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目的：揭示幽门螺杆菌（Ｈｐ）引起胃粘膜病变的可能机制。方法：对胃粘膜良恶性病变的ＨＥ切片，用油镜检测Ｈｐ；并对Ｈｐ阳性病例随机抽样，用聚合酶链反应（ＰＣＲ）法鉴定Ｈｐ。同时用免疫组化（ＬＳＡＢ）法检测增殖细胞核抗原（ＰＣＮＡ）的表达。结果：Ｈｐ在慢性浅表性胃炎活动性（ＣＳＧ）组最高（６５％），且与各组间均有差异（Ｐ＜０．０５）；ＰＣＮＡ在正常胃粘膜阳性率最低（３５％），与各组间均有差异（Ｐ＜０．０００５）。且随病变加重，阳性率呈递增趋势。结论：Ｈｐ在ＣＳＧ的发生中，具有病因学价值；Ｈｐ感染导致胃粘膜过度增生，为发展成癌前病变提供条件
Objective: To reveal the possible mechanism of Helicobacter pylori (Hp) causing gastric mucosal lesions. Methods: The HE slices of benign and malignant lesions of gastric mucosa were examined by Hp with oil mirror. Hp positive cases were randomly selected and Hp was identified by polymerase chain reaction (PCR). Meanwhile, the expression of proliferating cell nuclear antigen (PCNA) was detected by immunohistochemistry (LSAB). Results: Hp was the highest (65%) in chronic superficial gastritis activity group (CSG), with a significant difference (P <0.05). The positive rate of PCNA in normal gastric mucosa was the lowest (35% There was a significant difference between groups (P <0.0005). And with the increase of disease, the positive rate showed an increasing trend. Conclusion: Hp has etiological value in the pathogenesis of CSG. Hp infection leads to gastric mucosal hyperplasia, which provides conditions for the development of precancerous lesions