ArticleBMC endocrine disorders2026
Differential analysis of gut microbiota and metabolites in patients with Graves' disease and combined Helicobacter pylori infection.
Article in BMC endocrine disorders, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGraves' disease (GD) is one of the most common organ-specific autoimmune disorders. Current evidence indicates that GD pathogenesis results from complex gene-environment interactions, although the precise mechanisms remain incompletely elucidated. This study aims to investigate effects of environmental factors such as gut microbiota and Helicobacter pylori (H. pylori) infection on the pathogenesis of GD.
methodsThis study enrolled 88 treatment-naïve GD patients and 33 healthy controls. Plasma H.pylori-IgG levels were measured using enzyme-linked immunosorbent assay (ELISA). Varieties of gut microbiota in fecal specimens were examined using 16S rDNA sequencing. Gut metabolites were subjected to untargeted metabolomic analysis using liquid chromatography-mass spectrometry (LC-MS). Differences in gut microbiota composition and metabolites were analyzed between the GD group and the control group, as well as between the H. pylori-positive[H. pylori (+)] subgroup and the H. pylori-negative[H. pylori (-)] subgroup within the GD group.
resultsBacteroidota, f-Lactobacillaceae, and Prevotella-9 demonstrated significantly higher prevalence in the GD group compared to the control group. Clostridium_sensu_stricto_1 and Limosilactobacillus exhibited significantly greater abundance in the GD + H. pylori (+) subgroup compared to the GD + H. pylori (-) subgroup. Compared to the control group, in the GD group pregnanetriol, kynurenic acid, and several metabolites in the tryptophan metabolism pathway (serotonin, kynurenate, xanthurenate, and 3-Methyldioxyindole) increased significantly, while mulberrofuran T and fragransol B decreased. Significantly reduced levels of N-methyltyramine, N-isovalerylglycine, and cafestol were observed in the GD + H. pylori (+) subgroup relative to the GD + H. pylori (-) subgroup.
conclusionSignificant differences were identified in both gut microbiota composition and metabolites between the GD group and the control group. Alterations in the gut microbiota are potentially linked to GD pathogenesis via modulation of tryptophan metabolic pathway. Significant differences in both gut microbiota composition and metabolites were identified between the H. pylori (+) subgroup and the H. pylori (-) subgroup within the GD group.
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.