胃液总胆汁酸和幽门螺杆菌感染与胃黏膜肠化生的相关性研究

背景：幽门螺杆菌（Hp）感染和胃内胆汁反流与胃黏膜肠化生密切相关，但其机制尚不完全清楚。目的：研究胃液总胆汁酸（TBA）和Hp感染与肠化生指标CDX2、MUC2的相关性。方法：收集81例有胃内胆汁反流且无腹部手术史者和40例无胆汁反流对照者的胃液标本检测TBA浓度，于胃窦部取活检标本行HE染色、HID—AB—PAS染色肠化生分型和CDX2、MUC2免疫组化染色。同时行血清HpIgG抗体检测。结果：胆汁反流组慢性非萎缩性胃炎（CNAG）37例，慢性萎缩性胃炎（CAG）44例（均伴完全型肠化生），对照组40例均为CNAG。胆汁反流组胃液TBA浓度和胃黏膜CDX2、MUC2蛋白阳性表达率显著高于对照组（P〈0．01），其中CAG组显著高于CNAG组（P〈0．01）。胆汁反流组与对照组间血清HpIgG抗体阳性率无明显差异。胆汁反流组CDX2、MUC2蛋白阳性表达率随TBA浓度的增高呈上升趋势（P〈0．01），Hp感染阳性者CDX2、MUC2蛋白阳性表达率显著高于Hp感染阴性者（P〈0．05）。TBA〉3000μmol／L者的CDX2、MUC2蛋白阳性表达率显著高于Hp感染阳性者（91．2％对63．0％和91．2％对60．9％，P〈0．01）。结论：除Hp感染外，高浓度胆汁酸亦为引起胃黏膜肠化生和CDX2、MUC2表达的重要因素且其作用可能大于Hp感染。

Correlation of Total Bile Acid in Gastric Juice and Helicobacter pylori Infection with Gastric Intestinal Metaplasia

Background： Helicobacter pylori （Hp） infection and reflux of bile into the stomach may contribute to the induction of gastric intestinal metaplasia （ IM）, however, the mechanism underlying IM is not yet fully understood. Aims： To study the correlation of total bile acid （TBA） in gastric juice and Hp infection with two reliable IM markers, CDX2 and MUC2. Methods： Eighty-one patients with gastric bile reflux and without a history of abdominal operation were enrolled and forty subjects without gastric bile reflux were served as controls. When undergoing gastroscopy, gastric juice sample was collected for measurement of TBA concentration, and antral biopsy specimen was taken for HE staining, typing IM with HID-AB-PAS staining and immunohistochemical staining for assessing the expressions of CDX2 and MUC2. Serum Hp IgG was determined simultaneously. Results： Thirty-seven patients were identified as chronic non-atrophic gastritis （CNAG）, and 44 as chronic atrophic gastritis （CAG） in bile reflux group. All patients in CAG subgroup had complete IM. All control subjects were identified as CNAG. Concentration of gastric juice TBA and positivity rates of mucosal CDX2 and MUC2 proteins were significantly higher in bile reflux group than in control group （ P 〈 0.01 ）, and were significantly higher in CAG subgroup than in CNAG subgroup （ P 〈 0.01 ）. Difference in positivity rate of serum Hp IgG was insignificant between bile reflux group and control group. In bile reflux group, the positivity rates of CDX2 and MUC2 proteins were increased with the increase of TBA concentration （ P 〈 0.01 ）, and were significantly higher in Hp-positive subgroup than in Hp-negative subgroup （ P 〈 0.05）. The positivity rates of the two IM markers were significantly higher in TBA 〉 3000 μmol/L subgroup than in Hp-positive subgroup （91.2% vs. 63.0% and 91.2% vs. 60.9%, P 〈 0.01 ）. Conclusions： Besides Hp infection, high concentration of bile acid plays an important role in the induction of IM and expressions of CDX2 and MUC2 in the stomach. The effect of high concentration of bile acid might be greater than that of Hp infection.