What question did this study set out to answer?

To present a case of statin-induced refractory immune-mediated necrotizing myositis (IMNM).

May 20, 2026

C49-28 Refractory Statin-induced Seronegative Immune-mediated Necrotizing Myositis

Key Points

To present a case of statin-induced refractory immune-mediated necrotizing myositis (IMNM).
Case presentation of a 70-year-old man on rosuvastatin with muscle weakness and elevated creatine kinase levels.
Multiple therapies including high-dose methylprednisolone, plasma exchange, intravenous immunoglobulins, and rituximab administered without improvement.
Muscle biopsy performed to evaluate myopathy.
Elevated creatine kinase reached 101,030 U/L, with AST and ALT also rising despite treatment.
The patient experienced respiratory muscle weakness requiring intubation, leading to compassionate extubation and subsequent death.
Muscle biopsy demonstrated nonspecific myofiber atrophy with inadequate sampling concerns.

Abstract

Abstract Introduction Statins are among the most widely prescribed medications. Muscle toxicity is a well-known adverse effect and while commonly mild, may at times lead to severe myonecrosis. We present a case of statin-induced seronegative immune-mediated necrotizing myositis (IMNM) refractory to multiple therapies. Case Presentation A 70-year-old man on rosuvastatin for history of coronary artery disease and hyperlipidemia presented with dyspnea and progressive, painless, symmetric muscle weakness that involved the proximal muscles. Examination revealed bilateral upper and lower extremity weakness. Workup was notable for elevated creatine kinase(CK) levels (40,870U/L) and liver enzymes(AST 763U/L, ALT 210U/L) and acute kidney injury due to rhabdomyolysis. Magnetic resonance imaging of bilateral thighs demonstrated diffuse muscle edema consistent with myositis. Electromyography was consistent with irritative myositis. ANA, ANCA, myositis panel,SRP, andHMG-CoA reductase serologies were negative. Due to progressive decline despite statin discontinuation, high-dose methylprednisolone was administered for suspected seronegative IMNM with minimal response. The patient required intubation due to respiratory muscle weakness. Plasma exchange resulted in transient reduction in CK and liver enzymes without clinical improvement. He received intravenous immunoglobulins and rituximab, thoughCK, AST, andALT continued to increase to 101,030U/L, 4,000U/L, and9,252U/L, respectively. Muscle biopsy demonstrated nonspecific myofiber atrophy, with concern for inadequate sampling. The patient was compassionately extubated and expired. Discussion IMNM is a rare complication of statin use, with an estimated incidence of 8.3per million person-years1. The majority of cases present with subacute, progressive onset of muscle weakness. Evaluation for anti-HMG-CoA reductase antibodies is important in diagnosis, though up to 0.7% of patients are seronegative2. Patients are typically treated with immunosuppressive medications including steroids, rituximab, and methotrexate, often with at least partial recovery of muscle strength. Notably, statin withdrawal does not lead to improvement. Our case appears to be unique in the literature in terms of the lack of response to multiple therapies. This case makes clear the need for further research into the pathogenesis and therapeutic options for this condition. References 1. Li C, Liu H, Yang L, Liu R, YinG, XieQ. Immune-mediated necrotizing myopathy:A comprehensivereview of the pathogenesis, clinical features, andtreatments. J Autoimmun. 2024;148:103286. doi:10.1016/j.jaut.2024.103286 2. Pinal-Fernandez I, Casal-Dominguez M, MammenAL. Immune-MediatedNecrotizing Myopathy. Curr RheumatolRep. 2018Mar 26;20(4):21. doi:10.1007/s11926-018-0732-6. PMID:29582188;PMCID:PMC6019613. This abstract is funded by: none

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