Evidence map›Paper›PMID 33093664›Full record

ReviewNature reviews. Rheumatology2020

Immune-mediated necrotizing myopathy: clinical features and pathogenesis.

Yves Allenbach, Olivier Benveniste, Werner Stenzel, Olivier Boyer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed
20.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

155 citing papers in PubMed, 303 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Statins and Myasthenia Gravis: Clinical Implications and Pathogenesis.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Emerging therapies in idiopathic inflammatory myopathies.Journal of neuromuscular diseases · 2026
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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  20. Article

95 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Yves Allenbach *Sorbonne Université, Assistance Publique - Hôpitaux de Paris, Inserm U974, Department of Internal Medicine and Clinical Immunology, Pitié-Salpêtrière University Hospital, Paris, France.
Olivier Benveniste *Sorbonne Université, Assistance Publique - Hôpitaux de Paris, Inserm U974, Department of Internal Medicine and Clinical Immunology, Pitié-Salpêtrière University Hospital, Paris, France. olivier.benveniste@aphp.fr.ORCID http://orcid.org/0000-0002-1167-5797
Werner Stenzel *Department of Neuropathology, Charité -Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Olivier Boyer *Normandie University, UNIROUEN, Inserm U1234, Department of Immunology and Biotherapy, Rouen University Hospital, Rouen, France.ORCID http://orcid.org/0000-0002-7591-307X
Inserm · FRHumboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune-mediated necrotizing myopathy (IMNM) is a group of inflammatory myopathies that was distinguished from polymyositis in 2004. Most IMNMs are associated with anti-signal recognition particle (anti-SRP) or anti-3-hydroxy-3-methylglutaryl-coA reductase (anti-HMGCR) myositis-specific autoantibodies, although ~20% of patients with IMNM remain seronegative. These associations have led to three subclasses of IMNM: anti-SRP-positive IMNM, anti-HMGCR-positive IMNM and seronegative IMNM. IMNMs are frequently rapidly progressive and severe, displaying high serum creatine kinase levels, and failure to treat IMNMs effectively may lead to severe muscle impairment. In patients with seronegative IMNM, disease can be concomitant with cancer. Research into IMNM pathogenesis has shown that anti-SRP and anti-HMGCR autoantibodies cause weakness and myofibre necrosis in mice, suggesting that, as well as being diagnostic biomarkers of IMNM, they may play a key role in disease pathogenesis. Therapeutically, treatments such as rituximab or intravenous immunoglobulins can now be discussed for IMNM, and targeted therapies, such as anticomplement therapeutics, may be a future option for patients with refractory disease.

Indexed as

AnimalsAnti-Inflammatory AgentsAutoantibodiesAutoimmune DiseasesBiopsyHumansHydroxymethylglutaryl CoA ReductasesImmunologic FactorsMiceMuscle, SkeletalMyositisNecrosisPrognosisSignal Recognition ParticleAnti-Inflammatory AgentsAutoantibodiesHMGCR protein, humanHydroxymethylglutaryl CoA ReductasesImmunologic FactorsSignal Recognition Particle

Identifiers

PMID33093664
OpenAlexW3094476732

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.