[Epiphyseal bone pain caused by cyclosporin A in 28 patients with renal transplantation].
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Biomedical subjects
Publications and source records attributed to A Rossard.
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The authors report on 2 personal cases, and review 48 published cases of myasthenia induced by D-penicillamine (D-P) treatment in patients with rheumatoid arthritis. The clinical symptoms were not different from those of myasthenia gravis, and no correlation could be found between the total cumulative dose of D-P and the onset on the myasthenic syndrome. In 71% of the patients the neurological deficiency regressed after D-P was withdrawn, but in some cases anticholinesterase treatment had to be continued and thymectomy was contemplated. The most remarkable biological abnormalities were anti-striational antibodies (found in 58% of the cases) and anti-acetylcholine receptors antibodies (found in 4 out of 7 patients tested). These findings are in favour of a genuine myasthenia and against a myasthenic syndrome due to neuro-muscular blockade. While the mechanisms underlying the emergence of these antibodies remains unknown, their presence throws new light on immunological disorders in rheumatoid arthritis.
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We describe two patients who had a typical levamisole-induced agranulocytosis and a severe infection; the view of other cases found in the literature shows a fundamental fact: the complication can occur after a variable time of prescription (from thirteen days to eleven months), continuous or intermittent. The accidents are imprevisible, and circonspection must be used, not for its antihelminthic properties, but for its prolonged use for immunological purposes, even if some authors have not observed any cases of agranulocytosis in large series. Naturally, the purpose is quite different in the case of a severe rheumatoid arthritis or inesthetic warts, and our two observations are very demonstrative. Mechanism of agranulocytosis has not been totaly clarified: we have observed biological stigmates of immunological process against levamisole (responsible of agranulocytosis?), but essentially medullary lesions (successive regenerative aspects and necrosis) as has been described with pyramidon, and this could explain why the other blood cells are affected in an apparently isolated agranulocytosis.