Histological changes associated with pyloric and pseudopyloric metaplasia after Helicobacter pylori eradication

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ORIGINAL ARTICLE

Histological changes associated with pyloric and pseudopyloric metaplasia after Helicobacter pylori eradication Yasuhiro Wada 1,2 & Ryoji Kushima 2 & Masaaki Kodama 1 & Masahide Fukuda 1 & Kensuke Fukuda 1 & Kazuhisa Okamoto 1 & Ryo Ogawa 1 & Kazuhiro Mizukami 1 & Tadayoshi Okimoto 1 & Kazunari Murakami 1 Received: 19 December 2019 / Revised: 4 March 2020 / Accepted: 25 March 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020

Abstract Pyloric metaplasia (PM) and pseudopyloric metaplasia (PPM) are metaplastic changes resulting in pyloric-type glands in the gastric oxyntic mucosa that mainly occur in chronic gastritis caused by Helicobacter pylori (H. pylori) infection. Focusing on PM and PPM, we classified the histological changes in gastric mucosa according to the Updated Sydney System, using 314 biopsy specimens of gastric greater curvature of the middle body before H. pylori eradication (HPE). Next, the numbers of PM and PPM glands were counted in 47 specimens, and subjects were followed up over 10 years after HPE. PPM was recognized jointly with inflammation, activity, atrophy, and intestinal metaplasia, but PM was recognized more frequently than PPM as atrophy and intestinal metaplasia progressed. Both PM and PPM regressed significantly within 6 years after HPE. Additionally, we demonstrated that PM and PPM are not always coincident with spasmolytic polypeptide-expressing metaplasia (SPEM). In conclusion, PM and PPM are considered different modulations of the same line of differentiation, which are both reversible, with PM potentially emerging from PPM upon progression. Keywords Helicobacter pylori . Pyloric metaplasia . Pseudopyloric metaplasia . Spasmolytic polypeptide-expressing metaplasia (SPEM)

Introduction Helicobacter pylori (H. pylori) infection is a cause of various gastric lesions, such as chronic gastritis, gastric ulcers, and gastric cancer [1–4]. Pyloric metaplasia (PM) and pseudopyloric metaplasia (PPM) are metaplastic changes of gastric oxyntic mucosa caused by H. pylori infection [1, 5–8], and they are considered regenerative changes that serve to compensate for gastric mucosal damage [9, 10]. PM and PPM occur by replacing oxyntic glands with pyloric-type glands that are rich in mucin This article is part of the Topical Collection on Quality in Pathology * Ryoji Kushima [email protected] 1

Department of Gastroenterology, Faculty of Medicine, Oita University, Yufu, Oita 879-5593, Japan

2

Department of Pathology, Faculty of Medicine, Shiga University of medical science, Otsu, Shiga 525-2192, Japan

secreted from mucous neck cells [1, 5, 7, 8, 11]. Solcia classified PM and PPM as pepsinogen 1 (PG1)-negative and PG1-positive, respectively, whereas both PM and PPM were positive for MUC6 [12–14]. Previous studies demonstrated an improvement in chronic gastritis by H. pylori eradication (HPE) [15, 16], but to the best of our knowledge, investigations on the histological changes in PM and PPM after HPE remain to be conducted. In recent years, a metaplasia subt