幽门螺杆菌cagA基因和血清CagA抗体与VacA表达关系的研究

目的;探讨幽门螺杆菌cagA基因和血清CagA抗体与VacA表达的关系。方法：用聚合酶链反应法（PCR）测定由62例慢性胃炎、消化性溃疡和胃癌患者胃罕粘膜分离获得Hp菌株：用酶免疫技术测定患者血清HpCagA抗体;用Hela细胞培养法测定Hp菌株VacA活性。结果：cagA基因阳性和阴性Hp菌株表达VacA阳必班组分别为40.00%和33.33%(P>0.05);血清CagA抗体阳性和阴性患者感染Hp菌株体外产生VacA阳性率分别为33.33%和42.11%(P>0.05)。结论：HpcagA基因和血清CagA抗体与VacA表达之间无相互依赖关系,vacA基因是一个独立的标志物。     

幽门螺杆菌及VacA和CagA抗体与上消化道疾病关系的研究

目的：探讨幽门螺杆菌（Helicobacter pylori,Hp)与上消化道疾病的关系。方法：采用免疫印迹法,对慢性胃炎192例和十二指肠溃疡87例患者血清Hp进行检测分析,对Hp阳性的136例慢性胃炎和75例十二指肠溃疡患者进行VacA、CagA抗体检测。结果：慢性胃炎192例中检测出Hp阳性136例,阳性率为70.84%,十二指肠溃疡患者Hp阳性率为86.21%。在211例Hp阳性者中VacA、CagA抗体检测出阳性率为52.60%,而慢性胃炎与十二指肠溃疡有显著的差异。结论：提示Hp感染与上消化道疾病的发生有重要的生物学意义。     

幽门螺杆菌cagA基因和血清CagA抗体与VacA表达关系的研究

目的：探讨幽门螺杆菌cagA基因和血清CagA抗体与VacA表达的关系。方法：用聚合酶镇反应法（PCR）测定由62例慢性胃炎、消化性溃疡和胃癌患者胃窦粘膜分离获得Hp菌株;用酶免疫技术测定患者血清HpCagA抗体;用Hela细胞培养法测定Hp菌株VacA活性。结果：cagA基因阳性和阴性Hp菌株表达VacA阳性率分别为40．00％和33．33％（P＞0.05）;血清CagA抗体阳性和阴性患者感染Hp菌株体外产生VacA阳性率分别为33．33％和42．11％（P＞0.05）。结论：HpcagA基因和血清CagA抗体与VacA表达之间无相互依赖关系,vacA基因是一个独立的标志物。     

抗Hp-IgG检测在消化性溃疡治疗中的意义

目的：通过对检测血清抗幽门螺杆菌抗体（抗Hp-IgG）阳性的胃、十二指肠溃疡患者治疗前后抗Hp-IgC的变化观察，评价抗Hp-IgG检测在消化性溃疡治疗中的意义。方法：选择106例经胃镜检查诊断为胃或十二指肠溃疡患者，同时胃粘膜活检标本快速尿素酶试验、涂片染色联合检测Hp作为“金标准”，“金标准”阳性者为Hp感染的治疗观察对象。结果：服药2周后检查平均Hp清除率为75．65％，其中十二指肠球部溃疡为77．8％（56／72）、胃溃疡73．5％（25／34）溃疡愈合率为41．3％，其中十二指肠球部溃疡44．4％（32／72），胃溃疡38．2％（13／34）。治疗4周后溃疡愈合率为93．5％，其中十二指肠球部溃疡为95．8％（69／72），胃溃疡为91．2％（31／34），Hp清除率达93％。结论：检测血清中抗Hp- gG可以了解Hp清除情况．以指导临床用药，用于Hp根除后的随访。     

幽门螺杆菌多部位检测与临床及组织学表现的关系

目的 观察幽门螺杆菌（Hp）与胃及十二指肠粘膜病理组织学表现之间的关系。方法 对60例慢性胃炎和22例十二指肠溃疡患者经胃镜分别从胃窦、胃体、十二肠球部取活检,进行组织学检测。结果 在活动性胃炎中无论是胃窦部或胃体部Hp检出率近100％,显著地活动性十二指肠球炎的球部Hp的检出率,胃窦部Hp总检出率及活动性上的发生率均显著高于胃体部及十二指肠球部。22例十二指肠球部溃疡Hp在球部的检出率为54％,显著低于其在胃窦部组织中Hp100％的检出率。结论 Hp感染是胃粘膜活动性炎症的重要原因,并以此为基础发展为重度粘膜炎及溃疡病,因此,对某些慢性胃炎患者应及早进行Hp根除治疗。     

幽门螺杆菌感染与慢性胃病关系的检测分析

目的：了解消化性溃疡和慢性胃炎患者感染的幽门螺杆菌（Hp）cagA／vacA优势基因型及不同基因型Hp感染、混合感染与疾病的关系。方法：选择胃窦、胃体双份活检标本均培养出Hp的42例慢性胃炎（CG）和36例消化性溃疡（PU）患者作为研究对象，采用聚合酶链反应检测156份Hp分离株的cagA基因、vacA基因的信号区（s）和中间区（m）亚型，分析Hp基因型及多株Hp混合感染在CG和PU中的分布。部分优势基因型的扩增产物T—A克隆后进行核苷酸序列测定。结果：cagA基因的检测中，78例病人的胃窦标本中有？5例（96．2％）为cagA阳性，相应的胃体标本中，76例（97．4％）为cagA阳性，有1例（1．3％）患者胃窦、胃体检出cagA状态不一的Hp混合菌株。在胃窦标本的vacA基因分型中，sla／ml、sla／m2、sla／mlb、sla／mib—m．24种vacA基因型在78例患者中所占比例分别为6．4％（5／78）、55．1％（43／78）、26．9％（21／78）和1．3％（1／78），多株混合感染为3．8％（3／78）；而相应的胃体标本中，前述四种vacA基因型所占比例依次为6．4％（5／78）、53．8％（42／78）、25．6％（20／78）和3．8％（3／78），多株混合感染为5．1％（4／78）。c8gA＋sla／m2和cagA＋sla／mlb在胃窦标本中占51．3％（40／78）和26．9％（21／78），而在相应的胃体标本中占52．6％（41／78）和25．6％（20／78）。少量胃窦、胃体标本中vacA基因8区和m区不能分型，未发现8lb、82和mla型。联合胃窦、冒体标本分析，16例（20．5％）患者中检出不同基因型的多株Hp菌株，同一胃内多部位采样比单部位采样者有更高的混合感染检出率。HpcagA基因、vaeA基因型、cagA／vaeA基因组合及不同基因型菌株混合感染在CG和PU中的分布差异均无显著性（P〉0．05）。6株8h型Hp菌株的8区扩增产物与报道的ala型60190株核苷酸序列同源性为93．15—94．86％，4株n正型Hp菌株的m区扩增产物与报道的m2型87～203株核苷酸序列之间同源性为93．63—97．61％。结论：cagA＋sla／m2是本地区慢性胃炎或消化性溃疡中最主要的Hp菌株的优势基因型，其次为cagA＋sla／mlb，部分vacAsla／m2型优势分布菌株其核苷酸序列与国外报道的参考菌株比较有较高的同源性，部分患者同时感染不同基因型的多株Hp，但均与所致疾病类型和严重程度无密切相关。     

上海崇明地区幽门螺杆菌cagA基因多态性与感染临床结局的关系

目的探讨上海崇明地区幽门螺杆菌（Helicobacter pylori,Hp）的cagA基因的多态性与感染临床结局的关系。方法采用PCR法检测100株临床分离株cagA基因亚型,获得东亚型和西方型2种基因型。分析cagA基因亚型与消化道疾病间的关系。结果100株Hp中72株检出cagA基因,其中81．9％为cagA基因东亚型,15．3％为西方型,2．8％为同时存在着2种基因型。胃癌与慢性萎缩性胃炎患者中cagA基因东亚型菌株均显著高于胃溃疡、十二指肠溃疡患者,而十二指肠溃疡cagA基因西方型菌株的比率显著高于其余4种疾病类型。结论本地区感染Hp以cagA基因东亚型为主,cagA基因东亚型菌株与胃癌、慢性萎缩性胃炎密切相关,而cagA基因西方型菌株与十二指肠溃疡密切相关。推测cagA基因多态性对由Hp引起的感染性疾病的发病机制可能起一定的作用。     

不同消化性疾病患者幽门螺杆菌毒力基因类型及意义研究

目的分析用不同消化性疾病来源的幽门螺杆菌(Hp)毒力基因的检测结果及其意义。方法收集该院胃镜室于2015年1月至2016年7月采集的628例患者胃活检标本,分离培养Hp,检测其携带的毒力基因,并探讨Hp与慢性萎缩性胃炎(CAG)、慢性浅表性胃炎(CSG)、消化性溃疡(PUD)的相关性。结果 628份胃活检标本中成功分离出214株Hp,选取其中172株提取DNA,发现Hp携带cagA、vacA、dupA、iceA、oipA、luxS多种毒力基因,其中vacA s1m1是CSG的危险因素,vacA s1m2与iceA1+/iceA2+提高PUD的发生率,dupA+提高十二指肠溃疡危险度。结论不同消化性疾病与Hp感染密切相关,dupA可考虑作为Hp致十二指肠溃疡的标记基因,vacA s1m2与iceA1+/iceA2+增加了发生PUD的危险性。     

胃上皮化生、幽门螺杆菌感染和十二指肠溃疡的关系研究

目的：幽门螺杆菌（Hp）是引起消化性溃疡的重要致病因素，十二指肠溃疡（DU）患者HP感染率约90％。正常情况下HP主要定植于胃型上皮，也有DU患者十二指肠可见胃上皮化生，可供HP定植引起溃疡形成。本研究是经胃镜检查确诊为活动期十二指肠溃疡患者，检测十二指肠胃上皮化生、HP感染的情况，并与胃溃疡（GU）、功能性消化不良（FD）患者资料进行对照。结论：本组资料表明：十二指肠球部HP的检出率在DU、GU、FD三组差异无显著性。DU、GU、FD组的十二指肠胃上皮化生检出率分别为57．9％、11．1％、16．7％，3组患者在十二指肠球部均可出现胃上皮化生，但DU组显著高于其他2组，推测胃上皮化生与DU组的发病有关。     

幽门螺杆菌细胞毒素相关蛋白A、细胞毒素相关蛋白E、细胞空泡毒素A基因型与上消化道疾病的关系

目的分析幽门螺杆菌(Hp)的细胞毒素相关蛋白A(cagA)、细胞毒素相关蛋白E(cagE)、细胞空泡毒素A(vacA)基因型与上消化道疾病的关系。方法选取112例上消化道疾病患者,对其胃黏膜组织中Hp菌株的cagA、cagE、vacA基因型进行检测和分析。结果所有患者胃黏膜样本中的Hp菌株均为cagA基因和cagE基因阳性表达,阳性率均为100%。患者的vacAs1/m~2表型的阳性率最高,分别为54.1%和60.5%,其次为vacAs1/mlb表型和vacAs1/m~-表型,阳性率分别为13.2%~21.1%。消化性溃疡患者和慢性胃炎患者的Hp基因各表型的阳性率的差异均无统计学意义(P0.05)。结论上消化道疾病患者胃黏膜组织中的Hp菌株呈现cagA、cagE、vacAs1/m~2等基因亚型的优势表达,说明这些毒力因子表型在Hp引发和促进上消化道疾病的过程中具有重要的作用,但与上消化道疾病类型缺乏相关性。     

幽门螺杆菌cagA、vacA、iceA基因与儿童结节性胃炎的关系

目的：探讨幽门螺杆菌（HP）cagA、VaCA、iceA基因与儿童结节性胃炎的关系。方法：收集2007年5月-2008年1月行胃镜检查确诊Hp感染的22例结节性胃炎和22例非结节性胃炎患儿的胃粘膜组织,分别用聚合酶链反应（PCR）检测cagA、vacA和iceA基因。病理检查了解胃窦粘膜炎症程度。结果：结节性胃炎组中cagA基因单独检出率为68．2％,VaCAs1／ml单独捡出率为13．6％,vacAs1／m2单独检出率为45．5％,iceA1单独检出率为72．7％,iceA2单独检出率为18．2％．非结节性胃炎组中cagA基因单独检出率为68．2％,vacAs1／ml单独检出率为22．7％,vacAs1／m2单独检出率为27．3％。iceA1单独检出率为63．6％．iceA2单独检出率为22．7％。不同基因型菌株在结节性胃炎和非结节性胃炎中的检出率无统计学意义（P〉0．05）。在轻度、轻一中度、中度慢性结节性胃炎中,cagA型茵株检出率分别为66．7％、50％、75Voo,vacA s1／ml型菌株检出率分别为11．1％、0%、25%,VaCAs1／m2型菌株检出率分别为55．6％、25％、37．5％,iceA1型菌株检出率分别为88．9%、50％、75%．iceA2型菌株在轻度、轻一中度、中度慢性结节性胃炎中的检出率分别为0％、50％、25％,不同基因型菌株与结节性胃炎胃窦粘膜炎症的严重程度无关（P〉0．05）。结论：cagA、vacA、iceA基因与结节性胃炎、胃粘膜的炎症严重程度无关。提示除菌株因素外．宿主因素、环境因素在结节性胃炎的形成过程中可能发挥了重要作用。     

Genotyping of Helicobacter pylori strains from gastric biopsies by multiplex polymerase chain reaction. How advantageous is it?

Recent application of multiplex polymerase chain reaction (PCR) for genotyping Helicobacter pylori direct from biopsies revealed variable results (detection of amplicons from DNA extracted by boiling biopsies, variable size amplicons and deletions, uniform intensity of amplicon bands). We aimed to look at how applicable the technique is for determining cagA and vacA genotypes and to correlate the results with the severity of the disease. H. pylori strains from 52 patients (35 duodenal ulcers [DUs], 7 gastric ulcers [GUs], 10 gastritis) were included. Three antral biopsies were obtained for Campylobacter-like organism (CLO) and PCR. Primers for cagA, vacA s1s2, and m1m2 alleles were used. No PCR amplicons were detected from boiling biopsies; thus, DNA was extracted by QIAamp kit. H. pylori was positive in 84.6% of the patients (85.7% DU, 100% GU, and 70% gastritis). The cagA gene was detected in 86.6% DU, 71.4% GU, and 57.0% gastritis patients. The vacA allelic distribution among cagA-positive strains was 80.7% s1m1 in DU and 60.0% in GU patients, whereas 75.0% of gastritis had s1m2. No variability in the amplicon sizes was found, and the intensity of the amplicon bands was not uniform. A deleted band of approximately 420 bp below the m1 band was detected in strains from 2 DU and 1 GU patients. Although the multiplex PCR is a rapid and an effective tool for detecting several genes in a single-step system, one has to adjust for optimization of the technique when genotyping H. pylori direct from biopsies. A significant association was found between the cagA-positive vacA-s1m1 genotype and peptic ulcers.     

广州地区消化道疾病患者中H.pylori ureA和vacA s1基因及cagA基因亚型分布

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.

Abstract：

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.     

cagA vacA alelles and babA2 genotypes of Helicobacter pylori associated with gastric disease in Brazilian adult patients

Helicobacter pylori is an important human pathogen that causes chronic gastritis and is associated with development of peptic ulcer disease and gastric malignancies. The vacuolating cytotoxin (vacA), cagA gene, and babA2 gene are important virulence factor involving gastric diseases. Eighty-nine Helicobacter pylori-positive gastric biopsies were analyzed by polymerase chain reaction and Southern blotting for H. pylori detection and genotyping with primer pairs from each virulence gene. Fifty-three strains (59%) were common vacA genotype s1/m1, and only 14 (16%) were s2/m2, 12% of strains was found to have multiple infection. The cagA presence was detected in 48% (43 strains) and babA2 gene was detected in 44% of our H. pylori strains. We observed high percentage of s1/m1 strains with chronic gastritis and peptic ulcer and a significant correlation between cagA presence with the s1 allele and babA2 gene with chronic gastritis.     

Phospholipase C activity of Helicobacter pylori is not associated with the presence of the cagA gene

BACKGROUND: Knowledge about the possible role of phospholipase C (PLC) activity of microbial pathogens in the development of disease is increasing. Recently attention has focused on investigating PLC activity elaborated by Helicobacter pylori, but the role of this enzyme in H. pylori pathogenesis is still unknown. The aim of this study was to correlate PLC-activity of H. pylori on the basis of the cagA status with the clinical diagnosis of the patients. MATERIALS AND METHODS: Helicobacter pylori was isolated from patients with gastritis (G; n = 38), duodenal ulcer (DU; n = 15), gastric ulcer (GU; n = 11) and gastric cancer (GC; n = 12). Polymerase chain reaction primers DZ3/R009 which amplified a 1350-bp fragment were used to detect the cagA gene. PLC activity was determined using p-nitrophenylphosphorylcholine as substrate. RESULTS: Of the strains, 60% were cagA(+) and 40% were cagA(-). All strains showed PLC activity (2.20 +/- 0.91 U mg(-1) protein). PLC activity showed no association with the cagA status: cagA(+) (2.21 +/- 1.03 U mg(-1) protein), cagA(-) (2.18 +/- 0.79 U mg(-1) protein). Patients with GU had the highest PLC activity (2.77 +/- 1.26 U mg(-1) protein) and patients with GC had the lowest activity (1.8 +/- 0.57 U mg(-1) protein). CONCLUSIONS: Although PLC activity was present in all strains tested, it may only have pathological importance in patients with GU. However, the extent of PLC activity was independent of the presence of the cagA gene.     

胃肠相关疾病中幽门螺杆菌感染与胃黏膜白细胞介素-8含量的关系

目的　研究各种胃肠疾病幽门螺杆菌 (Hp)感染情况及其与胃黏膜白细胞介素 8(IL 8)含量的关系。 方法　采用双抗体夹心酶联免疫吸附试验检测 10 2例Hp感染与非感染患者胃黏膜匀浆上清液中的白细胞介素 8含量 ,其中胃镜下黏膜正常者 5例 ,单纯性慢性胃炎 (CG) 2 5例 ,十二指肠球部溃疡 (DU) 36例 ,胃溃疡 (GU) 15例 ,胃癌(Gca) 2 1例。结果　 10 2例中有 6 0例感染了Hp(5 8.8% ) ,其中以十二指肠球部溃疡组Hp感染率最高 (88.9% ) ,明显高于其他组 (均P <0 .0 5 ) ,Hp感染者胃黏膜IL 8含量明显高于非Hp感染者 (P <0 .0 1) ;GU、Gca、DU、CG组胃黏膜IL 8含量均明显高于黏膜正常组 (均P <0 .0 5 ) ,GU、Gca、DU组又明显高于CG组 (均P <0 .0 5 ) ,而GU、Gca、DU组间比较差异无统计学意义 (均P >0 .0 5 ) ;同时发现中度胃炎黏膜IL 8含量明显高于轻度胃炎 ,活动性胃炎又明显高于非活动性胃炎 (均P <0 .0 5 )。结论　Hp感染者与非感染者胃黏膜IL 8含量存在差异 ,疾病组胃黏膜IL 8含量明显高于正常黏膜 ,并与胃炎炎症程度和活动性有一定相关性 ,推测IL 8可能参与了Hp相关性胃炎胃黏膜损伤机制     

Frequencies of serum antibodies to Helicobacter pylori CagA and VacA in a Turkish population with various gastroduodenal diseases

Infection with Helicobacter pylori (H. pylori) strains secreting cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) proteins is associated with more severe gastroduodenal pathologies. However, this association varies among geographical regions and ethnic groups. We investigated the frequencies of antibodies to CagA and VacA proteins in 131 H. pylori-infected dyspeptic patients [40 duodenal ulcer (DU), 19 gastric ulcer (GU), 28 gastric cancer (GC), and 44 non-ulcer dyspepsia (NUD)] across 30 H. pylori-infected and endoscopically normal asymptomatic subjects (AS). Anti-CagA and anti-VacA antibodies were detected by Western blotting. The positivity rates of anti-CagA and anti-VacA antibodies were higher in patients with DU (92.5 and 75%), GU (89.5 and 84.2%) and GC (96.4 and 85.7%) than patients with NUD (70.5 and 50%) and AS (50 and 23.3%) (p < 0.05). CagA+ VacA+ phenotype was more frequent in patients with DU, GU and GC than patients with NUD and AS (75, 84.2, 85.7 vs. 47.7 and 20%, respectively) (p < 0.01). Our results showed that there is a significantly positive association between the presence of anti-CagA and anti-VacA antibodies and DU, GU and GC in our region.     

幽门螺杆菌感染与十二指肠胃上皮化生及胃泌素之间关系的研究

目的　通过对幽门螺杆菌 (Hp)感染与十二指肠胃上皮化生 (DGM )及胃泌素 (GAS)关系的研究 ,探讨Hp导致十二指肠溃疡 (DU)的发病机制。 方法　检测了 12 1例患者内镜、病理、Hp感染及DGM情况。同时测定了其中 6 6例患者的血清GAS浓度。结果　球部有溃疡者 ,胃及球部Hp检出率均显著高于球部无溃疡者 (P <0 .0 0 1) ;但球部Hp检出率在DU与CU、GU与CG之间无差别 (P >0 .0 5 ) ;球部有溃疡者DGM的检出率显著高于球部无溃疡者 (P <0 .0 0 1) ,且前者的DGM程度更重 (P <0 .0 0 1) ,但在DU与CU、GU与CG之间无差别 (P >0 .0 5 ) ;胃部Hp阳性者DGM的发生率 (73.0 % )显著高于胃部Hp阴性者 (37.5 % ,P <0 .0 0 1) ,DGM( )及以上者在Hp阳性组发生率 (47.2 % )也高于Hp阴性组 (2 1.9% ,P <0 .0 5 ) ;Hp阳性者血清GAS浓度显著高于Hp阴性者 (P <0 .0 1) ,但血清GAS浓度在Hp阳性的DU、CU、GU与CG之间无差别(P >0 .0 5 ) ;有DGM者血清GAS浓度也显著高于无DGM者 (P <0 .0 1) ,且随着DGM程度的加重 ,血清GAS浓度早递增趋势 ,两者呈正相关 (rs=0 .4 2 ,P <0 .0 1)。结论　Hp感染特别是十二指肠Hp定植及DGM是影响DU发生、发展的两大危险因素。Hp可影响DGM的发生与发展 ,其中部分可能通过增加血清GAS分泌的作用。