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World J Gastroenterol. Sep 14, 2014; 20(34): 11962-11965
Published online Sep 14, 2014. doi: 10.3748/wjg.v20.i34.11962
Potential mechanism of corpus-predominant gastritis after PPI therapy in Helicobacter pylori-positive patients with GERD
Ken-ichi Mukaisho, Tadashi Hagiwara, Takahisa Nakayama, Takanori Hattori, Hiroyuki Sugihara
Ken-ichi Mukaisho, Tadashi Hagiwara, Takahisa Nakayama, Takanori Hattori, Hiroyuki Sugihara, Department of Pathology, Division of Molecular Diagnostic Pathology, Shiga University of Medical Science, Seta-tsukinowa-cho, Otsu, Shiga 520-2192, Japan
Author contributions: Mukaisho K wrote the paper; Hagiwara T, Nakayama T, Hattori T and Sugihara H did critical reading of the manuscript.
Correspondence to: Ken-ichi Mukaisho, Associate Professor, Department of Pathology, Division of Molecular Diagnostic Pathology, Shiga University of Medical Science, Seta-tsukinowa-cho, Otsu, Shiga 520-2192, Japan. mukaisho@belle.shiga-med.ac.jp
Telephone: +81-77-5482167 Fax: +81-77-5439880
Received: October 25, 2013
Revised: March 7, 2014
Accepted: April 30, 2014
Published online: September 14, 2014
Core Tip

Core tip: It has been widely accepted that the long-term use of proton pump inhibitors (PPIs) exacerbates corpus atrophic gastritis in patients with Helicobacter pylori (H. pylori) infection. Recently, we successfully demonstrated that long-term PPI administration promotes corpus atrophic gastritis in Mongolian gerbils, which are excellent models of H. pylori-related gastritis and adenocarcinoma. Here, we suggest a potential mechanism for corpus-predominant gastritis after PPI therapy in H. pylori-positive patients with gastroesophageal reflux disease that includes interactions between bile acids, pH, and H. pylori.