the cause of the disease, including Epstein-Barr virus or mycobacterial infection and environmental factors (APS, 2002).
The criteria for diagnosing RA include:
■ Persistent symmetrical polyarthritis for more than 3 months, involving the small joints in the hands and feet
■ Presence of persistent systematic symptoms, such as fatigue, anemia, and weight loss
■ Presence of rheumatoid nodules
■ Exclusion of other causes of autoimmune systemic disorders, such as SLE
■ Elevated erythrocyte sedimentation rate (ESR)
■ Normocytic-normochromic anemia
■ Positive rheumatoid factor (RF) in 80% of the patients
■ Cyclic citrullinated peptide: 75% sensitive and 96% specific for RA
■ Radiographic studies in the early phase will show only articular osteopenia and soft-tissue swelling. Later studies can find similar findings as in OA, joint space narrowing, and erosion of the joint margins.
RA has a large number of systematic effects that are not present in OA patients. These include chronic synovitis, with erosion of the tendons, ligaments, and cartilage (Danter, 2009). Carpal tunnel syndrome is a common occurrence. Other organs may be affected as well. There is an increased risk of cardiovascular disease related to the ongoing inflammatory process (Danter, 2009), and lungs may develop RA lung disease, vasculitis, or Sjogren's disease (Strand, Scudder, & Fosam, 2009).
Patients who have a poorer prognosis with RA include the following:
■ Patients with limitation in function
■ Extra-articular manifestations (e.g., vasculitis)
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