Eradication of Helicobacter pylori after endoscopic resection of gastric lesions doesn’t prevent later development of new stomach tumors, researchers report in the May issue of Clinical Gastroenterology and Hepatology.
H pylori infection can lead to gastric atrophy, intestinal metaplasia, and dysplasia or cancer—specifically non-cardia gastric cancer. It does so by inducing inflammation and genetic and epigenetic alterations that promote genetic instability. The bacteria also cause mucosal damage that leads to hypochlorhydria and achlorhydria, allowing for overgrowth of other bacteria that produce carcinogens.
Eradication of H pylori stops the progression and can reverse some of the damage to the mucosa. Cancer risk is low when the bacteria are eradicated from patients with non-atrophic mucosa.
However, there have been conflicting results from studies to determine whether eradication of H pylori infection prevents development of new cancers in patients who have already been treated for gastric cancer or dysplasia.
Jeongmin Choi et al. performed a prospective study of 901 patients undergoing endoscopic resection for gastric dysplasia or cancer. After the lesions were removed, the patients were assigned to groups in which the H pylori infection was eradicated (with 20 mg omeprazole, 1 g amoxicillin, and 500 mg clarithromycin, twice daily for 1 week) or not treated. The patients then underwent endoscopic examination 3, 6, and 12 months later, and yearly thereafter, to identify any new carcinomas that developed the stomach (metachronous gastric carcinoma).
After a median follow-up period of 36.9 months, new cancers developed in 10 patients in the eradication group and in 17 patients in the control group—not a statistically significant difference. Furthermore, there was no significant difference in incidence of new cancers between patients ultimately positive or negative for H pylori infection.
Choi et al. conclude that these findings, along with those from previous studies, indicate that H pylori eradication does not benefit patients with precancerous lesions, dysplasia, or cancer.
A previous study reported that the incidence of metachronous cancer differed between the eradication and control groups only within 1 year of follow-up evaluation. Choi et al. propose that although H pylori eradication doesn’t prevent the development of later cancers, it might delay them.
In an accompanying editorial, David Y. Graham explains that by the time a gastric cancer becomes detectable, the stomach probably has other areas containing premalignant or even malignant microlesions. Eradicating H pylori could slow the progression of these lesions, reducing inflammation and further genetic damage and promoting healing of gastritis.
Graham proposes that eradication of H pylori does no harm and likely changes the gastric environment to improve patients’ outcomes. He says that markers are needed to identify patients at greatest risk for subsequent cancers and are most likely to benefit from H pylori eradication.
Choi et al. add that patients treated with endoscopic resection, compared with surgical resection, are at greater risk for development of gastric tumors, because the entire stomach is preserved. However, they observed that most of the new tumors that developed were intramucosal, and could be removed by endoscopy.
Choi et al. remind readers that careful surveillance endoscopy is important for detecting new lesions while they are still at a curable stage.