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Rheumatoid Arthritis
Rheumatoid arthritis (RA) is an autoimmune disorder that causes the immune system to attack the joints. It is a disabling and painful inflammatory condition, which can lead to substantial loss of mobility due to pain and joint destruction. The American College of Rheumatology has defined (1987) the following criteria for Rheumatoid Arthritis:
Four criteria have to be met, although many patients are treated despite not meeting the criteria. The symptoms that distinguish rheumatoid arthritis are inflammation and soft-tissue swelling of many joints at the same time (polyarthritis). The hands are generally affected in a symmetric fashion. The pain generally improves with use of the affected joints, and there is usually stiffness of all joints in the morning that lasts over 1 hour. If the arthritis has been longstanding, the inflammatory activity has led to erosion and destruction of the joint surface, which impairs their range of movement and leads to deformity. The fingers are typically deviated towards the little finger (ulnar deviation) and can assume unnatural shapes. Subcutaneous nodules on extensor surfaces, e.g. the elbows, are often present. When RA is being clinically suspected, immunological studies are required, such as rheumatoid factor (RF, a specific antibody). A negative RF does not rule out RA; rather, the arthritis is called seronegative. Usually, several other blood tests are done to allow for other causes of arthritis, such as lupus erythematosus. The erythrocyte sedimentation rate (ESR), C-reactive protein, full blood count, renal function, liver enzymes and immunological tests (e.g. antinuclear antibody/ANA) are all performed at this stage. Ferritin can reveal hemochromatosis, which can mimic RA. The cause of RA is unknown, but long suspected to be infectious. Mycoplasma, Erysipelothrix, Epstein-Barr virus, parvovirus and rubella have been suspected but never supported in epidemiological studies. As in other autoimmune diseases, the "mistaken identity" theory suggests that an offending organism causes an immune response that leaves behind antibodies that are specific to that organism. The antibodies are not specific enough, though. They begin an immune attack against, in this case, the synovium, because some molecule in the synovium "looks like" a molecule on the offending organism that created the initial immune reaction. Autoimmune diseases require that the affected individual have a defect in the ability to distinguish self from foreign molecules. This ability is acquired in the first year of life. There are markers on many cells that confer this self-identifying feature. However, some classes of markers allow for RA to happen. 90% of patients with RA have the cluster of markers known as the HLA-DR4/DR1 cluster, whereas only 40% of controls do. Thus, in theory, RA requires susceptibility to the disease through genetic endowment with specific markers AND an infectious event that triggers an autoimmune response. Once triggered, the immune response causes inflammation of the synovium. Once the inflammatory reaction is established, the synovium thickens, the cartilage and the underlying bone begins to disintegrate and evidence of joint destruction accrues.
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Rheumatoid Arthritis" and from Pain Busters Clinic
Rheumatoid Arthritis
Symptoms, Arthritis Symptoms
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