• Vol. 27 No. 1, 83–88
  • 15 January 1998

Rheumatoid Arthritis—A Review

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ABSTRACT

Rheumatoid arthritis, a common chronic inflammatory arthritis, tends to run a more benign course inpatients from the community than those seen at hospitals. The aetiology is unknown but the disease is postulated to result from the interaction between genetic and environmental factors. The strongest genetic association is with the major histocompatibility complex (MHC) Class II antigen HLA DR 4, although not more than 50% of the genetic susceptibility is due to MHC genes. In early disease the pathogenesis is thought to be T cell mediated whereas in late disease the mechanisms are T cell independent, with destruction contributed to by autonomous fibroblast like synoviocytes. The diagnosis is made on clinical grounds. Management is directed at controlling active synovitis so that joint damage is limited. The early use of a slow acting anti-rheumatic drug is now advocated, as studies have shown that they can potentially prevent or limit the progression of disease. Biological therapies are still experimental but may hold promise for the future.


Rheumatoid arthritis (RA) is a chronic inflammatory arthritis which is occasionally associated with extraarticular manifestations. Although the first good clinical description was by Landre-Beauvais in 1800, the term rheumatoid arthritis was first used only in 1878 by Alfred Garrod.

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