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Gut 2002;51:463-464; doi:10.1136/gut.51.4.463
Copyright © 2002 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 2002;51:463-464
© 2002 by Gut

COMMENTARY

Helicobacter pylori

FAP: another indication to treat H pylori

B Leggett

Department of Gastroenterology, Royal Brisbane Hospital, Herston 4029, Brisbane, Australia; barbara-leggett@health.qld.gov.au


Does infection of familial adenomatous polyposis (FAP) patients with Helicobacter pylori lead to chronic atrophic gastritis and an increased risk of gastric adenoma?

Keywords: familial adenomatous polyposis; fundic gland polyposis; gastric adenoma; atrophic gastritis; Helicobacter pylori

The first 150 words of the full text of this article appear below.

The report in this issue of Gut on the impact of Helicobacter pylori infection and mucosal atrophy on gastric lesions in patients with familial adenomatous polyposis (FAP)1 highlights the complex interplay between genetic and environmental factors in the genesis of malignancy and has therapeutic implications for the management of these patients [see page485]. A similar interplay has been observed in hereditary non-polyposis colorectal cancer where gastric cancer was quite common in earlier generations but has become less common recently, a change paralleling that seen in the general Western population.2

In Western patients with FAP the incidence of gastric adenoma is of the order of 2–6%. The incidence of gastric cancer is little if at all elevated above the general population3 and the major concern with these patients is the high risk of duodenal and periampullary cancer. However, in Japan the risk of gastric cancer in these . . . [Full text of this article]


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Relevant Article

Impact of Helicobacter pylori infection and mucosal atrophy on gastric lesions in patients with familial adenomatous polyposis
S Nakamura, T Matsumoto, Y Kobori, and M Iida
Gut 2002 51: 485-489. [Abstract] [Full Text] [PDF]

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