Eliminating H. pylori Reduces Risk of Gastric Cancer Recurrence

Patients underwent endoscopic resection and subsequent endoscopy at 6, 12, 24, and 36 months after surgery. Half the patients were randomized to receive treatment to eradicate H. pylori infection, with a combination of lansoprazole, amoxicillin, and clarithromycin twice daily for a week; the other half of the patients acted as a control group, but did not receive placebo. The primary endpoint was diagnosis of new carcinoma at another site in the stomach. For ethical reasons, after the final analysis, patients in the control group were also given eradication therapy, as were patients in the eradication group who still had an active H. pylori infection. The study results showed that at three-year follow-up, metachronous (not occurring at the same time) gastric carcinoma had developed in 9 patients in the eradication group and 24 in the control group. In the full intention-to-treat population, including all patients irrespective of length of follow-up (272 patients in each group), the odds ratio for metachronous gastric carcinoma was 0.353. In the eradication group, 19 (7%) patients had diarrhea and 32 (12%) had soft stools. The study was published in the August 2, 2008, issue of the Lancet.

"Prophylactic eradication of H. pylori after endoscopic resection of early gastric cancer should be used to prevent the development of metachronous gastric carcinoma,” concluded lead author Kazutoshi Fukase, M.D., and colleagues of the department of gastroenterology.

H. pylori is a gram-negative, microaerophilic bacterium that inhabits various areas of the stomach and duodenum. The bacterium causes a chronic low-level inflammation of the stomach lining and it is strongly linked to the development of peptic ulcers and stomach cancer. More people are infected with H. pylori than any other species of bacteria, and 50% or more of the population harbor it; it is more prevalent in developing countries. Two related mechanisms by which H. pylori could promote cancer have been proposed; one mechanism involves the enhanced production of free radicals near H. pylori and an increased rate of host cell mutation. The other mechanism involves enhancement of the transformed host cell phenotype by means of alterations in cell proteins such as adhesion proteins.

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