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April 05, 2016; 86 (16 Supplement) April 18, 2016

Inclusion Body Myositis (IBM) and HMG CoA Reductase Antibody Myopathy: A Rare Case (P3.127)

Ashish Kulhari, David Preston
First published April 4, 2016,
Ashish Kulhari
Case Western Reserve University Cleveland OH United States
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David Preston
University Hospitals - Case Medical center Cleveland OH United States
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Citation
Inclusion Body Myositis (IBM) and HMG CoA Reductase Antibody Myopathy: A Rare Case (P3.127)
Ashish Kulhari, David Preston
Neurology Apr 2016, 86 (16 Supplement) P3.127;

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Abstract

BACKGROUND: IBM is the most common inflammatory myopathy in individuals older than age 50. Statins are commonly prescribed in this age group. Statins may induce a variety of muscle related syndromes including HMG CoA reductase antibody myopathy. OBJECTIVE: To report a rare case with both IBM and HMG CoA reductase antibody myopathy. METHODS: Case report and literature pertinent to IBM and HMG CoA reductase antibody myopathy was reviewed. CASE: An 80 year-old African American man with a history of hypertension, mild diabetes, dyslipidemia on atorvastatin 80 mg daily for two years, and a prior right middle cerebral artery infarct without any residual neurological deficits was admitted for acute worsening of a slowly progressive quadriparesis and dysphagia over 2-3 years. On examination, he was not ambulatory with marked symmetrical proximal arm and leg weakness. Labs including CBC, CMP, ANA, ESR, CRP, and TSH were normal. Serum creatine kinase was 6,500. Electromyography showed increased fibrillations and short, small motor unit action potentials in multiple muscle groups suggestive of an inflammatory or necrotizing myopathy. Left tibialis anterior biopsy showed inclusion bodies suggestive of IBM along with myofibular necrosis and mild inflammatory cells suggestive of necrotizing myopathy. Anti-HMG CoA reductase antibody level was markedly elevated. He was treated with intravenous immunoglobulin. His strength improved; he now ambulates with a walker and takes care of his activities of daily living, but continues to be on tube feeds. Our patient had chronic progressive weakness due to IBM and acute worsening was presumably due to statin-induced autoimmune myopathy. CONCLUSION: In patients with IBM and abrupt worsening, secondary causes of myopathy should be considered. In patients with a history of statin exposure, HMG CoA reductase antibody myopathy should be included in the evaluation as it is potentially treatable with immune therapy.

Disclosure: Dr. Kulhari has nothing to disclose. Dr. Preston has nothing to disclose.

Monday, April 18 2016, 8:30 am-7:00 pm

  • Copyright © 2016 by AAN Enterprises, Inc.

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