Drug and Therapeutics Bulletin 1998;36:57-59; doi:10.1136/dtb.1998.36857
Copyright © 1998 by the BMJ Publishing Group Ltd.

This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content PubMed PubMed Citation

Helicobacter pylori and gastric cancer

Infection with Helicobacter pylori has been designated a cause of human cancer by the International Agency for Research on Cancer (part of the World Health Organization).¹ The infection, which affects 30-50% of adults in Europe and over 80% in parts of the developing world, is the commonest cause of chronic non-atrophic gastritis, which, if severe and prolonged, can lead to loss of gastric glands (atrophic gastritis) and intestinal metaplasia: both markedly increase the risk of developing gastric cancer.^1,2 H. pylori infection appears, by itself, capable of causing gastric mucosal atrophy,³ and there is some evidence that prolonged reduction in acid secretion, whether induced by disease or drugs, might accelerate this change.^4,5 These observations pose difficult dilemmas for doctors treating patients with gastric disorders, especially those needing long-term treatment with potent antisecretory drugs.