Evidence map›Paper›PMID 27103470›Full record

ReviewNature reviews. Neurology2016

Myasthenia gravis - autoantibody characteristics and their implications for therapy.

Nils Erik Gilhus, Geir Olve Skeie, Fredrik Romi, Konstantinos Lazaridis, Paraskevi Zisimopoulou, Socrates Tzartos

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

183 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. The associations of HLA-DRB1 gene polymorphisms with late-onset myasthenia gravis: a meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020
    Pooled it
  4. Thymectomy is a beneficial therapy for patients with non-thymomatous ocular myasthenia gravis: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017
    Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

123 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

6 authors.

Nils Erik GilhusDepartment of Clinical Medicine, University of Bergen, Postboks 7804, 5020 Bergen, Norway.
Geir Olve SkeieDepartment of Clinical Medicine, University of Bergen, Postboks 7804, 5020 Bergen, Norway.
Fredrik RomiDepartment of Clinical Medicine, University of Bergen, Postboks 7804, 5020 Bergen, Norway.
Konstantinos LazaridisDepartment of Neurobiology, Hellenic Pasteur Institute, 127 Vassilissis Sofias Avenue 115 21, Ampelokipi, Athens, Greece.
Paraskevi ZisimopoulouDepartment of Neurobiology, Hellenic Pasteur Institute, 127 Vassilissis Sofias Avenue 115 21, Ampelokipi, Athens, Greece.
Socrates TzartosDepartment of Neurobiology, Hellenic Pasteur Institute, 127 Vassilissis Sofias Avenue 115 21, Ampelokipi, Athens, Greece.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myasthenia gravis (MG) is an autoimmune disorder caused by autoantibodies that target the neuromuscular junction, leading to muscle weakness and fatigability. Currently available treatments for the disease include symptomatic pharmacological treatment, immunomodulatory drugs, plasma exchange, thymectomy and supportive therapies. Different autoantibody patterns and clinical manifestations characterize different subgroups of the disease: early-onset MG, late-onset MG, thymoma MG, muscle-specific kinase MG, low-density lipoprotein receptor-related protein 4 MG, seronegative MG, and ocular MG. These subtypes differ in terms of clinical characteristics, disease pathogenesis, prognosis and response to therapies. Patients would, therefore, benefit from treatment that is tailored to their disease subgroup, as well as other possible disease biomarkers, such as antibodies against cytoplasmic muscle proteins. Here, we discuss the different MG subtypes, the sensitivity and specificity of the various antibodies involved in MG for distinguishing between these subtypes, and the value of antibody assays in guiding optimal therapy. An understanding of these elements should be useful in determining how to adapt existing therapies to the requirements of each patient.

Indexed as

AutoantibodiesBiomarkersHumansMyasthenia GravisNeuromuscular JunctionAutoantibodiesBiomarkers

Identifiers

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.