Evidence map›Paper›PMID 29095917›Full record

ArticlePLoS pathogens2017

Comparison of the human gastric microbiota in hypochlorhydric states arising as a result of Helicobacter pylori-induced atrophic gastritis, autoimmune atrophic gastritis and proton pump inhibitor use.

Bryony N Parsons, Umer Z Ijaz, Rosalinda D'Amore, Michael D Burkitt, Richard Eccles, Luca Lenzi, Carrie A Duckworth, Andrew R Moore, Laszlo Tiszlavicz, Andrea Varro and 2 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 3 pooled it
19.1field-weighted citation impact, top 1% 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

116 citing papers in PubMed, 3 syntheses or guidelines pooled it, 200 citations in OpenAlex.

  1. Pooled it
  2. Effect ofFrontiers in cellular and infection microbiology · 2022
    Pooled it
  3. Pooled it
  4. Netazepide Inhibits Expression of Pappalysin 2 in Type 1 Gastric Neuroendocrine Tumors.Cellular and molecular gastroenterology and hepatology · 2020
    Trial
  5. Article
  6. Review
  7. Article
  8. Review
  9. Rethinking Oxidative Stress inLife (Basel, Switzerland) · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. The Potential Role ofMicroorganisms · 2025
    Review
  19. Review
  20. Article

56 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 2 countries.

Bryony N ParsonsDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UNITED KINGDOM.ORCID http://orcid.org/0000-0003-3599-1089
Umer Z IjazDepartment of Infrastructure and Environment University of Glasgow, School of Engineering, Glasgow, UNITED KINGDOM.ORCID http://orcid.org/0000-0001-5780-8551
Rosalinda D'AmoreCentre for Genomic Research, Institute of Integrative Biology, University of Liverpool, Liverpool, UNITED KINGDOM.ORCID http://orcid.org/0000-0002-2638-4466
Michael D BurkittDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UNITED KINGDOM.ORCID http://orcid.org/0000-0002-5055-6408
Richard EcclesCentre for Genomic Research, Institute of Integrative Biology, University of Liverpool, Liverpool, UNITED KINGDOM.
Luca LenziCentre for Genomic Research, Institute of Integrative Biology, University of Liverpool, Liverpool, UNITED KINGDOM.ORCID http://orcid.org/0000-0003-2697-691X
Carrie A DuckworthDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UNITED KINGDOM.
Andrew R MooreDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UNITED KINGDOM.ORCID http://orcid.org/0000-0001-7680-998X
Laszlo TiszlaviczDepartment of Pathology, University of Szeged, Szeged, HUNGARY.ORCID http://orcid.org/0000-0003-1134-6587
Andrea VarroDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UNITED KINGDOM.
Neil HallCentre for Genomic Research, Institute of Integrative Biology, University of Liverpool, Liverpool, UNITED KINGDOM.ORCID http://orcid.org/0000-0003-2808-0009
D Mark PritchardDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UNITED KINGDOM.ORCID http://orcid.org/0000-0001-7971-3561
University of Liverpool · GBUniversity of East Anglia · GBUniversity of Glasgow · GBUniversity of Szeged · HU

Funding

Medical Research Council G0900753Medical Research Council MR/K002279/1Wellcome TrustWorldwide Cancer Research 12-1028
6 · The paper itself

Abstract

Several conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Helicobacter pylori-induced atrophic gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk. 95 patients (in groups representing normal stomach, PPI treated, H. pylori gastritis, H. pylori-induced atrophic gastritis and autoimmune atrophic gastritis) were selected from a cohort of 1400. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq). Samples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. Patients with autoimmune atrophic gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. H. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. H. pylori-induced atrophic gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. Pathway analysis suggested that glucose-6-phospahte1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic gastritis versus autoimmune atrophic gastritis, and that both these groups showed increases in fumarate reductase. Autoimmune and H. pylori-induced atrophic gastritis were associated with different gastric microbial profiles. PPI treated patients showed relatively few alterations in the gastric microbiota compared to healthy subjects.

Indexed as

Gastrointestinal MicrobiomeAchlorhydriaAdultAgedAutoimmune DiseasesCluster AnalysisCohort StudiesEnglandFemaleGastric MucosaGastritis, AtrophicHelicobacter InfectionsHelicobacter pyloriHospitals, UniversityHumansMaleProton Pump Inhibitors

Identifiers

PMID29095917
PMCPMC5667734
OpenAlexW2620581837

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.