Evidence map›Paper›PMID 37249286›Full record

ReviewImmunity, inflammation and disease2023

COVID-19 as a trigger of Guillain-Barré syndrome: A review of the molecular mechanism.

Mahdi Malekpour, Shaghayegh Khanmohammadi, Mohammad Javad Entezari Meybodi, Dorsa Shekouh, Mohammad Reza Rahmanian, Sina Kardeh, Negar Azarpira

Open access · goldAbstract readReview
In one paragraph

Review in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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  13. Demyelination in Patients with POST-COVID Depression.Journal of clinical medicine · 2024
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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

7 authors at 3 institutions in 2 countries.

Mahdi MalekpourStudent Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID 0000-0003-2784-0002
Shaghayegh KhanmohammadiNetwork of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Mohammad Javad Entezari MeybodiStudent Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
Dorsa ShekouhStudent Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
Mohammad Reza RahmanianStudent Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
Sina KardehCentral Clinical School, Monash University, Melbourne, Australia.
Negar AzarpiraTransplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID 0000-0002-1518-1583
Shiraz University of Medical Sciences · IRMonash University · AUUniversal Scientific Education and Research Network · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a pandemic with serious complications. After coronavirus disease 2019 (COVID-19), several post-acute COVID-19 syndromes (PACSs) and long-COVID sequels were reported. PACSs involve many organs, including the nervous, gustatory, and immune systems. One of the PACSs after SARS-CoV-2 infection and vaccination is Guillain-Barré syndrome (GBS). The incidence rate of GBS after SARS-CoV-2 infection or vaccination is low. However, the high prevalence of COVID-19 and severe complications of GBS, for example, autonomic dysfunction and respiratory failure, highlight the importance of post-COVID-19 GBS. It is while patients with simultaneous COVID-19 and GBS seem to have higher admission rates to the intensive care unit, and demyelination is more aggressive in post-COVID-19 GBS patients. SARS-CoV-2 can trigger GBS via several pathways like direct neurotropism and neurovirulence, microvascular dysfunction and oxidative stress, immune system disruption, molecular mimicry, and autoantibody production. Although there are few molecular studies on the molecular and cellular mechanisms of GBS occurrence after SARS-CoV-2 infection and vaccination, we aimed to discuss the possible pathomechanism of post-COVID-19 GBS by gathering the most recent molecular evidence.

Indexed as

COVID-19Guillain-Barre SyndromeHumansPandemicsPost-Acute COVID-19 SyndromeSARS-CoV-2COVID-19GBSGuillain-Barré syndromelong COVIDpostacute COVID-19 syndromeSARS-CoV-2

Identifiers

PMID37249286
PMCPMC10187022
OpenAlexW4378745396

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.