الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Rheumatoid arthritis is a systemic autoimmune disease characterized by chronic inflammation of the synovial membrane resulting in joint destruction and disability. The clinical course of RA varies individually from mild joint symptoms to severe bone damage with loss of joint function. Traditionally, the diagnosis of RA relies on the history and physical examination, plain radiographs, and serologic tests according to the revised 1987 criteria set by the ACR. Unfortunately, however, RA can be difficult to diagnose. Many other conditions resemble it and its symptoms can develop insidiously. Blood tests and x-rays may show normal results for months after the onset of joint pain. So, clinical diagnosis of RA is not always straightforward. Even after RA has been diagnosed, it is extremely important to determine whether the course of the disease is benign or aggressive in order to treat the problem appropriately. Because RF has low specificity , a new serological test has been developed in recent years, which tests for the presence of so called anti-citrullinated protein (ACP) antibodies. As regard to imaging, conventional radiography demonstrates only the late changes of the RA. In addition, CR does not provide information about soft tissue structures or synovium. So, the role of US and MRI as novel imaging techniques in the diagnosis of early arthritis is being investigated, with promising results. The challenge for the clinician does not end with characterizing a patient’s disease severity ’profile’, but also includes decisions regarding treatment as none of the currently available medications are universally effective and free of side effects. There is no known cure for RA, but the goal of RA treatment is to reduce joint inflammation and pain, maximize joint function, and prevent joint destruction and deformity. Pharmacological treatment of RA can be divided into DMARDs, NSAIDs and analgesics. DMARDs have been found to produce durable remissions and delay disease progression. In particular they prevent bone and joint damage from occurring secondary to the uncontrolled inflammation. NSAIDs and analgesics improve pain and stiffness but do not prevent joint damage or slow the disease progression. Major advances in molecular biology and biotechnology have enabled the development of drugs aiming at therapeutic targets which are proinflammatory cytokines involved in signaling pathways and cells prominent in the pathogenesis of RA. Biologic DMARDs have several advantages over traditional DMARDs. They exhibit a rapid onset of action, provide significant clinical response, improve quality of life and most importantly, substantially inhibit radiographic progression. The therapeutic armamentarium for treatment of RA has significantly expanded in the last decade. Among the biologic DMARDs, the FDA-approved anti-TNF-α agents (infliximab, etanercept, adalimumab, golimumab and certolizumab), as well as treatments directed against IL1 (anakinra), a CTLA4-directed T-cell modulator (abatacept), a monoclonal antibody against CD20 that serves as a B-cell modulator (rituximab) and anti-IL6 (tocilizumab). Finally, It is now believed that early aggressive treatment with disease modifying drugs is important to inhibit the future structural joint damage.