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Successful treatment of Behçet’s disease with lenalidomide

tological examination revealed a disparity of fibre diameters, corresponding to scattered atrophic fibres and inflammatory infiltrates in septa. A massive mononuclear inflammatory cell infiltrate was seen in the endomysium, surrounding a capillary. Major histocompatibility complex (MHC) class I was positive in damaged and in intact areas. Pulmonary and digestive investigations did not reveal any anomaly. Carbimazole was stopped as the patient was euthyroid and there was a suspicion of drug-related dermatitis. Without any treatment, within a few weeks the asthenia and arthralgia disappeared. After 3 months, strength testing and muscle-derived enzymes had returned to normal levels and erythema had regressed. Nine months after carbimazole was stopped, the patient was still healthy and neuromuscular examination was normal. The papules on her hand started to decrease. She remains euthyroid. This observation was reported to the pharmacovigilance department and the case was entered in the national drug reactions database. Intrinsic imputability has been assessed as possible (I2), according to the method of Begaud et al. The patient was diagnosed as having JD because she had at least three criteria according to Bohan et al.: symmetrical proximal muscle involvement, elevated muscle-derived enzymes, electromyography changes of inflammatory myopathy. She also had characteristic skin lesions (facial erythema in association with Gottron’s papules). Apart from atrophy and inflammation, histological findings were not entirely specific of dermatomyositis as atrophic fibres were not focused on perifascicular areas, inflammatory infiltrates were seen in septa but also in endomysium, and class I MHC was positive in intact areas of the biopsy. The onset of the symptoms 3 months after the introduction of carbimazole and the rapid resolution after discontinuation of the drug were very suggestive of a causal association. To our knowledge, drug-induced JD has not been reported previously. In contrast, drug-induced dermatomyositis has been reported in adults. The reported drugs were as follows: statins, omeprazole, nonsteroidal anti-inflammatory drugs and D-penicillamine. Several cases of dermatomyositis-like eruption or Gottron’s papules were reported under hydroxyurea. The differential diagnosis of muscle involvement due to hyperthyroidism was excluded in our case as the patient was euthyroid when the symptoms appeared. Dermatomyositis is not a reported side-effect of carbimazole, but related diseases have been described. Shabtai et al. described a case of antithyroid arthritis syndrome due to carbimazole, including myalgia, arthralgia, arthritis, fever and rash. Four adults suffering from myositis associated with carbimazole have also been reported, with only one biopsy-proven case. One patient suffering from carbimazole-induced leukocytoclastic vasculitis has been described. The pathogenesis of carbimazole-related JD is unclear.