Introduction

Statins are widely prescribed for dyslipidemia and cardiovascular risk reduction. Although they are generally well tolerated, statin-associated muscle symptoms remain among the most common reasons for treatment interruption and may range from self-limited myalgia to severe myopathy and rhabdomyolysis [1,2]. Creatine kinase (CK) is an intracellular enzyme that helps maintain rapid energy availability in skeletal muscle, and serum CK rises when muscle-fiber injury releases the enzyme into the circulation. Statin-associated muscle injury is multifactorial and may involve altered muscle-cell energetics, membrane instability, and, in a small subset of patients, immune-mediated injury [1,2].

Marked CK elevation with progressive weakness should prompt urgent evaluation for severe statin-associated myopathy and alternative inflammatory myopathies. A particularly important diagnostic consideration is statin-associated immune-mediated necrotizing myopathy (IMNM), which may present with proximal weakness, persistent CK elevation, and antibodies against 3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR) [3-5]. Persistent marked CK elevation after statin discontinuation should prompt evaluation for anti-HMGCR antibody-associated IMNM. However, this diagnosis should not be considered confirmed without supportive serology and, when clinically indicated, electromyography, imaging, or muscle biopsy [3-5].

We present a case of severe rosuvastatin-associated myopathy recognized in the outpatient setting, complicated by marked hyperCKemia, transaminitis, and persistent CK elevation. This case highlights an important outpatient diagnostic challenge: distinguishing severe toxic statin myopathy from possible immune-mediated disease when CK remains markedly elevated after statin withdrawal and confirmatory investigations and long-term outcome data are not available to the initial clinician.