原发性胆汁反流性胃炎的胃黏膜损伤情况及与胃幽门螺杆菌感染的关系.doc

原发性胆汁反流性胃炎的胃黏膜损伤情况及与胃幽门螺杆菌感染的关系
【摘要】 目的:探討原发性胆汁反流性胃炎(primary bile reflux gastritis,PBRG)的胃黏膜损伤情况及与胃幽门螺杆菌(Helicobt difference between the two groups (P>), and the degree of bile reflux increased, no significant increase or decrease in Hp detection detection rate of gastric mucosal atrophy in Hp positive group of PBRG patients was significantly higher than that of Hp negative group. The serum G-17 level in the Hp positive group of PBRG patients was also significantly higher than that in the negative group (P<). Conclusion: Bile reflux can cause chronic inflammation, atrophy, and intestinal metaplasia in gastric mucosa. PBRG has no significant correlation with Hp infection, but PBRG patients with Hp infection can accelerate gastric mucosal atrophy and aggravate hypergastrinemia, leading to delayed bile reflux, so it is recommended that patients with PBRG actively anti-Hp treatment. [Key words] Primary bile reflux gastritis Atrophy Intestinal metaplasia Gastric Helicobacter pylori infection
First-author’s address: Chenggong Hospital Affiliated to Xiamen University, Xiamen 361001, China
胆汁反流又称为十二指肠胃反流,是机体普遍存在的一种生理现象,而过多的胆汁反流可致胃黏膜损伤,称之为胆汁反流性胃炎。针对由于非手术胃所致者称为原发性胆汁反流性胃炎(primary bile reflux gastritis,PBRG)。PBRG多考虑与幽门、十二指肠协调运动失调所致十二指肠液反流有关[1]。PBRG在临床上并不少见,%,长期反复的胆汁反流可对胃黏膜造成严重损伤:如肠化生、腺体萎缩、甚至癌变[2]。而幽门螺杆菌(Helicobacter pylori,Hp)感染与慢性胃炎、消化性溃疡及低度恶性胃MALT淋巴瘤的发生密切相关,世界卫生组织已将其列为Ⅰ类致癌因子。但是Hp感染是否在PBRG中起致病作用尚有争议。因此本研究通过检测PBRG患者胃黏膜病理及Hp感染情况,明确胆汁反流引起胃黏膜损伤情况及Hp感染在PBRG患者胃黏膜损伤中是否有协同关系。
1 资料与方法
一般资料
收集2017年9月-2018年6月在笔者所在医院就诊的PRBG患者48例为观察组。入选标准:(1)有间歇性上腹部不适或疼痛、恶心、胸骨后烧灼感,部分患者伴有呕吐症状,呕吐物伴有胆汁样胃内容物;(2)PBRG内镜下诊断需同时符合以下标准:检查中患者合作,无明显恶心、呕吐,胃黏膜尤其是胃窦部黏膜有水肿、出血或脆性增加;胃黏液湖有黄色或绿色胆汁染色和/或胃黏膜有胆汁染色[3]。同期收集根据《中国慢性胃炎共识意见(2012年,上海)》标准确诊慢性非萎缩性胃炎(chronic non-atrophic gastritis,CNAG)患者50例为对照组。排除标准:(1)消化系统恶性肿瘤史、胃十二指肠和胆道手术史、肠梗阻、胃十二指肠溃疡等引起的继发性胆汁反流;(2)1个月内有特殊用药史(包括抗生素、制酸剂、促胃动力药、胃黏膜保护剂等影响胃动力和分泌功能的药物);(3)伴有严重心、脑、肾、肝、肺等疾病者。PBRG组:男22例,女26例,年龄25~70岁,平均(40±18)岁;对