To characterise an elderly-onset case of anti-HMGCR IMNM manifesting with bulbar symptoms, asymmetric MRI findings and a rapid biochemical response to early IVIG therapy, thereby extending the clinical–radiologic phenotype described in literature.

Anti-HMG-CoA reductase (HMGCR) immune-mediated necrotising myopathy (IMNM) is a rare yet increasingly recognised myopathy that may evolve after statin withdrawal, reflecting loss of immune tolerance to the HMGCR antigen. Contemporary reviews report elderly-onset variants, but asymmetric muscle involvement with bulbar palsy and preserved renal function remain under characterised.

A 70-year-old man presented with ten weeks of progressive proximal weakness and dysphagia, seven weeks after cessation of rosuvastatin ( 2.5mg daily) Creatine kinase 8,897 U/L; AST 248 U/L; troponin T 267 ng/L (normal echocardiogram). MRI of the thighs showed asymmetric myositis; swallow fluoroscopy demonstrated safe swallow without aspiration. Muscle biopsy revealed necrotising myopathy with minimal infiltration. Anti-HMGCR IgG 118 U confirmed the diagnosis. He received prednisone 40 mg/day and IVIG 2 g/kg over 5 days

CK declined from 5,688 to 3,290 U/L within 72 hours of IVIG initiation, paralleling objective strength and dysphagia improvement. Troponin normalised, supporting skeletal cross-reactivity rather than myocarditis. The patient showed sustained functional recovery

This case underscores key refinements in the evolving understanding of anti-HMGCR IMNM:

1. Immune persistence can manifest weeks after statin withdrawal, confirming self-sustaining autoimmunity.
2. Asymmetric muscle involvement broadens the classical symmetric paradigm 
3. False-positive troponin T elevation necessitates cardiac evaluation with modality-specific interpretation.
4. Early IVIG initiation achieved rapid biochemical and clinical remission, aligning with modern endorsed protocols .

Recognition of such late-onset, post-statin, IVIG-responsive presentations broadens the therapeutic window for prompt, targeted intervention in immune-mediated necrotising myopathies.