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For the specialist... The first documentation of the role of IL-1a aAb in RA showed that IgG from patients with RA interfered with the biological effect of IL-1a, and sera from these patients interfered with the effect of both IL-1a and IL-1 beta (1). It was suggested that the levels of these Ab fluctuate with RA activity (2). This, however, was not found in other studies (3, 4). Common to these initial studies was that patients most positive for IL-1a aAb were the ones with milder disease manifestations and low titers of rheumatoid factor, and that a relative higher number of aAb-positive patients suffered from less severe forms of polyarthritis, e.g. primary Sjögren's syndrome or self-limiting inflammatory arthritis (4, 5). Recently, a three years study of unselected patients with chronic polyarthritis revealed that both incidence and levels of IL-1a aAb were higher in a subset characterized by an increased proportion of patients with primary Sjögren's syndrome or self-limiting inflammatory arthritis, diseases with a much better prognosis than RA (4). The relative risk of developing severe RA was 12 in the absence of high aAb levels and 18 when the absence of high aAb levels were associated with the presence of HLA-DR4. Conclusions and perspectives: If confirmed, detection of these aAb would be the best known predictor of non-erosive disease in patients with polyarthritis and might serve to select patients for less aggressive forms of anti-arthritic therapies. A lower frequency of IL-1a aAb than that seen in healthy controls has been detected in patients with systemic lupus erythematosus (SLE) and other chronic inflammatory diseases, e.g. Crohn's disease of the gut (2, 4, 6, 7). Cited references: 1. Suzuki H, Akama T, Okane M, Kono I, Matsui Y, Yamane K, Kashiwagi H. Interleukin-1-inhibitory IgG in sera from some patients with rheumatoid arthritis. Arthritis Rheum 1989; 32:1528-38.
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