Chronic atrophic gastritis and intestinal metaplasia surrounding diffuse-type gastric cancer: Are they just bystanders in the process of carcinogenesis?

Abstract

Background Gastric cancer (GC) is categorized as diffuse- and intestinal-type adenocarcinoma. Intestinal- type GC is associated with chronic gastritis, atrophic gastritis (AG), and intestinal metaplasia (IM), precursors of dysplastic changes. Diffuse-type GC is generally known to undergo de novo carcinogenesis and is not associated with chronic mucosal changes. However, clinically, AG and IM are frequently observed surrounding diffuse-type GC. This study aimed to evaluate the role of AG and IM in diffuse-type GC. Methods We retrospectively reviewed the data of patients undergoing surgery for early GC. We divided patients with diffuse-type GC into two groups according to the presence of AG and IM based on Kyoto classification of gastritis. The clinicopathological characteristics were compared between the groups. Results Among patients with diffuse-type GC, 52.5% patients had AG and 18.4% had severe AG. With regard to IM, 42.1% patients had IM and 17.1% had severe IM. Diffuse-type GC combined with severe AG or IM showed larger tumor size and higher submucosal invasion rate than that without severe AG or IM. However, the lymph node metastasis (LNM) rate was not significantly different between the two groups. In multivariate analysis, severe AG or IM was not an independent risk factor for LNM. Conclusions Severe AG or IM surrounding diffuse-type gastric cancer suggests a collapse of normal mucosal barriers and leads to the spread of cancer cells. Although the association between chronic mucosal changes and LNM is unclear, more caution is needed during endoscopy especially for complete resection of diffuse-type GC with these features. © 2019 Shin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.