Background and Aim: Metachronous recurrence often occurs after endoscopic submucosal dissection for early gastric cancer, and a method for preventing recurrence is unknown. We aimed to identify risk factors for metachronous lesions, and the effects of aspirin use and Helicobacter pylori eradication on preventing recurrence. Methods: A total of 1041 consecutive patients who underwent endoscopic submucosal dissection for early gastric cancer between January 2007 and December 2011 were retrospectively analyzed. Every patient was examined endoscopically at 2, 6, and 12 months after endoscopic submucosal dissection, and then annually. Patients were classified into the metachronous group or non-metachronous group according to the existence of metachronous lesions and subdivided by Helicobacter pylori status into three groups: not infected, eradicated after infection, and not eradicated. Results: At 39 months' median follow-up, metachronous gastric lesions had developed in 35 patients (3.4%), including 16 with dysplasia and 19 cancers. Metachronous group were significantly older than non-metachronous group (P=0.02). Although non-metachronous group took aspirin more frequently than metachronous group (15.5% vs 5.7%), the difference was statistically insignificant (P=0.11). In the not eradicated group, the odds ratio of metachronous lesion was 7.762 compared with the not infected group (95% confidence interval, 1.483-60.854; P=0.02). In the eradicated group, the odd ratio of metachronous lesion was 8.120 compared with not infected group (95% confidence interval, 1.950-58.985; P=0.01). Conclusion: Helicobacter pylori infection was an independent risk factor for metachronous gastric lesions. However, eradication of Helicobacter pylori alone does not prevent all metachronous lesions in an inflamed stomach.
|Number of pages||7|
|Journal||Journal of Gastroenterology and Hepatology (Australia)|
|Publication status||Published - 2015 Jan 1|
Bibliographical notePublisher Copyright:
© 2014 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd.
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