We report a case of a 75-year-old woman who was diagnosed with dermatomyositis presenting with isolated dysphagia. There were no obvious cranial nerve deficits with normal motor grade in all the limbs in neurological examinations, but a suspicious rash was observed in the anterior chest. The serum creatine kinase was 306 IU/L, and active myopathic changes in bilateral limb muscles were observed in the electromyography test. Muscle biopsy from vastus lateralis showed perivascular infiltration of mononuclear inflammatory cells, which was compatible with dermatomyositis. She had responded to oral prednisolone and azathioprine.
The inflammatory myopathies are divided into three major and distinct subsets as polymyositis(PM), dermatomyositis(DM), and inclusion body myositis(IBM). This distinction is based on unique clinical, demographic, laboratory, histologic,therapeutic, prognostic, and immunopathologic criteria.Although the causes of PM, DM, and IBM are unknown, autoimmune mechanisms are implicated, as supported bytheir association with other putative or definite autoimmune diseases or viruses, the evidence for a T cell-mediatedmyocytotoxicity or complement-mediated microangiopathy, the presence of various autoantibodies and their responseto immunotherapies. But in IBM the immune-mediated process is weaker and IBM patients do not readily respond toimmunotherapies, there are convincing immunopathological signs to suggest that a definite autoimmune component,similar to that seen in PM, also plays a role in the cause of IBM.
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