What question did this study set out to answer?

To highlight the potential severe consequences of statin-induced immune-mediated necrotizing myopathy and the need for early intervention.

May 20, 2026

A33-40 Statin-Induced Immune-Mediated Necrotizing Myopathy Leading to Respiratory Failure

Key Points

To highlight the potential severe consequences of statin-induced immune-mediated necrotizing myopathy and the need for early intervention.
A case presentation of a 68-year-old woman with a history of comorbidities and presenting symptoms of dyspnea and muscle weakness.
Diagnostic tools included muscle biopsy, serum CK levels, antibody testing, and imaging for evaluation of myopathy.
Intervention involved immunosuppressive treatments such as IV solumedrol and IVIG, transitioning to outpatient care.
Patient presented with CK levels of 3,379 U/L indicating severe muscle dysfunction.
Biopsy revealed predominant myofiber necrosis with minimal inflammatory infiltrate, confirming IMNM diagnosis.
Following treatment with immunosuppressive therapy, patient required long-term ventilatory support due to progressive symptoms.

Abstract

Abstract Introduction Immune-mediated necrotizing myopathy (IMNM) is a subset of idiopathic inflammatory myopathies, characterized by proximal muscle weakness, elevated creatine kinase (CK) levels, and muscle biopsy showing myofiber necrosis with minimal inflammatory infiltrate. IMNM may be associated with anti-signal recognition particle (anti-SRP) antibodies, anti-3-hydroxy-3-methylglutaryl-coA reductase (anti-HMGCR) antibodies, or be seronegative. Statin therapy can trigger anti-HMGCR antibodies, leading to statin-induced IMNM. We present a case of this condition. Case Presentation A 68-year-old woman with a history of diabetes, hypertension, and hyperlipidemia presented with dyspnea and required high-flow nasal cannula at 45 L/min with 70% FiO2. Initial chest X-ray was unremarkable, but a follow-up CTA chest revealed bilateral lower lobe pneumonia. She was started on empiric IV antibiotics; however, her condition worsened, necessitating intubation and norepinephrine support. Although her condition gradually improved, she could not be extubated. Further history from her daughter revealed a one-year history of chronic lower extremity weakness with recent onset of proximal muscle weakness and dysphagia. Neurology suspected that the patient may have statin-induced myopathy versus myasthenia gravis, so atorvastatin 40 mg daily was discontinued. HMG-CoA reductase (HMGCR) and acetylcholine receptor antibodies were ordered. CK was 3,379 U/L. MRI of the brain and cervical, thoracic, and lumbar spine were unremarkable. Rheumatology suspected an inflammatory myopathy and ordered a myositis panel and non-contrast MRI of the thighs, which showed fatty replacement of proximal muscles and areas of edema suggestive of active inflammation. General surgery performed a thigh muscle biopsy revealing predominant myofiber necrosis with minimal inflammatory infiltrate. HMGCR antibody returned strongly positive (200), while the myositis panel, acetylcholine receptor antibody, and Jo-1 were negative. The patient was treated with IV solumedrol 125 mg every 12 hours and IVIG 0.4 g/kg daily for five days, then transitioned to prednisone 60 mg daily with plans for continued outpatient IVIG. She underwent a tracheostomy and was discharged to a long-term acute care facility for ventilatory support. Discussion IMNM can progress rapidly, causing severe proximal muscle weakness and complications such as dysphagia, aspiration pneumonia, respiratory failure, and fatty muscle replacement, as seen in our patient. Early and aggressive immunosuppressive therapy is critical to improving outcomes and reducing long-term disability and mortality. This abstract is funded by: None

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