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Autoimmune myopathy, myonecrosis and transaminitis: case report A 54 year-old-man developed myonecrosis and transaminitis during treatment with atorvastatin. Additionally, he developed autoimmune myopathy following the concomitant administration of ticagrelor and atorvastatin [not all dosages stated; routes and durations of treatments to reactions onsets not stated]. The man was hospitalised due to increased muscle weakness, dyspnoea on exertion, worsened ambulation and dysphagia.His medical history was significant for non-alcoholic hepatitis steatosis (NASH), hypertension, hyperlipidaemia and type-2 diabetes. He reported that the symptoms started as upper extremity weakness about 7 weeks after the initiation of ticagrelor, atorvastatin and metoprolol for a stent placement following cardiac catheterisation of non-ST-elevation myocardial infarction (NSTEMI). Subsequently, his symptoms progressed. He developed lower extremity weakness with difficulty ambulating and also experienced a fall. Previously, he used to walk several miles every day. Blood test showed elevated creatine phosphokinase and ALT/AST. He had a history of using atorvastatin for 10 years for dyslipidaemia, which was temporarily stopped for 7 months due to NASH and elevated liver enzymes. Atorvastatin was restarted 2 months prior to the admission for a coronary stent. At that time, his ALT/AST was 164/88 IU/L. Prior to 7 days of his current admission, his primary care provider stopped the atorvastatin therapy due to elevated CK level and myopathy symptoms secondary to possible drug interaction between ticagrelor and atorvastatin. The man’s ticagrelor was changed to clopidogrel. On hospital day 1, his vital signs were unremarkable, while physical examination showed proximal muscle wasting, with muscle weakness in both upper and lower extremities. He was placed on aggressive IV fluid hydration for non-traumatic rhabdomyolysis. After 10 days of discontinuation of atorvastatin, he continued to exhibit tenderness, weakness and inability to ambulate despite 3 days of hydration. The creatine kinase level remained elevated (above 10000 IU/L) with normal urine output and serum creatinine. Subsequent MRI of both femurs and pelvis showed bilateral muscle oedema consistent with rhabdomyolysis or myositis. He was diagnosed with atorvastatin induced myonecrosis and accompanying transaminitis. Neurology consult suspected differential diagnosis of underlying inflammatory myositis, statin associated autoimmune myonecrosis or slowly resolving non-immunologic statin induced myopathy. Subsequently, he started receiving treatment with prednisone, which resulted in less weakness, dysphagia and increased ability to ambulate. The CK level also decreased (8700 IU/L); however, transaminases levels remained above 400 IU/L. After 5 days of hospitalisation, he was discharged with prednisone. In rheumatology clinic, anti-HMGCR antibody returned strongly positive at 102U, while muscle biopsy results were consistent with statin induced myonecrosis. After 12 days of discharge,