摘要
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。
Objective: To explore the probable meechanism that Helicobacter pylori (Hp) may induce gastric carcinoma. Methods: Hp was detected by using microscope (10×100) in H E staining sections, meanwhile, its reliability was decided by polymerase chain reaction (PCR). Proliferating cell nuclear antigen(PCNA) were examined by immunohistochemistry (LSAB). Results: (1)The positive rate of Hp was the highest in chronic superficial gastritis, active (CSG)(65%), and significant differences between it and other five lesions were found (P<0.05);(2)Normal mucosa had the lowest positive rate of PCNA(35%), meanwhile, there were significant differences between it and other five lesions (P<0.0005); with the advance of lesions, the positive rate raised gradually. Conclusion: Hp infection can cause CSG and induce excessive cell proliferation, and then predispose to malignant transformation.
关键词
胃肿瘤
胃粘膜
幽门螺杆菌
病变
proliferating cell nuclear antigen(PCNA)
dysplasia
intestinal metaplasia
carcinogenesis
helicobacter pylori(Hp)
