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Rheumatoid arthritis is a relatively common affliction of the joints which combines chronic inflammation, fibrosis and tissue degradation in its pathology. Little is known of the role in this disease of mediators normally associated with acute inflammation, such as histamine, kinins and the anaphylatoxins. The prostanoids, in particular PGE2′ are important in the pain associated with rheumatoid arthritis; they may also be partly responsible for the joint swelling. This explains the analgesic activity of non-steroidal anti-inflammatory drugs which inhibit prostaglandin synthesis. Small amounts of leukotriene B4 are found in rheumatoid synovial fluids. The importance of leukotrienes or platelet activating factor (PAF-acether) in joint pathology has not been investigated. In recent years it has been proposed that the monokine, interleukin 1, has a central role in the synovitis, fibrosis and tissue damage associated with rheumatoid arthritis. There is growing experimental support for this hypothesis. The inhibition of the synthesis of monokines or the antagonism of their action offers new hope for the treatment of the degenerative aspects of this crippling disease, which remain resistant to current therapies.
Henderson et al. (Wed,) studied this question.