Gut

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
[Advanced]

Published Online First: 7 April 2006. doi:10.1136/gut.2005.080358
Gut 2006;55:1545-1552
Copyright © 2006 BMJ Publishing Group Ltd & British Society of Gastroenterology

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
gut.2005.080358v1
55/11/1545    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this link to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Add article to my folders
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Naylor, G M
Right arrow Articles by Axon, A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Naylor, G M
Right arrow Articles by Axon, A

STOMACH

Why does Japan have a high incidence of gastric cancer? Comparison of gastritis between UK and Japanese patients

G M Naylor1, T Gotoda2, M Dixon1, T Shimoda2, L Gatta3, R Owen4, D Tompkins5, A Axon1

1 Centre for Digestive Disease, The General Infirmary at Leeds, Leeds, UK
2 Endoscopy Division, National Cancer Centre Hospital, Tokyo, Japan
3 Department of Internal Medicine and Gastroenterology, S Orsola-Malpighi Hospital, University of Bologna, Italy
4 Laboratory of Enteric Pathogens, Central Public Health Laboratory, London, UK
5 Health Protection Agencies, Leeds Laboratory, Leeds, UK

Correspondence to:
Correspondence to:
Dr G M Naylor
Chesterfield Royal Hospital, Chesterfield, N Derbyshire S44 5BL, UK; gregnaylor{at}doctors.org.uk

Background and aims: The incidence of gastric cancer in Japan is four times higher than in the UK. It usually arises in a stomach with corpus predominant or pangastritis that has undergone extensive atrophy and intestinal metaplasia. We hypothesised that a Japanese population would have a more severe gastritis with a corpus predominant or pangastritis pattern and a greater degree of atrophy and intestinal metaplasia than that found in the UK. To test this we designed a comparative trial.

Methods: A total of 252 age matched consecutive patients were recruited from the endoscopy services in Leeds and Tokyo. In each centre, 21 patients were prospectively selected from each decennial, between the ages of 20–80 years. All had epigastric discomfort as their predominant symptom. Patients with peptic ulcer, cancer, and oesophagitis were excluded. Five gastric biopsies were examined by two histopathologists using the updated Sydney system. Helicobacter pylori infection was assessed by histology and culture of biopsies and enzyme linked immunosorbent assay and immunoblot of plasma.

Results: Gastritis was found by both pathologists in 59 (47%) UK and 76 (60%) Japanese patients ({chi}2 test, p = 0.04). In those patients with gastritis, corpus predominant or pangastritis was commoner in the Japanese (63% Japan v 36% in the UK ({chi}2 test, p = 0.003) Atrophy and intestinal metaplasia were more extensive and severe (Mann-Whitney U test, p<0.001) and chronic inflammation and polymorph activity were also greater, especially in the corpus (Mann-Whitney U test, p<0.001). Fifty three of 59 UK gastritis patients (90%) and 67/76 (88%) ({chi}2 test, p = 1) Japanese gastritis patients were positive for H pylori. Using a previously described "gastric cancer risk index" among H pylori positive patients, there were significantly more Japanese than UK subjects with a "high risk" score.

Conclusion: In Japanese as opposed to English patients, gastritis is more prevalent and severe with more corpus predominant atrophy and intestinal metaplasia. These differences may partially explain the higher incidence of gastric cancer in Japan.


Abbreviations: IM, intestinal metaplasia; IQR, interquartile range; IL, interleukin; TNF-{alpha}, tumour necrosis factor {alpha}

Keywords: gastritis; Helicobacter pylori; population comparison; gastric cancer risk




This article has been cited by other articles:


Home page
Cancer Res.Home page
K. Kunii, L. Davis, J. Gorenstein, H. Hatch, M. Yashiro, A. Di Bacco, C. Elbi, and B. Lutterbach
FGFR2-Amplified Gastric Cancer Cell Lines Require FGFR2 and Erbb3 Signaling for Growth and Survival
Cancer Res., April 1, 2008; 68(7): 2340 - 2348.
[Abstract] [Full Text] [PDF]


Home page
MicrobiologyHome page
R. J. Owen and J. Xerry
Geographical conservation of short inserts in the signal and middle regions of the Helicobacter pylori vacuolating cytotoxin gene
Microbiology, April 1, 2007; 153(4): 1176 - 1186.
[Abstract] [Full Text] [PDF]


Home page
GutHome page
K. E L McColl
Helicobacter pylori and oesophageal cancer--not always protective
Gut, April 1, 2007; 56(4): 457 - 459.
[Full Text] [PDF]


Home page
J. Epidemiol. Community HealthHome page
G. Hughes
Hygieia
J Epidemiol Community Health, February 1, 2007; 61(2): 176 - 176.
[Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
Terms and conditions relating to subscriptions purchased online  ¦  Website terms and conditions  ¦  Privacy policy
Copyright © 2006 BMJ Publishing Group Ltd & British Society of Gastroenterology