Clinicopathological Features of Gastric Mucosa Prior to Helicobacter pylori Eradication May Predict Gastric Cancer

Abstract

Introduction: Although Helicobacter pylori eradication has been shown to inhibit gastric cancer, it does not completely suppress it. Therefore risk factors of gastric cancer development following H. pylori eradication were examined. Methods: A total of 2355 patients (1501 males, 824 females) underwent successful eradication of H. pylori. Endoscopical atrophy, and histological gastritis, atrophy, and intestinal metaplasia (IM), OLGA-system were evaluated after eradication. Results: Following eradication, 33/2355 patients (25 males, 8 females) developed gastric cancer. When a non-gastric cancer group was matched according to gender and age of the gastric cancer group, the incidence of endoscopic atrophy (3.52 ± 1.45 vs. 4.85 ± 1.18, P < 0.001), histological atrophy (1.42 ± 0.80 vs. 1.95 ± 0.86, P = 0.0059) at the greater curvature of the antrum, inflammation (2.05 ± 0.59 vs. 2.33 ± 0.66, P = 0.031), and IM (0.06 ± 0.30 vs. 0.24 ± 0.54, P = 0.029) at the greater curvature of the corpusfor the gastric cancer group was significantly higher than for the non-gastric cancer group. OLGA-stage 0-II/III, IV showed significant higher ratio in gastric cancer group than non-gastric cancer group (P=0.038). Multivariate analysis showed the highest odds ratio (6.26, 95% confidence interval, 1.28-30.60, P = 0.023) in IM at the corpus. Conclusion: Severe endoscopical atrophy, OLGA-sytem, histological atrophy at the antrum, inflammation, and particularly IM at the corpus, were identified as risk factors for gastric cancer development following H. pylori eradication. Therefore, eradication should be performed before these predictors develop.