An Unusual Case of Statin-Induced Myopathy: Anti-HMGCoA Necrotizing Autoimmune Myopathy

• Published in: Journal of general internal medicine : JGIM Vol. 30; no. 12; pp. 1879 - 1883
• Main Authors: Nichols, Laura, Pfeifer, Kurt, Mammen, Andrew L., Shahnoor, Nazima, Konersman, Chamindra G.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.12.2015; Springer Nature B.V
• Subjects: Acyl Coenzyme A - immunology; Atorvastatin Calcium - adverse effects; Autoantibodies - blood; Autoimmune Diseases - chemically induced; Autoimmune Diseases - pathology; Biopsy; Clinical Practice: Clinical Vignettes; Coenzyme A; Creatine; Creatine kinase; Creatine Kinase - blood; Electromyography; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - adverse effects; Internal Medicine; Medicine; Medicine & Public Health; Middle Aged; Muscle, Skeletal - pathology; Muscles; Muscular Diseases - chemically induced; Muscular Diseases - pathology; Myopathy; Patients; Statins; Therapy; idiopathic inflammatory myopathy; necrotizing autoimmune myopathy; statin; anti-HMGCR antibody
• ISSN: 0884-8734; 1525-1497
• DOI: 10.1007/s11606-015-3303-9

ABSTRACT Statins are some of the most widely prescribed medications, and though generally well tolerated, can lead to a self-limited myopathy in a minority of patients. Recently, these medications have been associated with a necrotizing autoimmune myopathy (NAM). Statin-associated NAM is characterized by irritable myopathy on electromyography (EMG) and muscle necrosis with minimal inflammation on muscle biopsy. The case presented is a 63-year-old woman who has continued elevation of creatine kinase (CK) after discontinuation of statin therapy. She has irritable myopathy on EMG and NAM is confirmed by muscle biopsy. She subsequently tests positive for an experimental anti-3-hydroxy-3-methylglutaryl-coenzyme A (anti-HMGCoA) antibody that is found to be present in patients with statin-associated NAM. Though statin-associated NAM is a relatively rare entity, it is an important consideration for the general internist in patients who continue to have CK elevation and weakness after discontinuation of statin therapy. Continued research is necessary to better define statin-specific and dose-dependent risk, as well as optimal treatment for this condition.