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.
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.
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.
摘要：
背景：胃上皮屏障破坏是胃癌（GC）的关键步骤。我们调查了Correa级联时间线期间的这些破坏与上皮屏障功能障碍相关。
方法：本研究以单中心，2019年5月至2022年10月在中国进行的非随机临床试验。慢性萎缩性胃炎（CAG）患者，胃肠上皮化生（GIM），低度上皮内瘤变（LGIN），高级别上皮内瘤变（HGIN），粘膜内癌接受了基于探针的共聚焦激光显微内镜（pCLE）。pCLE评分系统用于半定量评估胃上皮屏障破坏。
结果：我们招募了95名接受pCLE检查的患者。对照组由15个人组成，实验组包括17例CAG患者，27例GIM患者，20名LGIN患者，16例早期胃癌(EGC)。除了CAG,与对照组相比没有显着差异，在GIM中发现胃上皮屏障损伤的发生率明显更高，LGIN,和EGC组与对照组相比(Kruskal-WallisH检验=69.295,p<0.001)。GIM和LGIN区的LGIN患者没有差异，两组与EGC组比拟无差别。与非LGIN患者相比，LGIN患者的肠上皮化生区域会导致更严重的胃上皮损伤。此外,与对照组相比，幽门螺杆菌阳性萎缩性胃炎患者和IM患者之间存在显着差异（p<0.001），而在H.pylori阴性萎缩性胃炎患者间无显著性差异(p>0.05)。
结论：从幽门螺杆菌感染开始到GC进展，胃上皮屏障仍然功能失调。除了“不归路”之外，“随后的致癌过程可能归因于其他机制。
方法：本研究以单中心，2019年5月至2022年10月在中国进行的非随机临床试验。慢性萎缩性胃炎（CAG）患者，胃肠上皮化生（GIM），低度上皮内瘤变（LGIN），高级别上皮内瘤变（HGIN），粘膜内癌接受了基于探针的共聚焦激光显微内镜（pCLE）。pCLE评分系统用于半定量评估胃上皮屏障破坏。
结果：我们招募了95名接受pCLE检查的患者。对照组由15个人组成，实验组包括17例CAG患者，27例GIM患者，20名LGIN患者，16例早期胃癌(EGC)。除了CAG,与对照组相比没有显着差异，在GIM中发现胃上皮屏障损伤的发生率明显更高，LGIN,和EGC组与对照组相比(Kruskal-WallisH检验=69.295,p<0.001)。GIM和LGIN区的LGIN患者没有差异，两组与EGC组比拟无差别。与非LGIN患者相比，LGIN患者的肠上皮化生区域会导致更严重的胃上皮损伤。此外,与对照组相比，幽门螺杆菌阳性萎缩性胃炎患者和IM患者之间存在显着差异（p<0.001），而在H.pylori阴性萎缩性胃炎患者间无显著性差异(p>0.05)。
结论：从幽门螺杆菌感染开始到GC进展，胃上皮屏障仍然功能失调。除了“不归路”之外，“随后的致癌过程可能归因于其他机制。
