4.1 Article

A Case Series of Statin-Induced Necrotizing Autoimmune Myopathy

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CUREUS JOURNAL OF MEDICAL SCIENCE
卷 14, 期 1, 页码 -

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CUREUS INC
DOI: 10.7759/cureus.21613

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idiopathic rhabdomyolysis; statin-induced myopathy; proximal weakness; statin; sinam; statin-induced necrotizing autoimmune myopathy

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The use of statins for cardiovascular disease prevention has been increasing over the past decade, but it has also been associated with various side effects, including muscle-related complications. Among these, statin-induced necrotizing autoimmune myopathy (SINAM) stands out due to its unique characteristics and aggressive management. This article presents two cases of SINAM and discusses the clinical aspects of diagnosis, investigation, and treatment. SINAM typically presents with proximal myopathy and elevated creatinine kinase levels that do not improve with discontinuation of statins. Diagnosis is confirmed through biopsy and detection of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) antibodies. Additional investigations are necessary to rule out other causes of proximal myopathy. In most cases, rechallenging with statins is unsuccessful and immunosuppressive treatment is required.
The use of statins has been increasing over the past decade for the primary and secondary prevention of cardiovascular disease worldwide. Subsequently, various side effects have also been unfolding. Muscle-related side effects secondary to statins range from myalgia to rhabdomyolysis and need close monitoring for early detection. Statin-induced necrotizing autoimmune myopathy (SINAM) in particular is unique given its pathophysiology, trigger factor, genetic predisposition, and aggressive management strategy. We present two cases of SINAM and discuss the clinical aspects of diagnosis, investigation, and management. Statin-induced necrotizing autoimmune myopathy usually presents with proximal myopathy along with increased creatinine kinase (CK) levels which do not resolve with only statin discontinuation. Diagnosis should be made with biopsy and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) antibody detection. The investigation should also be directed to rule out other etiology of proximal myopathy. In most cases, rechallenge with a statin is unsuccessful and immunosuppressive treatment is essential.

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