A chronic inflammation of the synovial lining (see SYNOVIAL MEMBRANE) of several joints, tendon sheaths or bursae which is not due to SEPSIS or a reaction to URIC ACID crystals. It is distinguished from other patterns of inflammatory arthritis by the symmetrical involvement of a large number of peripheral joints; by the common blood-finding of anti-nuclear antibody; by the presence of bony erosions around joints; and, in a few, by the presence of subcutaneous nodules with necrobiotic (decaying) centres.
There is a major immunogenetic predisposition to rheumatoid arthritis in people carrying the HLA-DR4 antigen (see HLA SYSTEM). Other minor immunogenetic factors have also been implicated. In addition, there is a degree of familial clustering which suggests other unidentified genetic factors.
The primary lesion is an inflammation of the synovial membrane of joints. The synovial fluid becomes diluted with an outpouring of inflammatory exudate: if this persists for months it leads to progressive destruction of the joint CARTILAGE and adjacent BONE. Cartilage is replaced by inflammatory tissue known as pannus; a similar tissue invades bone to form erosions. Synovitis also affects tendon sheaths, and may lead to fibrosis or even rupture of tendons.
Rheumatoid arthritis varies from the very mild to the severely disabling. At least 50 per cent of patients continue to lead a reasonably normal life; around 25 per cent are significantly disabled in terms of work and leisure activities; and a minority become markedly disabled and are limited in their independence. There is often an early acute phase, followed by substantial remission, but in other patients gradual step-wise deterioration may occur, with progressive involvement of an increasing number of joints.
The diagnosis of rheumatoid arthritis is largely based on clinical symptoms and signs. Approximately 70 per cent of patients have rheumatoid factor ANTIBODIES in the SERUM. Radiological imaging may help in diagnosing early cases and is particularly helpful when considering surgery or possible complications such as pathological fracture. Patients commonly develop ANAEMIA, which may be partly due to gastrointestinal blood loss from anti-inflammatory drug treatment (see below).
involves physical, pharmacological, and surgical measures, together with psychological and social support tailored to the individual patient's needs. Regular activity should be maintained. Resting of certain joints such as the wrist with splints may be helpful at night or to assist prolonged manual activities. Sound footwear is important. Early use of anti-rheumatic drugs is designed to reduce long-term disability. They include simple ANALGESICS, NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS), and slow-acting drugs including GOLD SALTS (in the form of SODIUM AUROTHIOMALATE), PENICILLAMINE, SULFASALAZINE, METHOTREXATE and AZATHIOPRINE.
The non-steroidal agents are largely effective in reducing pain and early-morning stiffness but have no effect on the chronic inflammatory process. CORTICOSTEROIDS can be useful when injected into joints. Systemic corticosteroids carry serious problems if continued long term, but are useful under special circumstances. Tumour necrosis factor antagonists such as INFLIXIMAB and etanercept may be effective and are often used early in the course of the illness, not just when other drugs have failed.