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Factors predicting progression of gastric intestinal metaplasia: results of a randomised trial on Helicobacter pylori eradication
Open accessAbstract
BACKGROUND AND AIMS: Gastric intestinal metaplasia (IM) is generally considered to be a precancerous lesion in the gastric carcinogenesis cascade. This study identified the risk factors associated with progression of IM in a randomised control study. SUBJECTS AND METHODS: A total of 587 Helicobacter pylori infected subjects were randomised to receive a one week course of anti-Helicobacter therapy (omeprazole, amoxicillin, and clarithromycin (OAC)) or placebo. Subjects underwent endoscopy with biopsy at baseline and at five years. Severity of IM was graded according to the updated Sydney classification and progression was defined as worsening of IM scores at five years in either the antrum or corpus, or development of neoplasia. Backward stepwise multiple logistic regression was used to identify independent risk factors associated with IM progression. RESULTS: Of 435 subjects (220 in the OAC and 215 in the placebo group) available for analysis, 10 developed gastric cancer and three had dysplasia. Overall progression of IM was noted in 52.9% of subjects. Univariate analysis showed that persistent H pylori infection, age >45 years, male subjects, alcohol use, and drinking water from a well were significantly associated with IM progression. Duodenal ulcer and OAC treatment were associated with a reduced risk of histological progression. Progression of IM was more frequent in those with more extensive and more severe IM at baseline. With multiple logistic regression, duodenal ulcer (odds ratio (OR) 0.23 (95% confidence interval (CI) 0.09-0.58)) was found to be an independent protective factor against IM progression. Conversely, persistent H pylori infection (OR 2.13 (95% CI 1.41-3.24)), age >45 years (OR 1.92 (95% CI 1.18-3.11)), alcohol use (OR 1.67 (95% CI 1.07-2.62)), and drinking water from a well (OR 1.74 (95% CI 1.13-2.67)) were independent risk factors associated with IM progression. CONCLUSION: Eradication of H pylori is protective against progression of premalignant gastric lesions.
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Cited by
Pathogenesis of Helicobacter pylori Infection
Kusters, J. G., van Vliet, A. H. M., & Kuipers, E. J. (2006) · Clinical Microbiology Reviews · doi:10.1128/cmr.00054-05 · Cited by 2,526
McColl, K. E. L. (2010) · New England Journal of Medicine · doi:10.1056/nejmcp1001110 · Cited by 773
Banks, M., Graham, D., Jansen, M., Gotoda, T., Coda, S., di Pietro, M., Uedo, N., Bhandari, P., Pritchard, D. M., Kuipers, E. J., et al. (2019) · Gut · doi:10.1136/gutjnl-2018-318126 · Cited by 647
Capelle, L. G., de Vries, A. C., Haringsma, J., Ter Borg, F., de Vries, R. A., Bruno, M. J., van Dekken, H., Meijer, J., van Grieken, N. C. T., & Kuipers, E. J. (2010) · Gastrointestinal Endoscopy · doi:10.1016/j.gie.2009.12.029 · Cited by 608
Ford, A. C., Forman, D., Hunt, R. H., Yuan, Y., & Moayyedi, P. (2014) · BMJ · doi:10.1136/bmj.g3174 · Cited by 580
Metadata
- Authors
- Leung, W. K.
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2004-09-01
- Volume
- 53
- Issue
- 9
- Pages
- 1244-1249
- ISSN
- 0017-5749 (ISSN-L)
- OpenAlex
- W2107288240
- Cited by
- 437
- References
- 0
- FWCI
- 20.60
- Type
- journal article
- Language
- en
- Open access
- bronze
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