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Commentary on: the management of patients with gastric intestinal metaplasia
  1. David Y Graham1,
  2. Yi-Chia Lee2
  1. 1Medicine (111D), Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas, USA
  2. 2National Taiwan University Hospital, Taipei, Taiwan
  1. Correspondence to Dr David Y Graham, Medicine (111D), Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas, USA; dgraham{at}bcm.edu

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Recently, Gut published a review of guidelines for the management of gastric intestinal metaplasia (GIM) with the goal of promoting harmonisation of the guidelines regarding indications for endoscopic screening for gastric cancer and GIM detection/staging, metrics for high-quality endoscopy and non-endoscopic interventions for gastric cancer prevention in patients with GIM.1 GIM is not a disease per se but rather is a reparative response to gastric mucosal injury that may be present, at least temporarily, as part of healing such as of an ulcer.2 Clinically, widespread GIM is best considered a manifestation of healing of another disease, typically Helicobacter pylori infection or autoimmune gastritis. When present in autoimmune gastritis, GIM has no malignant potential and is potentially completely reversible.3 In contrast, when associated with chronic H. pylori infection, GIM is typically permanent and, at most, minimally reversible.4 The underlying H. pylori-induced inflammation is carcinogenic. H. pylori-related GIM is a manifestation of the duration, extent and severity of an H. pylori infection which, in turn, is related to the risk of gastric cancer. Because GIM is easily recognised and reflects the extent and severity of the infection, it is a valuable surrogate for the risk of developing gastric cancer. This has given GIM a role in the determination of an individual’s cancer risk. However, because GIM is neither a disease nor a cause of cancer, eradication of gastric cancer should focus on the eradication of the cause, that is, H. pylori infections.

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Footnotes

  • Collaborators None.

  • Contributors Both authors contributed equally to the manuscript. DYG is the guarantor.

  • Funding DYG is supported in part by the Office of Research and Development Medical Research Service Department of Veterans Affairs, Public Health Service, grant DK56338, which funds the Texas Medical Center Digestive Diseases Center and by the Cancer Prevention and Research Institute of Texas (RP220127). Y-CL is supported in part by the Health Promotion Administration, Ministry of Health and Welfare, Taiwan, which funds the H. pylori screening and monitoring programme (A1121003).

  • Competing interests DYG is an unpaid consultant for RedHill Biopharma and Phathom Pharmaceuticals regarding novel Helicobacter pylori therapies and has received research support for culture of H. pylori. He was also a consultant with Janssen Research and Development regarding potential GI effects of drugs under development and has collaborated on research projects with American Molecular Laboratories regarding molecular diagnostics for H. pylori. Y-CL has no conflicts of interests.

  • Provenance and peer review Commissioned; internally peer reviewed.

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