Gastric atrophy as an important risk factor for gastric cancer development after Helicobacter pylori eradication

Helicobacter pylori (H. pylori) infection plays an important role in gastric cancer development (1). Several studies have demonstrated the possibility of gastric cancer prevention by the H. pylori eradication (2,3). However, after successful H. pylori eradication, gastric cancers sometimes develop (4,5). Since little has been reported on the risk factors for primary gastric cancer after H. pylori eradication, Toyoshima et al conducted a retrospective, endoscopy-based, long-term, large-cohort study to clarify the risk factors for gastric cancer following H. pylori eradication (6). The author performed 10 years surveillance esophagogastroduodenoscopy of 1,232 cancer-free patients after successful H. pylori eradication. Gastric cancer developed in 15 patients (17 lesions) after successful H. pylori eradication. The cumulative incidence rates were 1.0% at 2 years, 2.6% at 5 years, and 6.8% at 10 years, respectively. Gastric cancers developed after H. pylori eradication were characterized as intestinal type histopathology, within the mucosal layer, and <20 mm in diameter. Multivariate analysis identified higher grade of endoscopic gastric atrophy at H. pylori eradication (hazard ratio 1.77; 95% confidence interval, 1.12–2.78; P=0.01) as the only independently associated parameter.

It is well known that the pathological state of gastritis, such as severe gastric mucosal atrophy or intestinal metaplasia is closely associated with the risk of gastric cancer among H. pylori infected patients (1). Recent studies have also suggested that the severe gastric atrophy at H. pylori eradication is associated with increased risk of metachronous gastric cancer (7). Our group has reported that severe gastric atrophy and intestinal metaplasia remained in the adjacent mucosa of the gastric cancer developed after H. pylori eradication (8). The effect of H. pylori eradication in preventing gastric cancer can be attributed to the improvement of chronic inflammation or atrophy. However, such effect would be limited in patients with baseline severe atrophic gastritis because gastric atrophy may not improve after H. pylori eradication.

The strength of the current study is that the author demonstrated a risk factor for gastric cancer after H. pylori eradication among larger cohort of cancer free patients. The author also demonstrated characteristics of gastric cancers developed after H. pylori eradication as tiny intra-mucosal cancer with intestinal type histopathology, which is in line with several other studies (4,5). Current result have provided useful information for many endoscopists to perform more appropriate clinical implementation reflecting individual risk for gastric cancer after H. pylori eradication.

Acknowledgments

Funding: None.

Footnote

Provenance and Peer Review: This article was commissioned by the editorial office, Annals of Laparoscopic and Endoscopic Surgery. The article did not undergo external peer review.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/ales.2016.12.12). The authors have no conflicts of interest to declare.

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