Evidence map›Paper›PMID 32484314›Full record

ArticleAnnals of clinical and translational neurology2020

Fc-gamma IIIa-V158F receptor polymorphism contributes to the severity of Guillain-Barré syndrome.

Shoma Hayat, Golap Babu, Avizit Das, Zakir Hossain Howlader, Ishtiaq Mahmud, Zhahirul Islam

Open access · goldAbstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 2 pooled it
0.3field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 2 syntheses or guidelines pooled it, 9 citations in OpenAlex.

  1. Association ofFrontiers in immunology · 2025
    Pooled it
  2. Triggers of Guillain-Barré Syndrome:International journal of molecular sciences · 2022
    Pooled it
  3. Article
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 at 2 institutions in 1 country.

Shoma HayatLaboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), icddr,b, Dhaka, 1212, Bangladesh.
Golap BabuLaboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), icddr,b, Dhaka, 1212, Bangladesh.
Avizit DasLaboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), icddr,b, Dhaka, 1212, Bangladesh.
Zakir Hossain HowladerDepartment of Biochemistry and Molecular Biology, University of Dhaka, Dhaka, 1000, Bangladesh.
Ishtiaq MahmudDepartment of Biochemistry and Molecular Biology, University of Dhaka, Dhaka, 1000, Bangladesh.
Zhahirul IslamLaboratory of Gut-Brain Signaling, Laboratory Sciences and Services Division (LSSD), icddr,b, Dhaka, 1212, Bangladesh.ORCID 0000-0003-0935-8079
International Centre for Diarrhoeal Disease Research · BDUniversity of Dhaka · BD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGuillain-Barré syndrome (GBS) is a rare, life-threatening disorder of the peripheral nervous system. Immunoglobulin G Fc-gamma receptors (FcγRs) mediate and regulate diverse effector functions and are involved in the pathogenesis of GBS. We investigated whether the FcγR polymorphisms FcγRIIa H/R131 (rs1801274), FcγRIIIa V/F158 (rs396991), and FcγRIIIb NA1/NA2, and their haplotype patterns affect the affinity of IgG-FcγR interactivity and influence GBS susceptibility and severity.

methodsWe determined FcγR polymorphisms in 303 patients with GBS and 302 ethnically matched healthy individuals from Bangladesh by allele-specific polymerase chain reaction. Pairwise linkage disequilibrium and haplotype patterns were analyzed based on D ́statistics and the genotype package of R statistics, respectively. Logistic regression analysis and Fisher's exact test with corrected P (Pc) values were employed for statistical comparisons.

resultsFcγRIIIa-V158F was associated with the severe form of GBS compared to the mild form (P = 0.005, OR = 2.24, 95% CI = 1.28-3.91; Pc = 0.015); however, FcγR genotypes and haplotype patterns did not show any association with GBS susceptibility compared to healthy controls. FcγRIIIa-V/V158 and FcγRIIIb-NA2/2 were associated with recent Campylobacter jejuni infection (P ≤ 0.001, OR = 0.36, 95% CI = 0.23-0.56; Pc ≤ 0.003 and P = 0.004, OR = 1.70, 95% CI = 1.18-2.44; Pc ≤ 0.012, respectively). Haplotype 1 (FcγRIIa-H131R- FcγRIIIa-V158F- FcγRIIIb-NA1/2) and the FcγRIIIb-NA2/2 genotype were more prevalent among anti-GM1 antibody-positive patients (P = 0.031, OR = 9.61, 95% CI = 1.24-74.77, Pc = 0.279; P = 0.027, OR = 1.62, 95% CI = 1.06-2.5, Pc = 0.081, respectively).

interpretationFcγR polymorphisms and haplotypes are not associated with susceptibility to GBS, though the FcγRIIIa-V158F genotype is associated with the severity of GBS.

Indexed as

Genetic Predisposition to DiseaseSeverity of Illness IndexAdolescentAdultFemaleGPI-Linked ProteinsGuillain-Barre SyndromeHumansMaleMiddle AgedPolymorphism, GeneticReceptors, IgGYoung AdultFCGR2A protein, humanFCGR3A protein, humanFCGR3B protein, humanGPI-Linked ProteinsReceptors, IgG

Identifiers

PMID32484314
PMCPMC7317642
OpenAlexW3030805195

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.