Statin-Induced Necrotizing Autoimmune Myopathy: Diagnosis and Treatment Approach

The widespread use of statins for cardiovascular diseases has unveiled a new subset of inflammatory myopathy, immune-mediated necrotizing myopathy (IMNM). We describe below an unusual case of anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR) myopathy. A 64-year-old male individual with type 2 diabetes, hyperlipidemia, and coronary artery disease presented with progressive proximal muscle weakness and pain for 3 months. He took atorvastatin 40 mg for 4 years, which was discontinued due to elevated liver enzymes and resumed treatment with rosuvastatin 5 mg later due to worsening hyperlipidemia. Physical examination showed significant weakness of the hip, shoulder girdle, and biceps/triceps. Creatinine kinase (CK) was found to be 232.48 µkat/L (13 921 IU/L) (normal: 0.833-5.133 µkat/L; 50-308 IU/L). Electromyography and left vastus lateralis muscle biopsy showed findings of myonecrosis. Anti-HMGCR assay was strongly positive with antibodies > 200 chemiluminescent units (CU) (normal: 0-20 CU). He was started on prednisone followed by human-immunoglobulin (IVIG) which led to a decline in CK. Statin-induced necrotizing autoimmune myopathy (SINAM) is an exceptionally rare side effect of statins. Although statins come with a good side-effect profile, one should be aware of marked, persistent elevations in muscle enzyme levels. Prompt confirmation with antibody levels, drug discontinuation, and early initiation of immunosuppression can lead to good outcomes.