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Rheumatoid arthritis is defined as a chronic inflammatory reaction in the synovial membrane of multiple diarthrodial joints. Joint inflammation leads to irreparable degrees of cartilage and bone damage within the joint. Thus, pain is a consequence not only of inflammation but mechanical factors as well. In an individual patient with rheumatoid arthritis, the ultimate extent of joint degradation is both variable and unpredictable. Although the etiology of rheumatoid arthritis remains unknown, rheumatoid arthritis, osteoarthritis, arthritis it clearly is a common prototypic autoimmune disease. At least 30% of rheumatoid arthritis patients end up with a degree of crippling.
Early diagnosis is important in order to justify early pharmacologic intervention. Most likely a patient has rheumatoid arthritis when at least four to six joints develop swelling in a symmetric distribution for a period of greater than six rheumatoid arthritis, osteoarthritis, arthritis weeks. Almost invariant is morning stiffness lasting for more than 30 minutes, with an abrupt onset and late afternoon fatigue. The diagnosis of rheumatoid arthritis is not dependent on laboratory parameters. Rheumatoid factor, is present in only approximately 20% of cases rheumatoid arthritis, osteoarthritis, arthritis in the earliest stages. Up to 5% of normal subjects are rheumatoid factor positive and the prevalence increases with age. Early on, the ESR is highly variable, joint x-rays are normal and anemia has not usually developed. The only pathognomonic sign of rheumatoid arthritis are small bone erosions on hand and foot films. Although it remains extremely difficult to predict the subsequent course and severity of disease in patients with early rheumatoid arthritis, the presence of serum antibodies to the cartilage type (type II) collagen has been recently reported to portend the development of crippling stages at a rumatoid.