Causes 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 unidenti?ed genetic factors. Genetic factors cannot alone explain aetiology, and environmental and chance factors must be important, but these have yet to be identi?ed.
Epidemiology Rheumatoid arthritis more commonly occurs in women from the age of 30 onwards, the sex ratio being approximately 4:1. Typical rheumatoid arthritis may occur in adolescence, but in childhood chronic SYNOVITIS usually takes one of a number of di?erent patterns, classi?ed under juvenile chronic arthritis.
Pathology The primary lesion is an in?ammation of the synovial membrane of joints. The synovial ?uid becomes diluted with in?ammatory exudate: if this persists for months it leads to progressive destruction of articular CARTILAGE and BONE. Cartilage is replaced by in?ammatory tissue known as pannus; a similar tissue invades bone to form erosions. Synovitis also affects tendon sheaths, and may lead to adhesion ?brosis or attrition and rupture of tendons. Subcutaneous and other bursae may be involved. Necrobiotic nodules also occur at sites outside synovium, including the subcutaneous tissues, the lungs, the pericardium and the pleura.
Clinical features Rheumatoid arthritis varies from the very mild to the severely disabling. Many mild cases probably go undiagnosed. At least 50 per cent of patients continue to lead a reasonably normal life; around 25 per cent are signi?cantly 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 but, because of the large number of false positives and false negatives, this test has very little value in clinical practice. It may be a useful pointer to a worse prognosis in early cases if the level is high. X-RAYS may help in diagnosing early cases and are 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 antiin?ammatory drug treatment (see below).
Treatment 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 antirheumatic drugs reduces long-term disability. Drug treatment includes 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 e?ective in reducing pain and early-morning sti?ness, and have no e?ect on the chronic in?ammatory process. It is important, especially in the elderly, to explain to patients the adverse effects of NSAIDs, the dosage of which can be cut by prescribing paracetamol at the same time. Combinations of anti-rheumatic drugs seem better than single agents. The slow-acting drugs take approximately three months to act but have a more global e?ect on chronic in?ammation, with a greater reduction in swelling and an associated fall in erythrocyte sedimentation rate (ESR) and rise in the level of HAEMOGLOBIN. Local CORTICOSTEROIDS are useful, given into individual joints. Systemic corticosteroids carry serious problems if continued long term, but may be useful under special circumstances. Much research is currently going on into the use of tumour necrosis factor antagonists such as INFLIXIMAB and etanercept, but their precise role remains uncertain.... rheumatoid arthritis
There is no cure, but first-line treatments include *coal tar, *dithranol, and topical corticosteroids and vitamin D analogues (e.g. *calcipotriol). Narrow-band UVB or *PUVA can also be effective as can systemic therapies, such as *methotrexate, *retinoids, and *ciclosporin. Biological treatments, such as *infliximab, *adalimumab, and *etanercept, are potent but expensive.... psoriasis
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