Case Presentation: We describe a 51-year-old male treated for statin-induced necrotizing autoimmune myopathy (SINAM). The patient presented to the emergency department (ED) with over a month of progressive proximal muscle weakness and dysphagia resulting in limited mobility, despite statin cessation from a recent hospitalization at outside hospital where was found to have rhabdomyolysis and elevated transaminases. In the ED, laboratory evaluation was notable for significantly elevated creatinine kinase (CK) 10,399 IU/L (N: 24-170), elevated aspartate transaminase (AST) 496 U/L (N: 5-40 U/L), elevated alanine transferase (ALT) 507 U/L (N: 4-41 U/L), and normal alkaline phosphatase. Given these abnormalities along with patient’s history of statin use, the patient was admitted to general medicine service for diagnosis and further evaluation (rheumatologic, infectious, and malignancy workups). Muscle biopsy during admission revealed necrotizing myositis and presence of HMG-CoA antibodies, confirming SINAM. Following rheumatology recommendation, the patient was treated with prednisone, solumedrol, mycophenolate, and intravenous immunoglobulin (IVIG) with marked improvement in muscle weakness and liver transaminases. The patient was discharged with continuation of prednisone, mycophenolate, and IVIG.
Discussion: Statins are highly effective lipid-lowering agents. Despite being relatively safe, statins are commonly associated with adverse muscle symptoms ranging in severity, including muscle pain, weakness, fatigue, and even rhabdomyolysis. About 10% – 25% of patients taking statins report such side effects. SINAM is an ultrarare and life-threatening complication on this spectrum, estimated to occur in 1/100,000 patients on statins; it may occur at any point after initiation and generally persists after statin discontinuation. SINAM is characterized by progressive proximal muscle weakness, elevated CK, and sometimes dysphagia and respiratory distress. It is likely mediated by an antibody-mediated immune reaction to HMG-CoA reductase, an enzyme upregulated by statins to achieve their lipid-lowering effects. Although certain risk factors may contribute to the development of SINAM, such as age > 50 years and African American descent, its epidemiological characteristics are unclear. This patient’s presentation of proximal muscle weakness, dysphagia, and elevated CK with onset years after statin initiation and persistence despite statin discontinuation was typical of SINAM, although nonspecific. However, the muscle biopsy findings allowed the patient to be definitively diagnosed and treated. SINAM is generally treated with steroids, IVIG, and steroid-sparing immunosuppressive agents, and treatment can be lifelong; this patient continues to receive therapy to this day.
Conclusions: This case of SINAM highlights the importance of screening patients on statin therapy for signs of muscle weakness indicative of myopathy even after years of uncomplicated use. Healthcare professionals should strongly consider reducing statin use or discontinuing the medication altogether to lower the risk of life-threatening complications such as SINAM and opt for other options to treat hyperlipidemia. Although statins are ubiquitously used, their adverse-muscle related events are not to be dismissed.