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目的 评价南昌地区幽门螺杆菌 (Helicobactcrpylori,Hp)表型在胃十二指肠疾病中的分布情况 ,并探讨其临床意义。方法 2 0 6例慢性胃炎 (CG)、消化性溃疡 (PU)和胃癌 (GC)的南昌患者经胃镜和组织学检查确诊 ,用免疫印迹法检测Hp细胞毒素相关蛋白 (CaSA)、空泡毒素 (VacA)和尿素酶 (Urease)及其亚型。结果 Hp感染人群中Hp表型CaZA、VacA和Urease的表达率分别为 5 7.1%、78.6 %和 10 0 %。Hp表型CagA、VacA及亚型 12 8KDCagA、116KDCagA、95 1KDVacA、91KDVacA、6 6KDUreB、30KDUreA ,无一在CG组、PU组和GC组中的表达率差异有显著性 (P >0 .0 5 )。表型CagA +/VacA +(CagA +或 /和VacA +)在CG组、PU组和GC组的表达率分别为 74 .4 %、85 .7%和 94 .4 % ,在CG组、PU组和GC组中 ,P =0 .0 2 4 ;在CG组和PU组中 ,P =0 .14 5 ;CG组和GC组中 ,P =0 .0 11:在PU组和GC组中 ,p =0 .2 75 ;在非CC(即CG和PU)组和CC组中 ,P =0 .0 2 4。116KDCagA在≤ 4 5岁患者的表达率 (6 0 .5 % )高于 >4 5岁患者的表达率 (42 .7% ) (P =0 .0 37)。结论 在Ca gA+ 南昌地区的Hp感染人群中 ,Hp的CaSA表达率明显低于VacA。Hp单一表型和亚型未显示其独立的致病作用。表型CagA+ /VacA +与GC有关 ,提示Hp可能通过多种表型和我们未提及的
Objective To evaluate the distribution of Helicobactcrpylori (Hp) phenotype in gastroduodenal diseases in Nanchang area and to explore its clinical significance. Methods Twenty-six patients with chronic gastritis (CG), peptic ulcer (PU) and gastric cancer (GC) were diagnosed by gastroscopy and histological examination. The expression of Hpa cytotoxin-related protein (CaSA), vacuolar toxin (VacA) and urease (Urease) and its subtypes. Results The expression rates of Hp phenotype CaZA, VacA and Urease in Hp infected individuals were 51.1%, 78.6% and 100% respectively. The expression rates of Hp phenotype CagA, VacA and subtype 12 8KDCagA, 116KDCagA, 95 1KDVacA, 91KDVacA, 6 6KDUreB and 30KDUreA were all significantly different between CG group, PU group and GC group (P> 0.05) ). The expression rates of CagA + / VacA + (CagA + or / and VacA +) in CG group, PU group and GC group were 74.4%, 85.7% and 94.4% In the CG and PU groups, P = 0.14 5; in the CG and GC groups, P = 0 .0 11: In the PU and GC groups, , p = 0.27 75; P = 0.024 4.116KDCagA in non-CC (CG and PU) group and CC group was higher than that in patients ≤ 45 years old (60.5%) > 4-year-old patients the expression rate (42.7%) (P = 0. 0 37). Conclusions In Ca gA + Nanchang population, the expression rate of CaSA in Hp was significantly lower than that in VacA. Hp single phenotype and subtype did not show its independent pathogenic role. Phenotype CagA + / VacA + is associated with GC, suggesting that Hp may pass multiple phenotypes and we have not mentioned