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Korean J Helicobacter  Up Gastrointest Res > Volume 11(2); 2011 > Article
The Korean Journal of Helicobacter  and Upper Gastrointestinal Research 2011;11(2):117-123.
DOI: https://doi.org/10.7704/kjhugr.2011.11.2.117    Published online September 10, 2011.
Helicobacter pylori Eradication Suppresses Metachronous Gastric Cancer and Cyclooxygenase-2 Expression after Endoscopic Resection of Early Gastric Cancer
Hwa Jong Kim, Su Jin Hong, Bong Min Ko, Won Young Cho, Joo Young Cho, Joon Seong Lee, Moon Sung Lee
Department of Internal Medicine, Soonchunhyang University College of Medicine, Bucheon, Korea. sjhong@schmc.ac.kr
Abstract
BACKGROUND/AIMS
The impact of Helicobacter pylori (H. pylori) eradication after endoscopic resection (ER) of early gastric cancer (EGC) has not been fully evaluated. We tried to find out the effect of H. pylori eradication therapy on the development of metachronous gastric cancers and changes in Cyclooxygenase-2 (COX-2) expression following attempts to eradicate H. pylori after ER of EGC. MATERIALS AND METHODS: We eradicated H. pylori in the patients with EGC after ER. Biopsy samples were taken according to the follow-up schedules for surveillance after ER. RESULTS: Fifty five patients were enrolled and finished the follow up schedules. Of the 55, 28 were successfully treated H. pylori infection, and the other 27 were failed eradication of H. pylori. The mean follow-up period was 60.8 months. Five in the H. pylori ongoing infection group developed metachronous gastric cancer, whereas no new gastric cancers were found in the 28 eradication group (P=0.023). COX-2 expression in the eradication group was significantly decreased (1.4+/-0.2, n=28), compared to that in H. pylori ongoing infection group (3.0+/-0.4, n=27, P=0.0001) after the follow-up. CONCLUSIONS: The eradication of H. pylori seems to have a preventative effect on the development of metachronous adenocarcinomas and a suppressive effect on COX-2 expression in the patients after ER for EGC.
Key Words: Helicobacter pylori; Gastric cancer; Cyclooxygenase 2


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