Rheumatoid arthritis is a chronic systemic inflammatory disease of of the peripheral joints. Articular inflammation may be remitting. Continued inflammation usually results in joint damage and disability. Certain extra-articular manifestations are characteristic, including rheumatoid nodules, arteritis, neuropathy, scleritis, pericarditis, and splenomegaly.
The exact cause of rheumatoid arthritis is unknown. There are several causes of chronic inflammation, including persistent infections, prolonged exposure to toxic elements, and autoimmune disease.
The immune system is activated in rheumatoid arthritis. Arthritogenic stimuli activate both humoral and cellular immune systems in the susceptible host. Antibodies (IgG, IgM, IgA anti-immunoglobulins) made by B cells and plasma cells in the joint space are complexed and fix complement, resulting in an inflammatory process. Infiltrating lymphocytes; primarily CD4 helper T-cells.
Risk factors for rheumatoid arthritis include HLA-DR4 (a genetic marker), family history, native American ethnicity, and female gender, age 20-50 years.
A CBC will usually show mild anemia. The sedimentation rate (ESR) is usually elevated and is helpful to follow disease activity. Increased rheumatoid factor is detectable in 70-80% of patients. Antinuclear antibodies (ANA) are present in 20-30%.
Complement (CH50), C3, C4 are useful to detect persons with early rheumatoid arhritis from those with early lupus, in whom compliment levels are decreased.
The synovial fluid has a variety of changes. The fluid is yellowish-white, turbid, with poor viscosity. A "Mucin clot" poor due to degradation of hyaluric acid by lysosomal enzymes is often found. Synovial WBC is increased (3500-50,000). Synovial total hemolytic complement assay (CH50) is lower than serum. Synovial protein is approximately 4.2 g/dL (42 g/L). The serum-synovial glucose difference is 30 mg/dL (1.67 mmol/L).
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