Rheumatoid arthritis:pathological mechanisms and modern pharmacologic therapies

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INTRODUCTIONrnRheumatoid arthritis (RA) is a chronic systemic autoimmune disease that arises more frequently in females than males, being predominantly observed in the elderly. The prevalence rate reported in 2002 ranged from 0.5%to 1%of the population and had regional variation.1 RA primarily affects the lining of the synovial joints and can cause progressive disability, premature death, and socioeconomic burdens. The clinical manifestations of symmetrical joint involvement include arthralgia, swelling, red?ness, and even limiting the range of motion. Early diagnosis is considered as the key improvement index for the most desirable outcomes (i.e., reduced joint destruction, less radiologic progres?sion, no functional disability, and disease modifying anti?rheumatic drugs (DMARD)?free remission) as well as cost?effectiveness as the first 12 weeks after early symptoms occur is regarded as the optimal therapeutic window.2–4 However, early diagnosis remains challenging as it relies heavily on the clinical information gathered from the patient’s history and physical examination supported by blood tests, and imaging analysis. The reasons for a delayed diagnosis vary markedly between countries with differing healthcare systems,5 while the reasons for a delay in initiating DMARD therapy in RA patients appear to be both patient? and physician?dependent. Noticeably, patient awareness of RA, the willingness of patients to seek medical advice, the time for the patients from symptom onset to receiving appropriate treatment, and the diagnostic capability of the physician all influence the treatment and outcome of RA. With poorly controlled or severe disease, there is risk that extra?articular manifestations such as keratitis, pulmonary granulomas (rheuma?toid nodules), pericarditis/pleuritis, small vessel vasculitis, and other non?specific extra?articular symptoms will develop.
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