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幽门螺杆菌感染与胃癌的关系
引用本文:周宗良,汤绍辉,罗和生.幽门螺杆菌感染与胃癌的关系[J].江汉大学学报(自然科学版),2001(1).
作者姓名:周宗良  汤绍辉  罗和生
作者单位:铁道部大桥局三处医院消化内科!湖北武汉430051(周宗良),武汉市职工医学院附属医院消化科!湖北武汉430015(汤绍辉),武汉大学医院消化内科!湖北武汉430060(罗和生)
摘    要:目的 :探讨幽门螺杆菌 (简称 Hp)感染与胃癌的关系。方法 :43例胃癌患者的新鲜癌手术标本及血清标本、36例十二提肠溃疡患者 (对照组 )的胃窦粘膜组织及血清标本入本组研究。分别采用 PCR及血清学试验检测其 Hp感染状况 ,两项检测均为阳性者即确立为 Hp感染。结果 :(1) 4 3例胃癌中 ,Hp阳性 30例 ,阳性率 6 9.77% ;36例十二指肠溃疡中 ,Hp阳性 30例 ,阳性率 83.33% ,两组阳性率相比差异无显著性。Hp阳性患者中 ,胃癌及对照组 cag A基因阳性分别为 2 4例、2 5例 ,阳性率分别为 80 .0 0 %、83.33% ,两组阳性率相比差异无显著性。(2 ) 4 3例胃癌中 ,高中分化腺癌组 Hp及 cag A检出率分别为 6 2 .5 0 %及 70 .0 0 % ,低未分化癌组 Hp及 cag A检出率分别为 74.0 7%及 85 .0 0 % ,但两组 Hp及 cag A检出率统计学上均无显著性差异。结论 :(1) Hp感染及 cag A+ 菌株感染不是胃癌发生的唯一或必须因素。 (2 )胃癌的分化程度与 Hp及cag A+菌株感染无明显相关性。

关 键 词:胃癌  十二指肠溃疡  幽门螺杆菌  cagA+菌株

Relation between Helicobacter pylori Infection and Gastric Cancer
Zhou Zongliang ,Tang Shaohui,Luo Hesheng.Relation between Helicobacter pylori Infection and Gastric Cancer[J].Journal of Jianghan University:Natural Sciences,2001(1).
Authors:Zhou Zongliang  Tang Shaohui  Luo Hesheng
Institution:Zhou Zongliang 1,Tang Shaohui,Luo Hesheng
Abstract:Objective: To investigate the relationship between Helicobacoter pylori (H.pylori) infection and gastric canccr. Methods: The carcinomatous tissues and serum samples of 43 patients with gastric cancer and the gastric mucosal tissues and serum samples of 36 patients with duodenal ulcer were studied. The status of H.pylori infection was determined by PCR and serological tests. The patient with positive PCR and serological tests was defined as H.pylori or cagA strain infection. Results: (1)In the 43 patients with gastric cancer, H.pylori infection was confirmed in the 30 patients and the positive rate was 69.77%;among 36 duodenal ulcers, H.pylori infection was detected in the 30 patients(83.33%). There was no significant difference between two groups(P>0.05). In the patients with H.pylori infection, cagA strains were found in 24(80.00%) of gastric cancers and in 25(83.33%) of duodenal ulcers, which had no statistical difference(P>0.05). (2)Among the 43 cases of gastric cancers, the detection rate of H.pylori was 62.5%(10/16) and cagA strains was 70.00%(7/10) in highly and moderately differential group, and 74.07%(20/27) and 85.00%(17/20) in poorly and non differential group respectively, but there were no statistical differences in H.pylori and cagA strain detection rate between the two groups(P>0.05). Conclusions: (1)H.pylori and cagA strain infection may not be the single or essential factor for the gastric carcinogenesis. (2)The differentiation of gastric cancer may not be correlated with H.pylori and cagA strain infection.
Keywords:Gastric cancer  Duodenal ulcer  Helicobacter pylori  CagA  strain
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