Evidence map›Paper›PMID 31828968›Full record

ReviewBrain and behavior2020

Hepatitis E virus-associated Guillain-Barre syndrome: Revision of the literature.

Hang Liu, Ying Ma

Open access · goldAbstract readReview
In one paragraph

Review in Brain and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Guillain Barre Syndrome as a Complication of COVID-19: A Systematic Review.The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques · 2022
    Pooled it
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Current perspectives of viral hepatitis.World journal of gastroenterology · 2024
    Review
  12. Article
  13. Observational
  14. Article
  15. Article
  16. Transfusion-transmitted hepatitis E: What we know so far?World journal of gastroenterology · 2022
    Review
  17. Review
  18. Review
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Hang LiuDepartment of Neurology, Shengjing Hospital, China Medical University, Shenyang, China.
Ying MaDepartment of Neurology, Shengjing Hospital, China Medical University, Shenyang, China.ORCID 0000-0001-7611-597X
China Medical University · CN

Funding

National Nature Science Foundation for Young Scholars of China 81200834
6 · The paper itself

Abstract

introductionThe association between preceding infection of hepatitis E virus (HEV) and Guillain-Barre syndrome (GBS) has been found for more than a decade, while hepatitis E virus-associated Guillain-Barre syndrome (HEV-associated GBS) still remains poorly understood. Initially discovered in 2000, the association between GBS and HEV has been focused by neurologists increasingly. Five percent of patients with GBS had preceding acute HEV infection in the Netherlands and higher rate was found in Bangladesh (11%) where HEV is endemic.

methodAn extensive review of relevant literature was undertaken.

resultsHepatitis E virus infection may induce GBS via direct viral damage according to recent research findings. On the other hand, the presence of antiganglioside GM1 or GM2 antibodies in serum of some HEV-associated GBS patients indicates that HEV infection may trigger GBS by activating autoimmune response to destroy myelin or axon mistakenly. Management of HEV-associated GBS has no obvious difference from GBS. It mainly consists of supportive therapy and immunotherapy. Intravenous immunoglobulin (IVIG) or plasma exchange (PLEX) was used in most reported cases, which is the main strategy for clinical treatment of HEV-associated GBS. Whether antiviral therapy could be additional strategy other than the routine therapy to shorten the length of disease course is one of the most urgent problems and requires further study.

conclusionsAn overview of possible pathogenesis will gain a first insight into why HEV, traditionally recognized as only hepatotropic, can induce many neurological disorders represented by GBS. Moreover, understanding of the underlying mechanisms may contribute to development of a novel therapeutic strategy. This review also summarizes management and clinical characteristics of HEV-associated GBS, aiming to achieve early recognition and good recovery.

Indexed as

Guillain-Barre SyndromeHepatitis EAutoimmunityDisease ManagementHepatitis E virusHumansantiganglioside antibodiesextrahepatic manifestationsGuillain-Barre syndromehepatitis E virusinfectionsperipheral neuropathiesviral replication

Identifiers

PMID31828968
PMCPMC6955827
OpenAlexW2994705720

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.