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Abstract

In the landscape of contemporary medicine, statins stand out as a cornerstone in the prevention and management of atherosclerotic cardiovascular diseases. By inhibiting the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase enzyme, statins effectively lower cholesterol levels, thus mitigating the risk of heart attacks and strokes.1 Despite their widespread adoption and generally well-tolerated nature, the clinical panorama of statin therapy is occasionally marred by side effects, including muscle-related adverse events. These range from relatively common and benign myalgias to the rare and severe statin-induced necrotizing autoimmune myopathy (SINAM), a condition marked by muscle weakness and profoundly elevated levels of creatine kinase (CK) that persist even after the discontinuation of the offending statin2 (Table 1).

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