Evidence map›Paper›PMID 35165857›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2022

Antibody Therapies in Autoimmune Neuromuscular Junction Disorders: Approach to Myasthenic Crisis and Chronic Management.

Fiammetta Vanoli, Renato Mantegazza

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

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  19. Starting eculizumab as rescue therapy in refractory myasthenic crisis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Fiammetta VanoliNeuroimmunology and Neuromuscular Disease Department, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.
Renato MantegazzaNeuroimmunology and Neuromuscular Disease Department, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. renato.mantegazza@istituto-besta.it.ORCID 0000-0002-9810-5737
Fondazione IRCCS Istituto Neurologico Carlo Besta · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myasthenia gravis (MG) is a neurological autoimmune disorder characterized by muscle weakness and fatigue. It is a B cell-mediated disease caused by pathogenic antibodies directed against various components of the neuromuscular junction (NMJ). Despite the wide range of adverse effects, current treatment is still based on non-specific immunosuppression, particularly on long-term steroid usage. The increasing knowledge regarding the pathogenic mechanisms of MG has however allowed to create more target-specific therapies. A very attractive therapeutic approach is currently offered by monoclonal antibodies (mAbs), given their ability to specifically and effectively target different immunopathological pathways, such as the complement cascade, B cell-related cluster of differentiation (CD) proteins, and the human neonatal Fc receptor (FcRn). Up to now, eculizumab, a C5-directed mAb, has been approved for the treatment of generalized MG (gMG) and efgartigimod, a FcRn inhibitor, has just been approved by the U.S. Food and Drug Administration for the treatment of anti-acetylcholine receptor (AChR) antibody positive gMG. Other mAbs are currently under investigation with encouraging preliminary results, further enriching the new range of therapeutic possibilities for MG. This review article provides an overview of the present status of mAb-based therapies for MG, which offer an exciting promise for better outcomes by setting the basis of a precision medicine approach.

Indexed as

Antibodies, MonoclonalMyasthenia GravisAutoantibodiesHumansNeuromuscular JunctionReceptors, CholinergicAntibodies, MonoclonalAutoantibodiesReceptors, CholinergicB cellBiological drugsImmunosuppressionMonoclonal antibodyMyasthenia gravis

Identifiers

PMID35165857
PMCPMC9294078
OpenAlexW4212901419

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.