Disruption of the gastric epithelial barrier in Correa's cascade: Clinical evidence via confocal endomicroscopy

IF 4.3 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter Pub Date : 2024-03-05 DOI:10.1111/hel.13065

Shao-Tong Wang, Hua-Wei Yang, Wen-Lin Zhang, Zhen Li, Rui Ji

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引用次数: 0

Abstract

Background

Gastric epithelial barrier disruption constitutes a crucial step in gastric cancer (GC). We investigated these disruptions during the Correa's cascade timeline to correlate epithelial barrier dysfunction.

Materials and Methods

This study was conducted as a single-center, non-randomized clinical trial in China from May 2019 to October 2022. Patients with chronic atrophic gastritis (CAG), gastric intestinal metaplasia (GIM), low-grade intraepithelial neoplasia (LGIN), high-grade intraepithelial neoplasia (HGIN), and intramucosal carcinoma underwent probe-based confocal laser endomicroscopy (pCLE). The pCLE scoring system was used to assess gastric epithelial barrier disruption semi-quantitatively.

Results

We enrolled 95 patients who underwent a pCLE examination. The control group consisted of 15 individuals, and the experimental group included 17 patients with CAG, 27 patients with GIM, 20 patients with LGIN, and 16 patients with early gastric cancer (EGC). Apart from CAG, which showed no significant difference compared to the control group, a significantly higher incidence of gastric epithelial barrier damage was found in the GIM, LGIN, and EGC groups compared to the control group (Kruskal–Wallis H test = 69.295, p < 0.001). There is no difference in LGIN patients between GIM and LGIN areas, and there is no difference between the two groups compared with the EGC group. The intestinal metaplasia area in LGIN patients causes more severe gastric epithelial damage compared to that in non-LGIN patients. Additionally, compared to control group, a significant difference (p < 0.001) was noted between individuals with Helicobacter pylori-positive atrophic gastritis and those with IM, whereas no significant difference (p > 0.05) was observed among individuals with H. pylori-negative atrophic gastritis.

Conclusions

The gastric epithelial barrier remains dysfunctional from the initiation of H. pylori infection to GC progression. Beyond the “point of no return,” subsequent carcinogenesis processes may be attributed to other mechanisms.

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科雷亚级联征中胃上皮屏障的破坏：共聚焦内窥镜的临床证据

背景：胃上皮屏障破坏是胃癌（GC）的关键步骤。我们研究了科雷亚级联时间线上的这些破坏，以关联上皮屏障功能障碍：本研究于2019年5月至2022年10月在中国进行了单中心、非随机临床试验。慢性萎缩性胃炎（CAG）、胃肠化生（GIM）、低级别上皮内瘤变（LGIN）、高级别上皮内瘤变（HGIN）和黏膜内癌患者接受了探针式共聚焦激光内镜（pCLE）检查。pCLE 评分系统用于半定量评估胃上皮屏障破坏情况：我们招募了 95 名接受 pCLE 检查的患者。对照组包括 15 人，实验组包括 17 名 CAG 患者、27 名 GIM 患者、20 名 LGIN 患者和 16 名早期胃癌（EGC）患者。除 CAG 与对照组相比无显著差异外，在幽门螺杆菌阴性的萎缩性胃炎患者中，GIM、LGIN 和 EGC 组的胃上皮屏障损伤发生率明显高于对照组（Kruskal-Wallis H 检验 = 69.295，P 0.05）：结论：从幽门螺杆菌感染开始到胃癌进展，胃上皮屏障一直处于功能失调状态。超过 "不归点 "后，随后的癌变过程可能归因于其他机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Helicobacter 医学-微生物学

CiteScore

8.40

自引率

9.10%

发文量

审稿时长

2 months

期刊介绍： Helicobacter is edited by Professor David Y Graham. The editorial and peer review process is an independent process. Whenever there is a conflict of interest, the editor and editorial board will declare their interests and affiliations. Helicobacter recognises the critical role that has been established for Helicobacter pylori in peptic ulcer, gastric adenocarcinoma, and primary gastric lymphoma. As new helicobacter species are now regularly being discovered, Helicobacter covers the entire range of helicobacter research, increasing communication among the fields of gastroenterology; microbiology; vaccine development; laboratory animal science.