All-cause mortality in statin-associated immune-mediated necrotizing myopathy compared with idiopathic inflammatory myopathy

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ID: 329818
2026
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Abstract
OBJECTIVES: Statin-associated immune-mediated necrotizing myopathy (IMNM) is a distinct idiopathic inflammatory myopathy (IIM) associated with anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR) antibodies. The present study determined all-cause mortality among patients with statin-associated IMNM. METHODS: In this retrospective cohort study of 142 adult patients with IIM evaluated at a tertiary academic medical center, statin-associated IMNM was defined by IMNM with recent statin exposure. IIM was defined by standard criteria. The primary outcome was all-cause mortality. Age-adjusted Cox proportional hazards models were the primary analyses with additional adjustments for age, diabetes mellitus, and hyperlipidemia with propensity score-weighted Cox models. RESULTS: Among 142 patients with IIM, 41 were statin-associated IMNM who were older and had shorter disease duration (p < 0.05). All-cause mortality was higher in statin-associated IMNM (31.7%, 13/41) than in IIM (23.8%, 24/101) (unadjusted HR 2.55, 95% CI 1.24-5.24; p = 0.011), with cardiopulmonary events and infections the major causes of death. In unadjusted analysis, statin-associated IMNM was associated with higher mortality (hazard ratio [HR] 2.55, 95% CI 1.24-5.24) and attenuated after age adjustment (HR 1.98, 95% CI 0.97-4.03) and was no longer statistically significant after adjustment for diabetes and hyperlipidemia (HR 1.70, 95% CI 0.71-4.08). Joint stratification by anti-HMGCR status and age (cutoff 60 years) demonstrated that older patients with statin-associated IMNM had the lowest survival among the four strata (log-rank P = 0.036). CONCLUSIONS: Statin-associated IMNM is associated with higher mortality than other myositis subtypes; this excess attenuates after adjustment for age and cardiometabolic comorbidity, indicating these pre-existing conditions identify a higher-risk clinical phenotype.
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Authors Oluoma Edeh, Tam Nguyen Dinh, Maheswari Muruganandam, Frank X. O'Sullivan, Avinash D Sahu, Wilmer L. Sibbitt
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Journal Lara D. Veeken
Year 2026
DOI
10.1093/rheumatology/keag536
URL
https://doi.org/10.1093/rheumatology/keag536
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