ArticleFrontiers in immunology2024
Case report: Rapid clinical improvement of anti-HMGCR immune-mediated necrotizing myopathy treated with efgartigimod.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Case Report - Anti-HMGCR-Associated Immune-Mediated Necrotizing Myopathy and Interstitial Lung Disease With Long-Term Use of Ezetimibe and Low-Dose Atorvastatin.International journal of rheumatic diseases · 2026Article
- Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Case Report: Balancing immunosuppression and infection-intravenous immunoglobulin in anti-HMGCR immune-mediated necrotizing myopathy complicated by severe pneumonia.Frontiers in medicine · 2026Article
- The Effect of Anti-3-Hydroxy-3-Methylglutaryl-CoA Reductase (HMGCR) Human Autoantibodies on Muscle Regeneration in Mice.Muscle & nerve · 2025Article
- Clinicopathological profiling and prognosis of idiopathic inflammatory myopathy overlapping with myasthenia gravis: a retrospective cohort study.Journal of neurology · 2025Article
- Patterns and predictors of therapeutic response to efgartigimod in acetylcholine receptor-antibody generalized myasthenia gravis subtypes.Therapeutic advances in neurological disorders · 2025Article
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Authors and funding
5 authors.
Funding
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Abstract
Immune-mediated necrotizing myopathy (IMNM) with anti-HMGCR antibody positivity is characterized by proximal extremity weakness, increased creatine kinase, and extensive muscle edema. There is an urgent need to find more appropriate treatment options for anti-HMGCR IMNM patients who do not respond well to conventional therapy in the acute phase. With the advent of targeted biologics, new treatment options are available. We report on a 66-year-old anti-HMGCR IMNM patient who initially presented with a 1-month history of progressive proximal extremity weakness and dysphagia with markedly elevated creatine kinase. The patient did not respond to conventional high-dose glucocorticoid and intravenous immunoglobulin therapy, and his symptoms rapidly deteriorated over the 2 weeks after this treatment, with worsening limb weakness that prevented walking, marked proximal muscle atrophy, and weight loss. After one cycle (four infusions) of efgartigimod, the patient's symptoms improved markedly and he has since (for several months) remained in a good clinical state.
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Registered trials
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