Evidence map›Paper›PMID 21088848›Full record

ArticleJournal of neurology2011

Comparison of muscle ultrastructure in myasthenia gravis with anti-MuSK and anti-AChR antibodies.

Giovanna Cenacchi, Valentina Papa, Papa Valentina, Marina Fanin, Fanin Marina, Elena Pegoraro, Pegoraro Elena, Corrado Angelini, Angelini Corrado

Erratum issuedAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Is paravertebral muscles edema a consequence of neurogenic changes in MuSK-positive myasthenia gravis?Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2022
    Article
  9. Article
  10. Muscle-Specific Kinase Myasthenia Gravis.Frontiers in immunology · 2020
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Animal models of antimuscle-specific kinase myasthenia.Annals of the New York Academy of Sciences · 2012
    Article
  17. Article
  18. Article
  19. Article
4 · The record

Corrections and comments

  • Erratum issued
    Valentina, Papa [corrected to Papa, Valentina]; Marina, Fanin [corrected to Fanin, Marina]; Elena, Pegoraro [corrected to Pegoraro, Elena]; Corrado, Angelini [corrected to Angelini, Corrado]
5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Giovanna CenacchiClinical Department of Radiological Histopathological Sciences, Alma Mater Studiorum University of Bologna, Bologna, Italy. giovanna.cenacchi@unibo.it
Valentina Papa
Papa Valentina
Marina Fanin
Fanin Marina
Elena Pegoraro
Pegoraro Elena
Corrado Angelini
Angelini Corrado
University of Padua · ITUniversity of Bologna · IT

Funding

Telethon GTB07001Telethon GTF02009
6 · The paper itself

Abstract

Patients with myasthenia gravis (MG) with antibodies to muscle-specific receptor tyrosine kinase (MuSK) differ from acetylcholine receptor (AChR)-positive MG patients, as they frequently present with severe oculobulbar muscle weakness or with neck, shoulder, and respiratory muscle involvement. The neuromuscular junction (NMJ) has been confirmed to be the main target of both AChR- and MuSK-MG. However, histopathological investigation disclosed that muscle fiber atrophy was prevalent in AChR-MG, whereas mild myopathic changes and mitochondrial abnormalities were more frequently observed in MuSK-MG. As the pathogenetic mechanism in MuSK-MG remains unclear, this study investigated the submicroscopic pattern of muscle histopathology to establish a possible correlation between clinical involvement and subcellular morphological findings. Muscle biopsies from seven MuSK-MG patients and from seven patients with AChR-MG were analyzed by transmission electron microscopy. Myopathic and mitochondrial abnormalities were more prominent in MuSK-MG and show giant, swollen, and degenerated mitochondria with fragmented cristae. The most common changes in AChR-MG muscles were fiber atrophy, myofibrillar disarray, and Z-line streaming, consistent with mild neurogenic abnormalities. A different pathogenetic mechanism is emerging in MuSK-MG compared to AChR-MG. Mitochondrial abnormalities seem to be more prominent in MuSK-MG, whereas neurogenic atrophy is observed in AChR-MG.

Indexed as

AdultAgedAutoantibodiesAutoantigensFemaleHumansMaleMicroscopy, Electron, TransmissionMiddle AgedMitochondriaMuscle, SkeletalMyasthenia GravisNeuromuscular JunctionReceptor Protein-Tyrosine KinasesReceptors, CholinergicYoung AdultAutoantibodiesAutoantigensMUSK protein, humanReceptor Protein-Tyrosine KinasesReceptors, Cholinergic

Identifiers

PMID21088848
OpenAlexW2084678609

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.