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Influence of potassium-competitive acid blocker on the gut microbiome of Helicobacter pylori-negative healthy individuals
  1. Taketo Otsuka1,
  2. Mitsushige Sugimoto2,
  3. Ryo Inoue3,
  4. Masashi Ohno1,
  5. Hiromitsu Ban2,
  6. Atsushi Nishida1,
  7. Osamu Inatomi1,
  8. Shunsuke Takahashi4,
  9. Yuji Naito5,
  10. Akira Andoh1
  1. 1Department of Medicine, Shiga University of Medical Science, Otsu, Japan
  2. 2Division of Gastrointestinal Endoscopy, Shiga University of Medical Science, Otsu, Japan
  3. 3Laboratory of Animal Science, Department of Agriculture and Life Science, Kyoto Prefectural University, Kyoto, Japan
  4. 4TechnoSuruga Laboratory, Shizuoka, Japan
  5. 5Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kyoto, Japan
  1. Correspondence to Professor Akira Andoh, Shiga University of Medical Science, Seta Tsukinowa, Otsu 520-2192, Japan; andoh{at}belle.shiga-med.ac.jp

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We read with great interest two recent reports by Imhann et al1 and Jackson et al.2 Through large population-cohort study, each group revealed that gastric acid inhibition by long-term use of proton pump inhibitors (PPIs) changes the gut microbiome to predispose to enteric infection including Clostridium difficile (CD). Potassium-competitive acid blockers (P-CABs) have been reported to exert more potent gastric acid suppression than PPIs.3 ,4 The inhibitory effect of vonoprazan (TAK-438), a new P-CAB, on H+, K+-ATPase in vitro is approximately 400 times more potent than that of PPI (lansoprazole) (inhibitory concentration (IC)50 of vonoprazan 0.019 μM and lansoprazole 7.6 μM).5 We describe below that vonoprazan induces more complex alteration of the gut microbiome as compared with lansoprazole.

We enrolled serum Helicobacter pylori IgG-negative healthy individuals to eliminate the influence of H. pylori infection on gastric acid secretion (see online supplementary table S1). The PPI group (n=11) took 30 mg of lansoprazole daily for 4 weeks, and the P-CAB group …

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Footnotes

  • Contributors AA, MS and YN designed the study and wrote the protocol. TO collected faecal samples and wrote the manuscript. RI and MO prepared the statistical analyses. HB, AN, ST and OI recruited patients to the study and performed molecular analyses of faecal samples. RI performed the bioinformatics of this study. All authors commented on the drafts and approved the final version. All authors had full access to the data and participated in the decision to submit for publication.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was approved by the Ethics Committee of Shiga University of Medical Science (permission No. 27-131).

  • Provenance and peer review Not commissioned; internally peer reviewed.

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