Absence of anti–HMG‐CoA reductase autoantibodies in severe self‐limited statin‐related myopathy |
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Authors: | James S Floyd MD MS Jennifer A Brody BA Eleni Tiniakou MD Bruce M Psaty MD PhD Andrew Mammen MD PhD |
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Institution: | 1. Department of Medicine, University of Washington, Seattle, Washington, USA;2. Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA;3. Department of Epidemiology, University of Washington, Seattle, Washington, USA;4. Health Services, University of Washington, Seattle, Washington, USA;5. National Institutes of Health, Bethesda, Maryland, USA |
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Abstract: | Introduction: Patients with self‐limited statin‐related myopathy improve spontaneously when statins are stopped. In contrast, patients with statin‐associated autoimmune myopathy have autoantibodies recognizing 3‐hydroxy‐3‐methyl‐glutaryl‐coenzyme A reductase (HMGCR) and usually require immunosuppressive therapy to control their disease. On initial presentation, it can sometimes be difficult to distinguish between these 2 diseases, as both present with muscle pain, weakness, and elevated serum creatine kinase (CK) levels. The goal of this study was to determine whether patients with severe self‐limited statin‐related myopathy also make anti‐HMGCR autoantibodies. Methods: We screened 101 subjects with severe self‐limited cerivastatin‐related myopathy for anti‐HMGCR autoantibodies. Results: No patient with severe self‐limited cerivastatin‐related myopathy had anti‐HMGCR autoantibodies. Conclusion: Anti‐HMGCR autoantibody testing can be used to help differentiate whether a patient has self‐limited myopathy due to cerivastatin or autoimmune statin‐associated myopathy; these findings may apply to other statins as well. Muscle Nerve 54 : 142–144, 2016 |
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Keywords: | adverse drug reaction autoimmune myopathy rhabdomyolysis statins |
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