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The Capital Region of Denmark - a part of Copenhagen University Hospital
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Gastric cancer and gastrin: on the interaction of Helicobacter pylori gastritis and acid inhibitory induced hypergastrinemia

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  4. Bilio-enteric flow and plasma concentrations of bile acids after gastric bypass and sleeve gastrectomy

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Gastric cancer, a disease with a reduced frequency for decades, now appears to be on the rise again in young Americans. The epidemiology of gastric cancer differs between tumors in the cardia and those of the more distal parts of the stomach. The tumors are divided into the intestinal type showing glandular growth pattern and the diffuse type with a different pattern. The latter often expresses neuroendocrine and more specifically ECL-cell markers suggesting that they originate from the ECL cell, the target cell for the antral hormone, gastrin. Helicobacter pylori gastritis is accepted as the major cause of gastric cancer, but only after having induced oxyntic atrophy which reduces gastric acid secretion and thus induces hypoacidity leading to hypergastrinemia. Long-term hypergastrinemia is known to induce malignant neoplasia in the stomach of animals as well as man. Recently treatment with proton pump inhibitor after Helicobacter pylori eradication in patients with gastroesophageal reflux disease, has been reported to predispose to gastric cancer. Since profound acid inhibition is a well-known cause of gastric neoplasia, it is to be expected that Helicobacter pylori infection and profound acid inhibition has an additive or possibly potentiating effect on the development of gastric cancer.

Original languageEnglish
JournalScandinavian Journal of Gastroenterology
Volume54
Issue number9
Pages (from-to)1118-1123
Number of pages6
ISSN0036-5521
DOIs
Publication statusPublished - Sep 2019

    Research areas

  • Classification of gastric cancer, ECL cell, gastric cancer, gastrin, gastritis, Helicobacter pylori, inhibitors of gastric acid secretion, proton pump inhibitors

ID: 58076743