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目的研究肠化胃粘膜幽门螺杆菌（Ｈｐ）阳性率与ＰＣＮＡ，ｃｅｒｂＢ２表达率之间关系，以探讨Ｈｐ感染在胃肠化发生、发展中作用．方法经病理检查证实的慢性胃炎伴肠化１１６例，对照组非溃疡性消化不良．应用改良ＷａｒｔｈｉｎＳｔａｒｙ法检测Ｈｐ，免疫酶组化ＳＰ法检测ＰＣＮＡ，ｃｅｒｂＢ２的表达，比较Ｈｐ阳性组和阴性组间ＰＣＮＡ，ｃｅｒｂＢ２的阳性表达率．结果胃粘膜肠化者Ｈｐ感染率增高（５８６％ｖｓ１８８％，χ２＝１０７９，Ｐ＜００１），肠化胃上皮内少见Ｈｐ粘附，Ｈｐ阳性组ＰＣＮＡ，ｃｅｒｂＢ２表达高于阴性组（４８／６８ｖｓ１２／４８，χ２＝９０５，Ｐ＜００５；３６／７４ｖｓ２／４２，χ２＝１３２８，Ｐ＜００１）．结论Ｈｐ感染促进胃粘膜肠化，并使肠化胃粘膜细胞增殖迅速而启动恶性变，故Ｈｐ感染可能促进胃癌的形成．
Objective To study the relationship between the positive rate of Helicobacter pylori (Hp) in intestinal mucosa and the expression of PCNA and cerbB2 in order to investigate the role of Hp infection in the occurrence and development of gastrointestinal. Methods 116 cases of chronic gastritis with intestinal metaplasia confirmed by pathological examination and non-ulcer dyspepsia in the control group. Application of modified Warthin Stary method for detection of Hp, immunohistochemical SP method of PCNA, c erbB 2 expression, compared Hp positive group and negative group of PCNA, c erbB 2 of the positive expression rate. Results Hp infection rate of gastric mucosal metaplasia increased (58.6% vs18.8%, χ2 = 10.79, P <0.01), intestinal metaplasia rare Hp adhesion, Hp positive group PCNA, c erbB 2 expression was higher than the negative group (48 / 68vs12 / 48, χ2 = 9 05, P <0 05; 36 / 74vs2 / 42, χ2 = 1328, P <001). Conclusion Hp infection promotes gastric mucosal intestinal metaplasia and prompts the proliferation of intestinal mucosal cells to initiate malignant transformation. Therefore, Hp infection may promote the formation of gastric cancer.