Evidence map›Paper›PMID 32871870›Full record

Trial reportMedicine2020

Celiac disease serology and gut microbiome following proton pump inhibitor treatment.

Sophie Jang, Benjamin Lebwohl, Julian A Abrams, Peter H R Green, Daniel E Freedberg, Armin Alaedini

Erratum issuedOpen access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Sophie JangDepartment of Medicine.
Benjamin LebwohlDepartment of Medicine.
Julian A AbramsDepartment of Medicine.
Peter H R GreenDepartment of Medicine.
Daniel E FreedbergDepartment of Medicine.
Armin AlaediniDepartment of Medicine.
Columbia University Irving Medical Center · USNew York Medical College · US

Funding

Clinical and Translational Science AwardUL1TR000040 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2012 to 2015
$26.2M
Loss of Gastrointestinal Colonization Resistance and Antibiotic-Resistant Infections in the Intensive Care UnitK23DK111847 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FREEDBERG, DANIEL E. · 2017 to 2020
$608k
NCATS NIH HHS UL1 TR000040NIDDK NIH HHS K23 DK111847
6 · The paper itself

Abstract

backgroundCeliac disease is an autoimmune enteropathy characterized by an aberrant immune response to ingested gluten in genetically predisposed individuals. Studies have pointed to a rising prevalence of celiac disease in recent decades. Changes in diet and use of medication that may impact the gut microbiome have been suggested as potential contributors. Exposure to proton pump inhibitors (PPIs) was recently found to be associated with an increased risk for subsequent diagnosis of celiac disease. We aimed to investigate potential mechanisms for this link by examining the relationship between PPI use and gluten-related immune responses in the context of changes in gut microbiome.

methodsWe performed a post hoc analysis of blood and fecal samples from a recent randomized trial in order to assess the potential association between PPI use and development of celiac disease serology in conjunction with alterations in gastrointestinal microbial composition. The study included 12 healthy participants who were administered a PPI (Omeprazole; 40 mg twice daily) for 4 or 8 weeks.

resultsThe analysis did not reveal an overall significant change in levels of serologic markers of celiac disease for the study cohort in response to PPI treatment. However, one individual developed a marked increase in the celiac disease-specific autoantibody response to transglutaminase 2 in conjunction with enhanced immune reactivity to gluten during the trial. Genotyping revealed positivity for the celiac disease-associated HLA-DQ2 and -DQ8 alleles. Furthermore, the observed elevation in antibody responses was closely associated with a sharp increase in fecal abundance of bacteria of the order Actinomycetales.

conclusionsThe results of this exploratory analysis support further investigation of molecular mechanisms involved in the contribution of PPIs to celiac disease risk through the potential enhancement of gluten immunopathology and changes in gut microbial population.

Indexed as

ActinomycetalesAdultAllelesCeliac DiseaseFecesFemaleGastrointestinal MicrobiomeGastrointestinal TractGenotypeGlutensGTP-Binding ProteinsHLA-DQ AntigensHumansMaleMiddle AgedOmeprazoleGlutensGTP-Binding ProteinsHLA-DQ2 antigenHLA-DQ AntigensOmeprazoleProtein Glutamine gamma Glutamyltransferase 2Proton Pump InhibitorsTransglutaminasesantibodyceliac diseaseglutenhost–microbe interactionmicrobiomeproton pump inhibitor

Identifiers

PMID32871870
PMCPMC7458245
OpenAlexW3080916775

What OpenQuestion holds

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LicenceCC BY-NC
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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.