早期胃癌和进展期胃癌患者幽门螺杆菌感染与胃黏膜组织学特点的关系

背景幽门螺杆菌(H.pylori)感染已被确认为慢性胃炎的主要病因,由慢性非萎缩性胃炎、慢性萎缩性胃炎至肠化生,经过数十年最终可能导致胃癌发生。目的评价H.pylori感染与胃镜检查正常者、慢性胃炎、早期胃癌和进展期胃癌患者胃黏膜组织学特点的关系。方法在受检者胃窦大弯侧、胃体大弯侧和胃角处各取一块黏膜活检标本,以Giemsa染色和免疫组化染色检测H.pylori感染情况;以HE染色评价胃黏膜炎症、活动性、萎缩和肠化生情况。结果慢性胃炎、早期胃癌和进展期胃癌患者的总体H.pylori感染率均显著高于胃镜检查正常者(52.4%、52.4%和81.2%对44.9%,P<0.05),慢性胃炎与早期胃癌患者的感染率无显著差异,但均显著低于进展期胃癌患者(P<0.05)。胃镜检查正常和慢性胃炎组H.pylori感染者的胃黏膜炎症、活动性、萎缩和肠化生检出率均显著高于无感染者(P<0.05);早期胃癌和进展期胃癌组H.pylori感染者的炎症活动性检出率显著高于无感染者(P<0.05),而炎症、萎缩和肠化生检出率与无感染者无显著差异。结论由H.pylori感染引起的胃黏膜慢性炎症、萎缩和肠化生可能在胃癌的发生、发展过程中起直接或间接作用。

Helicobacter pylori Infection and its Relationship with Histological Features of Gastric Mucosa in Patients with Early and Advanced Gastric Cancer

Background: It has been confirmed that the development of gastric cancer spans over several decades sequentially starting with Helicobacter pylori () infection, and then, chronic active gastritis, atrophy and intestinal metaplasia. Finally, gastric cancer will eventually arise in a subset of these patients. Aims: To evaluateinfection and its relationship with the histological features of gastric mucosa in patients with normal endoscopy, chronic gastritis, early and advanced gastric cancer. Methods: The biopsy specimens were taken from the greater curvature of antrum, greater curvature of corpus and the angulus, respectively. HE staining, Giemsa staining and -specific antibody immunohistochemical staining were performed for histological diagnosis of infection, chronic gastritis with atrophy and intestinal metaplasia, as well as early or advanced gastric cancer. Results: The overall prevalence ofinfection in chronic gastritis, early and advanced gastric cancer patients was significantly higher than that in patients with normal endoscopy (52.4%, 52.4% and 81.2% vs. 44.9%, P<0.05). There was no obvious difference ofinfection rate between chronic gastritis and early gastric cancer, but both were lower than that of advanced gastric cancer (P<0.05). In endoscopically normal and chronic gastritis patients, the positivity rates of inflammation, atrophy and intestinal metaplasia in gastric mucosa were significantly higher in those withinfection than in those without (P<0.05), and no differences were found in patients with early and advanced gastric cancer. Conclusions: Chronic inflammation, atrophy and intestinal metaplasia of the gastric mucosa induced byinfection possibly have direct and/or indirect effects on the development of gastric cancer.