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分析不同病变胃粘膜端粒酶活性的差异及其与幽门螺杆菌（H．pylori）感染的关系，探讨端粒酶活性、H.pylori感染与胃粘膜癌变的关系。方法：应用瑞粒重复扩增法测定正常胃粘膜、癌前病变和胃癌组织中的端粒酶活性，用酶免疫法检测H.Pylori感染患者的血清H．Pylori-CagA-IgG水平，并分析端粒酶活性与H.Pylori-CagAriIgG水平的关系。结果：172例胃镜活检标本中，正常胃粘膜、浅表性胃炎、慢性萎缩性胃炎无肠化、伴1度、2度肠化和胃癌组织的端粒酶阳性率分别为0％、0％、25％、37．5％和88．89％。45例手术切除的胃癌组织和相应的非癌胃组织也呈相似结果。正常胃粘膜、浅表性胃炎、慢性萎缩性胃炎无肠化及伴1度、2度肠化组织的H．pylori阳性率分别为0％、52.17％、60％、70％和75％。45例手术切除胃癌的非癌胃组织无肠化、伴1度、2度肠化的H．pylori感染强度分别为10．8±9．6个／50腺体、41．3±31．1个／50腺体和86．4±47．8个／50腺体。慢性浅表性胃炎患者的H、pylori-CagA-IgG抗体水平显著低于胃癌患者（P＜0.01），22例HPylori阳性胃癌患者感染的HPylori全部为cagA阳性菌株，其非癌胃粘膜有12例呈现端粒酶活性（54．55％）；相反H.pylori阳性的22例慢性浅表性胃炎患者感染的H.Pylori只有8例为cagA阳?
To analyze the difference of telomerase activity in gastric mucosa with different pathological changes and its relationship with H.pylori infection and to explore the relationship between telomerase activity, H.pylori infection and gastric mucosal carcinogenesis. Methods: The telomerase activity in normal gastric mucosa, precancerous lesion and gastric cancer tissues was determined by repeated replica amplification method. Serum H was detected by enzyme immunoassay in patients with H. pylori infection. Pylori-CagA-IgG levels and analyze the relationship between telomerase activity and H. pylori-CagAriIgG levels. Results: The positive rates of telomerase in normal gastric mucosa, superficial gastritis and chronic atrophic gastritis were 0%, 0% , 25%, 37.5% and 88.89% respectively. Forty-five resected gastric cancer tissues and corresponding non-cancerous gastric tissues also showed similar results. Normal gastric mucosa, superficial gastritis, chronic atrophic gastritis and intestinal metaplasia with 1 degree, 2 degrees of intestinal metaplasia H. The positive rates of pylori were 0%, 52.17%, 60%, 70% and 75% respectively. Forty-five cases of non-cancerous gastric tissue resected from gastric cancer without intestinal metaplasia, with 1 degree and 2 degree intestinal metaplasia. The infection rates of pylori were 10.8 ± 9.6 / 50 gland, 41.3 ± 31.1 / 50 gland and 86.4 ± 47.8 / gland respectively. The levels of H and pylori-CagA-IgG antibodies in patients with chronic superficial gastritis were significantly lower than those in patients with gastric cancer (all P <0.01). All 26 HPylori-positive gastric cancer patients were infected with cagA-positive HPylori, and 12 patients with non-cancerous gastric mucosa Showed telomerase activity (54.55%). In contrast, only 8 of H.pylori infected with H.pylori-positive chronic superficial gastritis were cagA positive