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Necrotizing myopathies: beyond statins.

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Necrotizing myopathy on muscle biopsy is often immune-mediated. Recent findings reveal distinct subtypes based on autoantibodies, including anti-signal recognition particle and anti-HMG-CoA reductase, impacting treatment strategies for autoimmune myopathy.

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Area of Science:

  • Neurology
  • Immunology
  • Pathology

Background:

  • Necrotizing myopathy on muscle biopsy can be associated with various conditions, including toxic, endocrine, and heritable myopathies.
  • Immune-mediated myopathies are a significant cause of necrotizing myopathy and are the focus of this review.

Purpose of the Study:

  • To review the spectrum of diseases presenting with necrotizing muscle biopsy.
  • To emphasize the role of immune-mediated myopathies in necrotizing myopathy.
  • To discuss the classification and implications of distinct autoantibody profiles in immune-mediated necrotizing myopathy.

Main Methods:

  • Literature review of studies on necrotizing myopathy and immune-mediated myopathies.
  • Analysis of recent evidence classifying immune-mediated necrotizing myopathy based on autoantibodies.
  • Discussion of distinct clinical entities within autoimmune myopathy with necrotizing features.

Main Results:

  • Immune-mediated necrotizing myopathy (IMNM) is now understood to encompass distinct entities based on autoantibodies.
  • Key autoantibodies identified include those targeting signal recognition particle (anti-SRP) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (anti-HMGCR).
  • Anti-HMGCR-positive IMNM can be further stratified by statin exposure, with statin-naïve cases potentially being more resistant to immunosuppression.

Conclusions:

  • A substantial subset of autoimmune myopathy patients exhibit predominantly necrotizing muscle biopsies with minimal inflammation.
  • This finding is observed across various myositis types, including antisynthetase syndrome, anti-SRP, and anti-HMGCR-associated myopathies (statin-exposed and -naïve).
  • Recognizing these distinct entities is crucial for advancing understanding of pathogenic mechanisms and optimizing treatment for autoimmune myopathies.