Endoscopic Gastritis: What Does It Mean?

Abstract

One can confidently assume that there is no evidence of endoscopic gastritis when the gastric mucosa has a regular pinkish color without discoloration or structural alteration, the gastric rugae are not thicker than 5 mm, and if the gastric mucosa expands well upon inflation with air. However, inflammatory changes induce subsequent apoptosis and gland damage, which can lead to regeneration, fibrosis, or metaplasia [1]. Inflammatory changes such as color and/or structural changes are noted in endoscopic findings, and are thus labeled endoscopic gastritis. Endoscopic gastritis can be classified into seven types: (a) superficial, (b) hemorrhagic, (c) erosive, (d) verrucous, (e) atrophic, (f) metaplastic, and (g) hypertrophic [2]. Erosive gastritis is diagnosed when endoscopy reveals small elevations with central umbilication, mimicking octopus’ suckers, which are usually observed in the antrum. It can also be defined as a flat or minimally depressed white spot surrounded by a reddish area that is sometimes accompanied by small superficial bleeding [3]. Since the distinction between erosion and tiny shallow ulcer is arbitrary, the latter might be included under the term ‘‘erosion.’’ When the erosion is elevated, it is generally defined as verrucous gastritis or gastritis varioliformis rather than as erosive gastritis. In this issue of Digestive Diseases and Sciences, Yamamoto et al. [3] provide an interesting finding that lower serum levels of adiponectin are associated with an increased risk of endoscopic erosive gastritis, independently of body mass index (BMI). BMI is known to be associated with abnormal upper endoscopic findings, such as erosive gastritis, gastric ulcer, duodenal ulcer, and reflux esophagitis [4]. Interestingly, when Yamamoto et al. analyzed factors including age, sex, alcohol habits, smoking habits, BMI, blood pressure, cholesterol, triglyceride, glucose, and insulin in 2,400 participants, BMI was significantly higher and the serum adiponectin level was significantly lower in gastritis-positive participants than in gastritis-negative participants. That study indicated a possible role of hypoadiponectinemia in erosive gastritis, in addition to a previous study that showed a link between low plasma adiponectin levels and gastric cancer [5]. Erosive gastritis has been considered relatively less significant than Helicobacter pylori-related endoscopic gastritis, since H. pylori infection involves a multistep progression from gastritis to glandular atrophy, intestinal metaplasia (IM), dysplasia, and ultimately to intestinaltype gastric cancer [6]. We have recently shown that the endoscopic diagnosis of open-type atrophic gastritis is related to the histological diagnosis of IM and Cdx2 expression [7]. Higher levels of Cdx2 expression are related to open-type atrophic gastritis and metaplastic gastritis, but not to closed-type atrophic gastritis and nonatrophic/ nonmetaplastic cases. The location of the atrophic gastric border was found to be strongly related to histological IM and Cdx2 expression. Our findings suggest that Cdx2 expression is an early change that is correlated with the presence of histological IM, and which occurs before endoscopic metaplastic gastritis, and that the risk of development of intestinal-type gastric cancer will continue to remain high during the process of gastric carcinogenesis in open-type atrophic gastritis and metaplastic gastritis, but not in closed-type atrophic gastritis and nonatrophic/ S.-Y. Lee (&) Department of Internal Medicine, Konkuk University School of Medicine, Seoul 143-729, Korea e-mail: sunyoung@kuh.ac.kr