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Modern Rheumatology 2020-Aug

Tumour necrosis factor inhibitor-induced myositis in a patient with ulcerative colitis

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Akitsu Yoshida
Yasuhiro Katsumata
Shinya Hirahara
Masanori Hanaoka
Moeko Ochiai
Masaki Kobayashi
Masayoshi Harigai

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Tumour necrosis factor (TNF) inhibitors are known to induce autoimmune diseases, such as lupus-like syndrome; in rare cases, TNF inhibitor-induced myositis has been reported. This report documents the case of a male patient with ulcerative colitis (UC) complicated by TNF inhibitor-induced myositis. After UC diagnosis and treatment with azathioprine and infliximab, he was evaluated for a recent 5-month history of muscle weakness and pain. Laboratory tests revealed elevated muscle enzymes, such as serum creatine kinase (CK) and aldolase. He also tested positive for anti-nuclear antibodies and anti-double stranded DNA antibodies. High-intensity signals in his quadriceps on magnetic resonance image (MRI) and fibrillation potentials in his proximal muscles on electromyography were demonstrated. Muscle biopsy revealed the endomysial infiltration of mononuclear cells surrounding myofibers. Eventually, the patient fulfilled the classification criteria for idiopathic inflammatory myopathies. Although an adverse drug reaction of infliximab had been speculated, his muscle involvements did not improve in 6 weeks from the last administration of infliximab; therefore, treatment with prednisolone was initiated. Subsequently, his muscle symptoms ameliorated, and his serum CK levels returned to normal. Repeat MRI revealed a complete resolution of the signal intensity, and he reported no symptoms of UC or myositis while prednisolone was tapered without resumption of infliximab. Clinicians should consider the diagnosis of drug-induced myositis if muscle symptoms develop in patients treated with TNF inhibitors.

Keywords: Anti-double stranded DNA antibody; infliximab; myositis; tumour necrosis factor inhibitor; ulcerative colitis.

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