*5-1-1, Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
Jpn J Clin Oncol. 2014 Jan;44(1):65-71. doi: 10.1093/jjco/hyt167. Epub 2013 Nov 11.
Although many gastric cancers arise in chronic gastritis, the association between adenocarcinoma of the esophagogastric junction and the status of background gastritis remains unclear. We aim to investigate the histological status of gastritis in the background fundic gland mucosa of adenocarcinoma of the esophagogastric junction.
The present study included 121 consecutive patients with superficial adenocarcinoma of the esophagogastric junction obtained by surgical and/or endoscopic resection. We re-evaluated the histogenesis of adenocarcinoma of the esophagogastric junction, including the background fundic gland mucosa using the Updated Sydney System. The prevalence of histologic atrophic gastric mucosa with gastritis (positive gastritis), non-atrophic gastric mucosa without gastritis (negative gastritis) and Barrett's adenocarcinoma was examined.
Histologic-positive gastritis was found in 67 (55%) of all patients, in 24 (38%) of 63 Barrett's adenocarcinoma patients and in 43 (74%) of 58 non-Barrett's adenocarcinoma patients (P < 0.01). A higher female ratio in non-Barrett's adenocarcinoma with gastritis patients `and younger age in non-Barrett's adenocarcinoma without gastritis patients were shown. There were no differences in clinicopathological features related to the gastritis status in Barrett's adenocarcinoma patients. Reflux esophagitis was observed in most (81%) of all patients, and 32 (74%) of the non-Barrett's adenocarcinoma with gastritis patients. In the 67 positive gastritis patients, the mean Updated Sydney System scores of glandular atrophy and intestinal metaplasia were 1.45 and 1.10, respectively, and these scores were higher in the non-Barrett's adenocarcinoma patients than in the Barrett's adenocarcinoma patients.
This study suggests that about half of the patients with adenocarcinoma of the esophagogastric junction harbor histological gastritis. Adenocarcinoma of the esophagogastric junction is considered to be a heterogeneous entity, including Barrett's esophagus-related, positive gastritis-related, and Barrett's esophagus and gastritis-unrelated adenocarcinoma of the esophagogastric junction.
尽管许多胃癌起源于慢性胃炎，但食管胃交界部腺癌与背景性胃炎的关系仍不清楚。本研究旨在探讨食管胃交界部腺癌背景下胃底腺黏膜的炎症状态。
本研究纳入了 121 例经手术和/或内镜切除的浅表性食管胃交界部腺癌连续患者。我们使用更新的悉尼系统重新评估了食管胃交界部腺癌的发生机制，包括胃底腺黏膜的背景。检查了组织学萎缩性胃炎伴胃炎（阳性胃炎）、非萎缩性胃炎无胃炎（阴性胃炎）和 Barrett 腺癌的患病率。
所有患者中，组织学阳性胃炎为 67 例（55%），其中 Barrett 腺癌患者为 24 例（38%），非 Barrett 腺癌患者为 43 例（74%）（P < 0.01）。非 Barrett 腺癌伴胃炎患者中女性比例较高，非 Barrett 腺癌无胃炎患者年龄较轻。Barrett 腺癌患者的胃炎状态与临床病理特征无差异。大多数（81%）患者均有反流性食管炎，非 Barrett 腺癌伴胃炎患者中 32 例（74%）。在 67 例阳性胃炎患者中，胃底腺萎缩和肠上皮化生的平均悉尼系统评分分别为 1.45 和 1.10，非 Barrett 腺癌患者的评分高于 Barrett 腺癌患者。
本研究表明，约一半的食管胃交界部腺癌患者存在组织学胃炎。食管胃交界部腺癌被认为是一种异质性实体，包括与 Barrett 食管相关、与阳性胃炎相关以及与 Barrett 食管和胃炎无关的食管胃交界部腺癌。
