Kyoto classification of gastritis: Advances and future perspectives in endoscopic diagnosis of gastritis

Abstract

This editorial provides an update of the recent evidence on the endoscopy-based Kyoto classification of gastritis, clarifying the shortcomings of the Kyoto classification, and providing prospects for future research, with particular focus on the histological subtypes of gastric cancer (GC) and Helicobacter pylori (H. pylori) infection status. The total Kyoto score is designed to express GC risk on a score ranging from 0 to 8, based on the following five endoscopic findings: Atrophy, intestinal metaplasia (IM), enlarged folds (EF), nodularity, and diffuse redness (DR). The total Kyoto score reflects H. pylori status as follows: 0, ≥ 2, and ≥ 4 indicate a normal stomach, H. pylori-infected gastritis, and gastritis at risk for GC, respectively. Regular arrangement of collecting venules (RAC) predicts non-infection; EF, nodularity, and DR predict current infection; map-like redness (MLR) predicts past infection; and atrophy and IM predict current or past infection. Atrophy, IM, and EF all increase the incidence of H. pylori-infected GC. MLR is a specific risk factor for H. pylori-eradicated GC, while RAC results in less GC. Diffuse-type GC can be induced by active inflammation, which presents as EF, nodularity, and atrophy on endoscopy, as well as neutrophil and mononuclear cell infiltration on histology. In contrast, intestinal-type GC develops via atrophy and IM, and is consistent between endoscopy and histology. However, this GC risk-scoring design needs to be improved.

Keywords: Kyoto classification; Gastritis; Endoscopy; Gastric cancer; Histology; Helicobacter pylori

Core Tip: Endoscopy-based Kyoto classification of gastritis assesses gastric cancer (GC) risk and Helicobacter pylori (H. pylori) infection status. Total Kyoto scores of 0, ≥ 2, and ≥ 4 indicate a normal stomach, H. pylori-infected gastritis, and gastritis at risk for GC, respectively. Atrophy, intestinal metaplasia (IM), and enlarged folds (EF) increase H. pylori-infected GC incidence. Map-like redness is a specific risk factor for H. pylori-eradicated GC, while regular arrangement of collecting venules result in less GC risk. Diffuse-type GC is induced by active inflammation, depicting EF, nodularity, and atrophy. Intestinal-type GC develops through atrophy and IM; however, the GC risk-scoring design still needs to be improved.