The gastritis connection: Prevention and early detection of gastric neoplasms

Robert M. Genta

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Most gastric polyps, adenocarcinomas, carcinoids, and B cell lymphomas arise on a gastric mucosa damaged by long-standing chronic gastritis. The most common form of chronic gastritis is caused by infection with Helicobacter pylori. All patients with H. pylori infection develop lymphoid aggregates with germinal centers that interact intimally with the gastric mucosa (mucosa-associated lymphoid tissue [MALT]); these follicles are the condition sine qua non for the development of primary B cell mantle lymphomas, also known as MALT lymphomas. As the infection progresses, atrophy of the gastric mucosa develops in a subset of patients, which is replaced by an intestinal-type epithelium (intestinal metaplasia). On this background, dysplasia and adenocarcinomas of the intestinal type may develop. When atrophy is sufficiently severe to impair acid production, the gastrin-producing cells of the antrum increase their secretion of gastrin and stimulate endocrine cells in the corpus, which may eventually proliferate, become dysplastic, and give raise to carcinoids. This development is more frequent in advanced cases of autoimmune gastritis associated with pernicious anemia. On this background, there is also extensive epithelial hyperplasia and the formation of hyperplastic or inflammatory polyps, a small percentage of which may become dysplastic and progress to adenocarcinoma. Chronic exposure of the corpus mucosa to pancreaticoduodenal secretions ("bile reflux") causes reactive mucosal changes that may predispose to neoplasia. Thus, the progression of inflammation to atrophy to metaplasia, and in some cases chronic chemical injury, may give rise, at different times and under the influence of other, unknown stimuli, to most types of gastric tumors. Other types of gastritis, including lymphocytic and granulomatous gastritis, are rare and have not been associated with gastric neoplasia. Awareness of these associations, appropriate treatment policies, and implementation of endoscopic surveillance programs would dramatically reduce the incidence of most types of gastric neoplasms and would allow the detection of many tumors at a stage when endoscopic resection or conservative treatment would still be possible.

Original languageEnglish (US)
JournalJournal of Clinical Gastroenterology
Volume36
Issue number5 SUPPL.
DOIs
StatePublished - May 2003

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Gastritis
Stomach Neoplasms
Gastric Mucosa
Atrophy
Stomach
Adenocarcinoma
Carcinoid Tumor
Metaplasia
B-Cell Lymphoma
Polyps
Helicobacter pylori
Neoplasms
Mucous Membrane
Bile Reflux
Pernicious Anemia
Marginal Zone B-Cell Lymphoma
Gastrin-Secreting Cells
Germinal Center
Endocrine Cells
Gastrins

Keywords

  • Gastric
  • Gastric cancer
  • Gastric lymphoma

ASJC Scopus subject areas

  • Gastroenterology

Cite this

The gastritis connection : Prevention and early detection of gastric neoplasms. / Genta, Robert M.

In: Journal of Clinical Gastroenterology, Vol. 36, No. 5 SUPPL., 05.2003.

Research output: Contribution to journalArticle

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