Epidemiology and Etiology
Despite the years of intensive study of endocrine, metabolic, and nutritional factors as well as geographic, occupational, and psychological variables, the etiology of rheumatoid arthritis has not been elucidated.
A genetic predisposition is suspected (because certain histocompatibility markers are found frequently); however, bacterial and viral infections are often associated with acute polyarthritis in humans, and thus an infection followed by an altered or sustained immunologic response could be instrumental for development of the disease. Certainly, immunologic abnormalities appear to play a role in both the aggravation and perpetuation of the inflammatory process. Cellular and humoral immunologic reactions occur at the local site (joints) and often systemically. The production of antiimmunoglobulins or rheumatoid factors occurs initially in the inflammatory tissue of the joint and can subsequently be detected in the serum of 80 percent of the patients treated for the condition. Those patients with rheumatoid arthritis who are seropositive for rheumatoid factor show a more marked progression of the disease than do those who are seronegative.
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