Proton Pump Inhibitors and Helicobacter Pylori-Associated Pathogenesis

Hagiwara, Tadashi; Mukaisho, Ken-Ichi; Nakayama, Takahisa; Hattori, Takanori; Sugihara, Hiroyuki

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자료유형: 학술저널

저자정보: Hagiwara, Tadashi (Department of Pathology, Division of Molecular and Diagnostic Pathology, Shiga University of Medical Science) Mukaisho, Ken-Ichi (Department of Pathology, Division of Molecular and Diagnostic Pathology, Shiga University of Medical Science) Nakayama, Takahisa (Department of Pathology, Division of Molecular and Diagnostic Pathology, Shiga University of Medical Science) Hattori, Takanori (Department of Pathology, Division of Molecular and Diagnostic Pathology, Shiga University of Medical Science) Sugihara, Hiroyuki (Department of Pathology, Division of Molecular and Diagnostic Pathology, Shiga University of Medical Science)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제16권 제4호

발행연도: 2015.1

수록면: 1,315 - 1,319 (5page)

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The fact that long-term use of proton pump inhibitors (PPIs) aggravates corpus atrophic gastritis in patients with Helicobacter pylori infection has been proven clinically and experimentally. Corpus atrophic gastritis is a known risk factor for gastric cancer. Therefore, gastric neoplasia might be associated with the long-term use of PPIs. One of the causes of worsening corpus atrophic gastritis, leading to the development of adenocarcinoma, might be bacterial overgrowth under conditions of hypochlorhydria. The production of potentially carcinogenic N-nitrosocompounds by nitrosating organisms under conditions of hypochlorhydria might be associated with carcinogenesis. Interactions between bile acids, pH, and H. pylori might also contribute to carcinogenicity, especially in patients with gastro-esophageal reflux disease (GERD). The concentration of soluble bile acids, which have bactericidal or chemorepellent properties toward H. pylori, in gastric contents is considerably higher in patients undergoing continuous PPI therapy than in healthy individuals with normal acid production. Under these circumstances, H. pylori might colonize the stomach body rather than the pyloric antrum. Hypergastrinemia induced by PPI administration might promote the development of gastric cancer. Because the main cause of corpus atrophic gastritis is H. pylori infection, and not PPI administration, H. pylori infection should be eradicated before starting long-term PPI therapy.

#Helicobacter pylori #proton pump inhibitors #gastric cancer #corpus atrophic gastritis #GERD #gatrin

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