Ohno K, Nakatani E, Kurokami T, Kawai A, Itai R, Matsuda M, Masui Y, Satoh T, Ikeda S, Hirata T, Takeda S, Suzuki M, Haruma K. Relationship between gastric mucosal atrophy by endoscopy and non-ampullary duodenal epithelial tumors. World J Gastrointest Oncol 2025; 17(2): 100545 [DOI: 10.4251/wjgo.v17.i2.100545]
Corresponding Author of This Article
Ken Haruma, PhD, Researcher, Department of General Internal Medicine 2, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 700-8505, Japan. kharuma@med.kawasaki-m.ac.jp
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Retrospective Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Kazuya Ohno, Takafumi Kurokami, Asami Kawai, Ryosuke Itai, Masanori Matsuda, Yuichi Masui, Tatsunori Satoh, Shinya Ikeda, Taiyo Hirata, Shodai Takeda, Department of Gastroenterology, Shizuoka General Hospital, Shizuoka 420-8527, Japan
Eiji Nakatani, Research Support Center, Graduate School of Public Health, Shizuoka Graduate University of Public Health, Shizuoka 420-0881, Japan
Makoto Suzuki, Department of Pathology, Shizuoka General Hospital, Shizuoka 420-8527, Japan
Ken Haruma, Department of General Internal Medicine 2, Kawasaki Medical School, Okayama 700-8505, Japan
Co-first authors: Kazuya Ohno and Eiji Nakatani.
Author contributions: Ohno K and Nakatani E contributed equally; Ohno K designed and performed the experimental studies and drafted the manuscript; Nakatani E designed the research and contributed to the analysis; Kurokami T, Kawai A, Itai R, Matsuda M, Masui Y, Satoh T, Ikeda S, Hirata T, and Takeda S contributed to appropriate endoscopic diagnosis and accumulation of cases; Suzuki M contributed to specimen preparation and pathological diagnosis; Haruma K designed the experimental studies and supervised the study.
Institutional review board statement: This study was approved by the ethics committee of Shizuoka General Hospital (No. SGHIRB #2021033) and conducted in compliance with the Declaration of Helsinki.
Informed consent statement: Personal information was strictly managed, and patients provided consent to participate in the study using an opt-out method. The study was conducted at an institution; therefore, patients who did not wish to participate could be excluded. The data were analyzed anonymously and did not contain personally identifiable information.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ken Haruma, PhD, Researcher, Department of General Internal Medicine 2, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 700-8505, Japan. kharuma@med.kawasaki-m.ac.jp
Received: August 20, 2024 Revised: October 21, 2024 Accepted: November 14, 2024 Published online: February 15, 2025 Processing time: 151 Days and 20.6 Hours
Abstract
BACKGROUND
The pathogenesis of non-ampullary duodenal epithelial tumors (NADETs) is not fully understood. NADETs that express gastric-type mucin phenotypes (G-NADETs) are noteworthy because of their high malignancy. Gastric foveolar metaplasia, from which G-NADETs originate, protects the duodenal mucosa from gastric acidity. As gastric acid secretion is affected by endoscopic gastric mucosal atrophy (EGMA), we hypothesized that EGMA would be associated with G-NADETs.
AIM
To evaluate the association between EGMA and the occurrence of G-NADETs.
METHODS
This cross-sectional retrospective study investigated the relationship between EGMA and NADETs in 134 patients. The duodenum was divided into parts 1 (bulb), 2 (superior duodenal angle to the papilla), and 3 (anal side of the papilla to the horizontal part). The effects of gastric acidity and presence of Brunner’s glands were considered. EGMA was divided into types C (no or mild atrophy) and O (severe atrophy). Mucin phenotype expressions in NADETs were divided into gastric, intestinal, gastrointestinal, and unclassifiable.
RESULTS
When NADETs were classified according to EGMA, 105 were classified as type C and 29 as type O. G-NADETs were present in 11.9% (16 cases) of all cases, and all 16 cases were of type C. Among G-NADETs, 93.8% (15 cases) were present in part 1 or 2. There was an association between G-NADETs and type C in part 1, and 50.0% (eight of 16 cases) of G-NADETs were associated with a current or previous Helicobacter pylori infection status. Additionally, all eight cases occurred in part 1.
CONCLUSION
G-NADETs were significantly associated with type C. Gastric acidity and Brunner's gland growth may be associated with G-NADETs.
Core Tip: This retrospective study evaluated effects of endoscopic gastric mucosal atrophy (EGMA) on the occurrence of highly malignant gastric-type non-ampullary duodenal epithelial tumors (G-NADETs). G-NADETs were observed in 16 patients with no or mild EGMA (type C). On dividing NADETs into parts 1 (bulb), 2 (superior duodenal angle to the papilla), and 3 (anal side of the papilla), type C and G-NADETs were mainly observed in part 1. Half of the G-NADETs had a history of Helicobacter pylori infection and were found in part 1. These results suggest that G-NADET occurrence is related to gastric acidity.
