原发性病理性十二指肠胃反流致病的因素分析

目的 探讨原发性病理性十二指肠胃反流(DGR)胃黏膜病变、幽门螺杆菌(Hp)感染、胆汁反流之间的关系.方法 应用便携式胆汁监测仪监测86例原发性病理性DGR患者胃内24 h胆汁反流情况;另取胃黏膜组织活检,分别行快速尿素酶试验、改良Giemsa染色和HE染色,判断有无Hp感染,并观察胃黏膜慢性炎症、活动性、萎缩、肠化等组织学特征.结果 ①将患者根据有无Hp感染分为Hp阳性组和Hp阴性组,Hp阳性组胃窦部黏膜病理积分、胆红素吸收值≥0.25的时间百分比均显著低于Hp阴性组(P均＜0.05);两组胆红素吸收值≥0.25的时间百分比和胃窦、胃角部黏膜病理积分均呈显著正相关(P均＜0.05).②将患者根据胆汁反流程度分为高反流组和低反流组,高反流组Hp阳性率显著低于低反流组(P＜0.05),胃窦和胃角部黏膜肠上皮化生的检出率、胃窦部黏膜病理积分均显著高于低反流组(P均＜0.05).结论 原发性病理性DGR导致胃窦黏膜损伤的主要因素可能为胆汁反流,随胆汁反流程度加重,胃窦黏膜损伤程度加重;胆汁反流可能抑制Hp在胃窦部定植,Hp感染可能与胆汁反流协同作用导致胃体部黏膜损伤.

Pathogenic factors of primary pathological duodenogastric reflux

Objective To study the relationship among the gastric mucosal lesions caused by primary pathological duodenogastric reflux , the Hp infection, the bile reflux assessed with bilirubin absorbance. Methods 24 hours intragastric bile reflux of 86 cases in primary pathological duodenogastric reflux were measured using Bilitec 2000. Endoscopy and gastric mucosa biopsies were performed in all cases for examination with rapid urease test, improved Giemsa staining and HE staining in order to diagnose Hp infection and define the lesions of gastric mucosa. The degree of chronic inflammation, activity, atrophy, intestinal metaplasia of gastric mucosa were observed. Results ① All cases were divided into two groups, Hp positive group and Hp negative group, based on the diagnosis of Hp infection. The time percentage of bilirubin absorbance≥0.25 in Hp positive group was significantly lower than that in Hp negative group(P＜0.05). The time percentage of bilirubin absorbance≥0.25 was positively correlated with New Sydney system pathological scores of gastric antrum and gastric anguli in two groups. ②Based on the severity of bile reflux, all cases were divided into two groups, high reflux group and low reflux group. Hp infection rate in high reflux group was significantly lower than that in low reflux group(P＜0.05). The frequency of intestinal metaplasia of gastric antrum and anguli, the New Sydney system pathological scores of gastric antrum in high reflux group were significantly higher than that in low reflux group(P＜0.05). Conclusions Bile reflux is possibly the main cause to mucosal lesions of gastric antrum in primary pathological duodenogastric reflux. Bile reflux may inhibit Hp to locate in gastric antrum. Hp infection and bile reflux can contribute to mucosal lesions of gastric body cooperatively.