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Gastroenterology. 2015 Oct;149(4):883-5.e9. doi: 10.1053/j.gastro.2015.06.043. Epub 2015 Jul 9.

Proton Pump Inhibitors Alter Specific Taxa in the Human Gastrointestinal Microbiome: A Crossover Trial.

Author information

1
Department of Medicine, Division of Digestive and Liver Diseases, Columbia University Medical Center, New York, New York.
2
New York Genome Center, New York, New York.
3
College of Physicians and Surgeons, Columbia University Medical Center, New York, New York.
4
Department of Pediatrics, Division of Infectious Diseases, Columbia University Medical Center, New York, New York.
5
Department of Pathology and Cell Biology, Columbia University, New York, New York.
6
Department of Pathology and Cell Biology, Columbia University, New York, New York; Department of Systems Biology, Columbia University, New York, New York. Electronic address: hw2429@cumc.columbia.edu.
7
Department of Medicine, Division of Digestive and Liver Diseases, Columbia University Medical Center, New York, New York. Electronic address: ja660@cumc.columbia.edu.

Abstract

We conducted an open-label crossover trial to test whether proton pump inhibitors (PPIs) affect the gastrointestinal microbiome to facilitate Clostridium difficile infection (CDI). Twelve healthy volunteers each donated 2 baseline fecal samples, 4 weeks apart (at weeks 0 and 4). They then took PPIs for 4 weeks (40 mg omeprazole, twice daily) and fecal samples were collected at week 8. Six individuals took the PPIs for an additional 4 weeks (from week 8 to 12) and fecal samples were collected from all subjects at week 12. Samples were analyzed by 16S ribosomal RNA gene sequencing. We found no significant within-individual difference in microbiome diversity when we compared changes during baseline vs changes on PPIs. There were, however, significant changes during PPI use in taxa associated with CDI (increased Enterococcaceae and Streptococcaceae, decreased Clostridiales) and taxa associated with gastrointestinal bacterial overgrowth (increased Micrococcaceae and Staphylococcaceae). In a functional analysis, there were no changes in bile acids on PPIs, but there was an increase in genes involved in bacterial invasion. These alterations could provide a mechanism by which PPIs predispose to CDI. ClinicalTrials.gov ID NCT01901276.

KEYWORDS:

Acid Suppression; Clostridium difficile Infection; Gastroesophageal Reflux Disease; Pharmacology

PMID:
26164495
PMCID:
PMC4584196
DOI:
10.1053/j.gastro.2015.06.043
[Indexed for MEDLINE]
Free PMC Article
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