胆汁反流、胃酸和幽门螺杆菌感染共同作用对胃黏膜损伤程度和分布的影响

The Influence of Bile Reflux, Gastric Acid and Helicobacter pylori Infection on Gastric Mucosal Injury: Severity and Localization

背景:胆汁反流、胃酸和幽门螺杆菌（H.pylori）感染均是胃黏膜损伤的独立致病因素。然而,它们共同存在时有无协同致病作用尚不清楚。目的:探讨胆汁反流、胃酸和H.pylori感染共同作用对胃黏膜损伤程度和分布的影响。方法:37例胃镜检查疑有十二指肠胃反流者均经24h胃内胆汁监测证实,同时行胃内PH监测。胃体和胃窦黏膜有或无活动性炎症、萎缩、肠化和不典型增生分别记2分或1分。分别以胃体和胃窦黏膜的各项病理学改变为应变量,以胃内胆红素吸收值>0.14的时间百分比、pH<4的时间百分比和H.pylori感染状态指标为自变量进行多变量逐步Logistic回归分析。结果:37例患者胃内胆红素吸收值>0.14的时间百分比为34.49％±22.69％,pH<4的时问百分比为78.68％土 9.91％,H.pylori阳性率为29.73％。胆汁反流出现在以胃体和胃窦黏膜肠化以及胃体黏膜活动性炎症为应变量的Logistic回归模型中,H.pylori出现在以胃体黏膜活动性炎症为应变量的回归模型中。结论:胆汁反流是胃黏膜肠化的危险因素;胃内有胆汁反流存在时,H.pylori感染是导致胃体新膜炎症的重要病因。

Background: It is well known that bile reflux, gastric acid and Helicobacter pylori (H. pylori) in-fection cause gastric mucosal injury. However, the combinative roles of these factors were obscure. Aims: To investigate the damage of bile reflux, gastric acid and H. pylori infection to gastric mucosa on severity and localization. Methods: A total of consecutive 37 patients who were suspected with duo-deno-gastric reflux, performed the 24-hour bile and gastric pH monitoring tests simultaneously. Active inflammation, atrophy, intestinal metaplasia and hyperplasia in the gastric mucosa of the corpus and antrum were investigated and scored. A stepwise Logistic regression analysis between gastric patho-logical changes and the time percentage of bilirubin absorption value > 0.14, the time percentage of pH <4, and the presence of H. pylori was carried out. Results: The time percentage of bilirubin absorp-tion value>0.14 and pH<4 were 34.49% ?2.69% and 78.68% ?.91%, respectively. The H. pylori infec-tion rate was 29.73%. Bile reflux was present in the Logistic regression models when there was intes-tinal metaplasia in the gastric mucosa of the corpus and antrum and active inflammation in the gastric mucosa of the corpus. H. pylori was present when there was active inflammation. Conclusions: Bile reflux causes intestinal metaplasia, and H. pylori is the most important etiological factor for corpus gastritis in the presence of bile reflux.