CAJ | 학술논문

目的分析研究广州地区消化道疾病患者中H.pylori ureA、vacA s1基因和cagA基因亚型(ABC、ABD、ABAB、AAD等)的分布状况及其与胃黏膜病理检测结果间的相关性.方法随机选取227例消化道疾病患者的胃黏膜标本,分别来自病理组织学检测无病理改变者46例,慢性胃炎130例,消化性溃疡29例,萎缩性胃炎15例,胃癌7例.并用实时荧光定量PCR检测H.pylori ureA基因、vacA s1基因,用PCR扩增cagA羧基端EPIYA基序所在区,然后测序确定其亚型.以保守基因ureA的存在判断H.pylori感染.结果 227例消化道疾病患者中,有50.7% (115/227)的患者H.pylori阳性,其中,vacA s1基因阳性91.3%(105/115),cagA基因阳性78.3%(90/115).4种cagA-EPIYA亚型分布为,ABC 17.8%(16/90)、ABD 78.9%(71/90)、AAD 2.2%(2/90)、ABAB 1.1%(1/90).无病理改变组中H.pylori 阳性32.6%(15/46),vacA s1基因阳性28.3%(13/46),cagA基因阳性26.1%(12/46);慢性胃炎组H.pylori 阳性48.5%(63/130),vacA s1基因阳性43.8%(57/130),cagA基因阳性36.2%(47/130);溃疡组H.pylori 阳性72.4%(21/29),vacA s1基因阳性65.5%(19/29),cagA基因阳性55.2%(16/29);萎缩性胃炎组H.pylori 阳性66.7%(10/15),vacA s1基因阳性66.7%(10/15),cagA基因阳性66.7%(10/15);胃癌组H.pylori阳性85.7%(6/7),vacA s1基因阳性85.7%(6/7),cagA基因阳性71.4%(5/7).H.pylori在不同胃黏膜病理组的分布差异有统计学意义(χ2=16.72;P<0.01),溃疡、萎缩性胃炎、胃癌组中H.pylori的分布明显高于无病理改变与炎症组(χ2=16.02;P<0.01).但在H.pylori阳性患者中,强毒力因子vacA s1基因(χ2=2.00;P=0.74)、cagA基因(χ2=3.44;P=0.49)及cagA-EPIYA亚型(χ2=3.66;P=0.45)在无病理改变、炎症、溃疡、萎缩性胃炎及胃癌组中的分布差异均无统计学意义.结论广州消化道疾病患者中H.pylori的感染与胃黏膜病理改变显著相关,而广州地区消化道疾病患者中H.pylori高毒力亚型的强致病性并不明显,需扩大标本量,再细化疾病种类进一步分析高毒力H.pylori对胃肠道疾病发生的影响. 目的分析研究廣州地區消化道疾病患者中H.pylori ureA、vacA s1基因和cagA基因亞型(ABC、ABD、ABAB、AAD等)的分佈狀況及其與胃黏膜病理檢測結果間的相關性.方法隨機選取227例消化道疾病患者的胃黏膜標本,分彆來自病理組織學檢測無病理改變者46例,慢性胃炎130例,消化性潰瘍29例,萎縮性胃炎15例,胃癌7例.併用實時熒光定量PCR檢測H.pylori ureA基因、vacA s1基因,用PCR擴增cagA羧基耑EPIYA基序所在區,然後測序確定其亞型.以保守基因ureA的存在判斷H.pylori感染.結果 227例消化道疾病患者中,有50.7% (115/227)的患者H.pylori暘性,其中,vacA s1基因暘性91.3%(105/115),cagA基因暘性78.3%(90/115).4種cagA-EPIYA亞型分佈為,ABC 17.8%(16/90)、ABD 78.9%(71/90)、AAD 2.2%(2/90)、ABAB 1.1%(1/90).無病理改變組中H.pylori 暘性32.6%(15/46),vacA s1基因暘性28.3%(13/46),cagA基因暘性26.1%(12/46);慢性胃炎組H.pylori 暘性48.5%(63/130),vacA s1基因暘性43.8%(57/130),cagA基因暘性36.2%(47/130);潰瘍組H.pylori 暘性72.4%(21/29),vacA s1基因暘性65.5%(19/29),cagA基因暘性55.2%(16/29);萎縮性胃炎組H.pylori 暘性66.7%(10/15),vacA s1基因暘性66.7%(10/15),cagA基因暘性66.7%(10/15);胃癌組H.pylori暘性85.7%(6/7),vacA s1基因暘性85.7%(6/7),cagA基因暘性71.4%(5/7).H.pylori在不同胃黏膜病理組的分佈差異有統計學意義(χ2=16.72;P<0.01),潰瘍、萎縮性胃炎、胃癌組中H.pylori的分佈明顯高于無病理改變與炎癥組(χ2=16.02;P<0.01).但在H.pylori暘性患者中,彊毒力因子vacA s1基因(χ2=2.00;P=0.74)、cagA基因(χ2=3.44;P=0.49)及cagA-EPIYA亞型(χ2=3.66;P=0.45)在無病理改變、炎癥、潰瘍、萎縮性胃炎及胃癌組中的分佈差異均無統計學意義.結論廣州消化道疾病患者中H.pylori的感染與胃黏膜病理改變顯著相關,而廣州地區消化道疾病患者中H.pylori高毒力亞型的彊緻病性併不明顯,需擴大標本量,再細化疾病種類進一步分析高毒力H.pylori對胃腸道疾病髮生的影響.
목적 분석연구엄주지구소화도질병환자중H.pylori ureA、vacA s1기인화cagA기인아형(ABC、ABD、ABAB、AAD등)적분포상황급기여위점막병리검측결과간적상관성.방법 수궤선취227례소화도질병환자적위점막표본,분별래자병리조직학검측무병리개변자46례,만성위염130례,소화성궤양29례,위축성위염15례,위암7례.병용실시형광정량PCR검측H.pylori ureA기인、vacA s1기인,용PCR확증cagA최기단EPIYA기서소재구,연후측서학정기아형.이보수기인ureA적존재판단H.pylori감염.결과 227례소화도질병환자중,유50.7% (115/227)적환자H.pylori양성,기중,vacA s1기인양성91.3%(105/115),cagA기인양성78.3%(90/115).4충cagA-EPIYA아형분포위,ABC 17.8%(16/90)、ABD 78.9%(71/90)、AAD 2.2%(2/90)、ABAB 1.1%(1/90).무병리개변조중H.pylori 양성32.6%(15/46),vacA s1기인양성28.3%(13/46),cagA기인양성26.1%(12/46);만성위염조H.pylori 양성48.5%(63/130),vacA s1기인양성43.8%(57/130),cagA기인양성36.2%(47/130);궤양조H.pylori 양성72.4%(21/29),vacA s1기인양성65.5%(19/29),cagA기인양성55.2%(16/29);위축성위염조H.pylori 양성66.7%(10/15),vacA s1기인양성66.7%(10/15),cagA기인양성66.7%(10/15);위암조H.pylori양성85.7%(6/7),vacA s1기인양성85.7%(6/7),cagA기인양성71.4%(5/7).H.pylori재불동위점막병리조적분포차이유통계학의의(χ2=16.72;P<0.01),궤양、위축성위염、위암조중H.pylori적분포명현고우무병리개변여염증조(χ2=16.02;P<0.01).단재H.pylori양성환자중,강독력인자vacA s1기인(χ2=2.00;P=0.74)、cagA기인(χ2=3.44;P=0.49)급cagA-EPIYA아형(χ2=3.66;P=0.45)재무병리개변、염증、궤양、위축성위염급위암조중적분포차이균무통계학의의.결론 엄주소화도질병환자중H.pylori적감염여위점막병리개변현저상관,이엄주지구소화도질병환자중H.pylori고독력아형적강치병성병불명현,수확대표본량,재세화질병충류진일보분석고독력H.pylori대위장도질병발생적영향.
Objective To detect the distribution of H.pylori ureA, vacA s1 gene and cagA subtype(ABC, ABD, ABAB, AAD, et al) in patients with digestive diseases in Guangzhou and investigate the relationship with the pathological findings of gastric mucosa.Methods A total of 227 randomly selected gastric mucosa from patients with digestive diseases were enrolled in the research, including 46 without pathological changes, 130 with chronic gastritis, 29 with peptic ulcer, 15 with atrophic gastritis and 7 with gastric cancer.Real-time PCR assay were used to detect Helicobacter pylori ureA gene and vacA s1 gene.EPIYA motifs in the 3′ region of cagA were amplified by conventional PCR followed by subtype sequencing. The conserved gene ureA was used to detect H.pylori infection.Results Among the 227 patients with digestive diseases, 50.7% (115/227) patients were H.pylori positive, in which 91.3%(105/115) carried vacA s1 and 78.3% (90/115) carried cagA. Four types of cagA-EPIYA subtype were detected, including ABC 17.8%(16/90), ABD 78.9%(71/90), AAD 2.2%(2/90) and ABAB 1.1%(1/90).In the non-pathological change group, 32.6% (15/46) were H.pylori positive, in which 28.3% (13/46) carried vacA s1 and 26.1% (12/46) carried cagA;in chronic gastritis group, it was 48.5% (63/130), 43.8% (57/130) and 36.2% (47/130), respectively;in ulcer group, it was 72.4% (21/29), 65.5% (19/29) and 55.2% (16/29), respectively;in atrophic gastritis group, it was 66.7% (10/15), 66.7% (10/15) and 66.7% (10/15), respectively;in gastric cancer group, it was 85.7% (6/7), 85.7% (6/7) and 71.4% (5/7), respectively.The distribution of H.pylori among the 4 groups had statistical significance (χ2=16.72;P<0.01). H.pylori was more prevalent in ulcer, atrophic gastritis and cancer group than in inflammation group and non-pathological change group (χ2=16.02;P<0.01).In patients infected by H.pylori, there was no significant difference in the distribution of vacA s1 gene as high virulence factors among non-pathological change, inflammation, ulcer, atrophic gastritis and cancer group (χ2=2.00;P=0.74), as well as cagA (χ2=3.44;P=0.49) and EPIYA subtypes (χ2=3.66;P=0.45).Conclusions H.pylori infection is significantly associated with the pathological change of gastric mucosa for patients with digestive diseases in Guangzhou, while the relationship with the pathogenicity of H.pylori with high virulence genotype is not significant.More samples and diseases reclassification are needed to make an advanced analysis of the effect of H.pylori with high virulence in gastrointestinal diseases development.