ArticleBMC neurology2026
Association between Guillain-Barré syndrome and 7 autoimmune diseases: a mendelian randomization study.
Article in BMC neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe genetic and environmental factors influencing an individual's susceptibility to develop Guillain-Barré syndrome (GBS) remain largely unidentified. This study aims to evaluate the genetically predicted associations between GBS and candidate autoimmune diseases using a Mendelian randomization (MR) framework.
methodsGenetic instruments for autoimmune diseases were extracted from large-scale genome-wide association study (GWAS) datasets. Following stringent quality control, seven autoimmune diseases were ultimately retained for the primary analysis. Summary statistics for GBS were obtained from the FinnGen consortium. We employed the inverse variance weighted (IVW) method as the primary approach, supplemented by sensitivity analyses to ensure robustness. Furthermore, a high-throughput two-step MR screening of 731 immune traits was integrated to explore potential biological mediators.
resultsGenetic liability to type 1 diabetes was suggestively associated with an increased risk of GBS [OR (95% CI) = 1.26 (1.04-1.52), p = 0.0176]. Conversely, genetic predisposition to psoriasis vulgaris showed a suggestive protective association [OR (95% CI) = 0.784 (0.623-0.986), p = 0.0375]. No significant or suggestive associations were observed for rheumatoid arthritis (p = 0.990), sarcoidosis (p = 0.993), systemic lupus erythematosus (p = 0.240), asthma (p = 0.906), or Graves' disease (p = 0.926). No circulating immune trait emerged as a significant mediator between these conditions.
conclusionThis study identifies suggestive genetically predicted associations between specific autoimmune diseases and GBS susceptibility, specifically a potential risk-increasing effect of type 1 diabetes and a protective effect of psoriasis vulgaris. The absence of significant peripheral immune mediators suggests that these neuro-immune interactions may be driven by more localized or complex tissue-resident mechanisms.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.