A 78 year-old woman was admitted to our hospital because of subacutely progressive
dysarthria,
dysphagia, proximally dominant
muscle weakness and
erythema in the neck and back. She was diagnosed as having
rheumatoid arthritis (RA) at the age of 60 and treated with
bucillamine (BUC) for 8 years. Laboratory tests included a
rheumatoid factor of 1,472U/ml. Serum
creatine kinase level was slightly elevated. The activated T cells in the peripheral blood were markedly increased. Needle EMG demonstrated myogenic changes. The magnetic resonance image of the left upper arm showed diffuse
muscle atrophy and inflammatory changes in the triceps muscle. The muscle biopsy revealed perivascular inflammatory cell infiltraton and type II fiber
atrophy. A biopsy from the skin showed mild perivascular inflammatory cell infiltraton. According to the results of these findings, she was thought to have
dermatomyositis due to BUC. After withdrawal of BUC followed by the administration of
prednisolone 1mg/kg, her symptoms improved and activated T cells in the peripheral blood were decreased. In Japan, BUC is widely accepted as an effective drug in the treatment of RA, even though it is known to induce some
autoimmune diseases. However, the mechanism of the development of
autoimmune disease is unclear. We considered that the long-term use of
bucillamine could trigger an autoimmune response such as an increase in activated T cells and the development of
dermatomyositis-like clinical features in our patient. In conclusion, when RA patients treated with BUC show a clinical picture compatible with
dermatomyositis, its causative relationship has to be considered.