Gastroesophageal flap valve status distinguishes clinical phenotypes of large hiatal hernia

作     者：Haruka Kaneyama Mitsuru Kaise Hiroshi Arakawa Yoshinori Arai Keisuke Kanazawa Hisao Tajiri 

作者机构：Department of EndoscopyThe Jikei University School of Medicine Department of Gastroenterology and HepatologyThe Jikei University School of Medicine 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2010年第16卷第47期

页      面：6010-6015页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

主　　题：Large hiatal hernia Reflux esophagitis Cameron lesion Gastroesophageal flap valve Nonsteroidal anti-inflammatory drug 

摘      要：AIM: To investigate two distinct clinical phenotypes of reflux esophagitis and intra-hernial ulcer (Cameron lesions) in patients with large hiatal hernias. METHODS: A case series study was performed with 16 831 patients who underwent diagnostic esophagogastroduodenoscopy for 2 years at an academic referral center. A hiatus diameter ≥ 4 cm was defined as a large hernia. A sharp fold that surrounded the cardia was designated as an intact gastroesophageal flap valve (GEFV), and a loose fold or disappearance of the fold was classified as an impaired GEFV. We studied the associations between large hiatal hernias and the distinct clinical phenotypes (reflux esophagitis and Cameron lesions), and analyzed factors that distinguished the clinical phenotypes. RESULTS: Large hiatal hernias were found in 49 (0.3%) of 16 831 patients. Cameron lesions and reflux esopha-gitis were observed in 10% and 47% of these patients, and 0% and 8% of the patients without large hiatal hernias, which indicated significant associations between large hiatal hernias and these diseases. However, there was no coincidence of the two distinct disorders. Univariate analysis demonstrated significant associations between Cameron lesions and the clinico-endoscopic factors such as nonsteroidal anti-inflammatory drug (NSAID) intake (80% in Cameron lesion cases vs 18% in non-Cameron lesion cases, P=0.015) and intact GEFV (100% in Cameron lesion cases vs 18% in non-Cameron lesion cases, P=0.0007). In contrast, reflux esophagitis was linked with impaired GEFV (44% in reflux esophagitis cases vs 8% in non-reflux esophagitis cases, P = 0.01). Multivariate regression analysis confirmed these significant associations. CONCLUSION: GEFV status and NSAID intake distinguish clinical phenotypes of large hiatal hernias. Cameron lesions are associated with intact GEFV and NSAID intake.