Ten-year prospective follow-up study on the relationship between Helicobacter pylori infection and progression of atrophic gastritis, particularly assessed by endoscopic findings
Article first published online: 20 APR 2002
DOI: 10.1046/j.1365-2036.16.s2.13.x
Issue
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Alimentary Pharmacology & Therapeutics
Volume 16, Issue Supplement s2, pages 198–203, April 2002
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How to Cite
Sakaki, N. , Kozawa, H. , Egawa, N. , Tu, Y. and Sanaka, M. (2002), Ten-year prospective follow-up study on the relationship between Helicobacter pylori infection and progression of atrophic gastritis, particularly assessed by endoscopic findings. Alimentary Pharmacology & Therapeutics, 16: 198–203. doi: 10.1046/j.1365-2036.16.s2.13.x
Publication History
- Issue published online: 20 APR 2002
- Article first published online: 20 APR 2002
- Abstract
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Aim:
To ascertain the progression of atrophic gastritis due to Helicobacter pylori infection, we conducted a 10-year prospective follow-up study with annual endoscopy of the stomach.
Methods:
Prospective endoscopic observation was started in 53 subjects in 1989 and 1990 after informed consent was obtained. The progression of atrophic gastritis was evaluated mainly by the endoscopic pattern of atrophy. Histological assessment was performed on biopsy specimens taken from the lesser curvature of the lower corpus. By 2000, 43 patients (20 males, 23 females, mean age 56.7 years at entry) had completed at least 10 years of endoscopic follow-up.
Results:
Eight H. pylori-negative patients with normal fundic mucosa showed no change endoscopically or histologically. In 35 H. pylori-positive patients, the progression of histological atrophy was observed in 46% and intestinal metaplasia was observed in 49%. Fifteen of 35 H. pylori-positive cases exhibited a cephaloid shift of the endoscopic atrophic border. The cephaloid shift of the atrophic area occured suddenly. The cumulative progression rate of atrophic patterns was 6% after 2 years, 22% after 4 years, 34% after 6 years and 43% after 10 years. These atrophic changes were related to neutrophil infiltration.
Conclusion:
The progression of atrophic gastritis is a result of chronic active gastritis caused by H. pylori infection.

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