硒酵母胶囊治疗慢性萎缩性胃炎疗效观察

慢性萎缩性胃炎是公认的癌前病变,通常为慢性浅表性胃炎-萎缩性胃炎-肠上皮化生-异型增生-胃癌是一个相对时间较长的演变过程,故慢性萎缩性胃炎伴肠上皮化生和（或）异型增生的诊治,一直是医学界的研究热点。     

胃癌形成中survivin与cyclinD1的表达及临床意义

目的:探讨survivin及cyclinD1基因表达在胃癌发生发展过程中的作用及其临床意义。方法:采用免疫组织化学染色(SP法)检测12例慢性浅表性胃炎、32例胃黏膜肠上皮化生、32例异型增生和50例胃癌组织中survivin与cyclinD1的表达。结果:慢性浅表性胃炎、肠上皮化生、异型增生和胃癌组织中survivin阳性率分别为0、21.9%、37.5%和54.0%,cyclinD1表达阳性率8.3%、15.6%、34.4%和48.0%,survivin与cyclinD1在肠上皮化生中的表达均明显低于在胃癌组织中的表达(P<0.05),而两者在肠上皮化生与异型增生、异型增生与胃癌组织间差异均无显著性(P>0.05)。survivin阳性表达在不同肿瘤大小、临床分期、血管浸润、淋巴结转移间差异均无显著性(P>0.05),而在不同组织分化程度中差异有显著性(P<0.05);cyclinD1表达在不同组织分化程度、血管浸润及淋巴结转移间差异有显著性(P<0.05),在肿瘤大小及临床分期间差异无显著性(P>0.05)。胃癌组织中,survivin与cyclinD1表达正相关。结论:Survivin及cyclinD1基因表达在胃癌发生发展过程中起着重要作用,它们的检测对胃癌的早期诊断、恶性度及预后评估提供有效的依据。     

慢性萎缩性胃炎的胃镜下表现与病理诊断

正1988年,有学者[1]提出了胃癌发生模式是正常胃黏膜-浅表性胃炎-萎缩性胃炎-小肠型肠上皮化生-大肠型肠上皮化生-异型增生(中重度)-胃癌,对于慢性萎缩性胃炎(CAG)进行早期诊断和及时治疗是降低胃癌发生率的有效手段。CAG是一种临床常见的慢性消化系统疾病,病程常呈迁延不愈,而CAG合并胃黏膜异型增生是一种常见的癌前病变[2]。CAG患者的胃黏膜组织存在着黏膜炎症、腺体萎缩、肠上皮化生和异型增生等     

胃粘膜中Survivin与cyclinD1表达及其相关性

目的 探讨Survivin及CyclinD1基因表达在胃癌发生发展过程中的作用。 方法 采用免疫组织化学染色(SP法)检测12例慢性浅表性胃炎、32例胃粘膜肠上皮化生、32例异型增生和50例胃癌组织中Survivin与CyclinD1 表达。结果 慢性浅表性胃炎、肠上皮化生、异型增生和胃癌组织中Survivin阳性率分别为0、21.9%、37.5%和54%，CyclinD1 表达阳性率8.3%、15.6%、34.4%和48%，Survivin与CyclinD1肠上皮化生组表达均明显低于胃癌组（p<0.05）,而两者在肠上皮化生与异型增生、异型增生与胃癌组间均无显著性差异（p>0.05）。Survivin阳性表达与肿瘤大小、临床分期、血管浸润、淋巴结转移均无显著性差异（p >0.05），而组织分化关系密切（p<0.05）；CyclinD1表达与肿瘤分化程度、血管浸润及淋巴结转移关系密切（p<0.05），而肿瘤大小及临床分期无关（p>0.05）。胃癌中，Survivin与CyclinD1表达正相关。结论 Survivin及CyclinD1基因表达在胃癌发生发展过程中起着重要作用，它们的检测对胃癌的早期诊断、恶性度及预后评估提供有效的依据。     

胃癌前病变环氧合酶-2蛋白的表达及中医辨证

目的:探讨胃癌前病变中环氧合酶-2蛋白的表达及中医辨证.方法:采用免疫组织化学方法,研究20例慢性胃炎、16例萎缩性胃炎、15例肠上皮化生、19例不典型增生、12例早期胃癌及28例进展期胃癌患者的环氧合酶-2蛋白的表达情况,比较各种辨证分型与病理的关系.结果:环氧合酶-2蛋白在浅表性胃炎、萎缩性胃炎、肠化生、不典型增生、早期胃癌及进展期胃癌中的表达逐渐增强;其中肠上皮化生、不典型增生、早期胃癌及进展期胃癌与慢性胃炎相比有显著差异(P均<0.01);不典型增生与早期胃癌相比无显著差异(P>0.05),与进展期胃癌相比有显著差异(P<0.01).在疾病发展的不同阶段,中医辨证不同,浅表性胃炎-肠上皮化生阶段多属脾胃虚弱型,肠上皮化生-早期胃癌阶段多属湿热邪毒型,进展期胃癌阶段多属气滞血瘀型.结论:环氧合酶-2蛋白可能参与胃癌的发生发展过程.     

胃上皮细胞动力学变化与胃癌关系研究

目的研究胃上皮细胞动力学变化与胃癌关系,探讨胃癌发病的分子机制。方法分别用切口末端标记法(TUNEL)、免疫组织化学(SP)法对12例正常胃黏膜、38例浅表性胃炎、28例萎缩性胃炎伴肠上皮化生、10例异型增生和40例胃癌的活检组织进行细胞凋亡、增殖细胞核抗原(PCNA)的检测。结果正常胃黏膜、浅表性胃炎、肠上皮化生、异型增生和胃癌的细胞凋亡指数分别为(2.1±0.5)%、(6.2±2.1)%、(9.8±3.1)%、(5.8±1.6)%和(5.3±1.5)%;细胞增殖指数分别为(3.20±1.03)%、(12.3±3.4)%、(22.1±7.2)%、(43.5±10.7)%、(65.7±12.1)%,浅表性胃炎组、肠上皮化生组凋亡指数与增殖标记指数呈显著正相关(P<0.05),异型增生组、胃癌组凋亡指数与增殖标记指数呈显著负相关(P<0.01)。结论从浅表性胃炎到胃癌的演化序列中,胃上皮细胞动力学出现紊乱,这可能是胃癌发病的分子机制之一。     

幽门螺杆菌感染及PCNA表达与胃腺癌的相关性研究

目的 :探讨幽门螺杆菌感染及PCNA表达与胃癌发生的关系。方法 :对 183例手术切除或胃镜活检标本采用简易快速尿素酶反应检测HP感染情况 ,免疫组化采用SP法检测PCNA的表达强度。结果 :慢性浅表性胃炎 ,慢性萎缩性胃炎伴肠上皮化生、中重度不典型增生及胃癌的HP感染与PCNA表达的强度不同 ,均呈递增趋势 ,同时在慢性萎缩性胃炎伴肠上皮化生及中重度不典型增生组中 ,HP阳性患者PCNA表达显著高于HP阴性患者 ,两者比较差异有显著性(P <0 .0 5 )。结论 :HP感染的胃粘膜处于高增殖状态 ,可能具有较高的癌变易感性     

SHH在肠型胃癌发展中的表达及意义

目的检测人类刺猬因子（SHH）在肠型胃癌各阶段病变的表达情况及与尾型同源盒转录因子2（CDX2）的相关性,探讨SHH在肠型胃癌发生、发展中的作用。方法采用免疫组织化学方法,检测慢性浅表性胃炎、慢性萎缩性胃炎伴肠化生、不典型增生及肠型胃癌组织SHH和CDX2蛋白的表达情况。结果 SHH在萎缩性胃炎伴肠化生胃黏膜组织表达率低于在慢性浅表性胃炎的表达率（χ2=3.914,P〈0.05）,在肠型胃癌组织的表达率高于在浅表性胃炎的表达率（χ2=10.286,P〈0.05）。CDX2蛋白在慢性浅表性胃炎组织不表达,在萎缩性胃炎肠化生胃黏膜的表达率高于在不典型增生和肠型胃癌组织的表达率（χ2=9.619、4.904,P〈0.05）。慢性萎缩性胃炎伴肠化病人胃黏膜组织SHH和CDX2蛋白的表达呈负相关（r=-0.384,P〈0.05）。结论 SHH与胃黏膜肠上皮化生和肠型胃癌的发生有关,在胃黏膜肠上皮化生的过程中SHH与CDX2可能互相调节。     

幽门螺旋杆菌感染和FasL蛋白表达在胃癌发生中的变化

目的 探讨幽门螺旋杆菌(H.pylori)感染和Fas配体(FasL)蛋白表达在胃癌(GC)发生发展中的变化.方法 选取2010年1月至2011年9月在上海浦东新区南汇中心医院诊断的胃部病变169例患者,其中慢性浅表性胃炎(CSG)25例、慢性萎缩性胃炎(CAG)28例、肠化生(IM)37例、异型增生(Dy)38例和胃癌(GC)41例.分别检测胃黏膜组织中H.pylori感染和FasL的蛋白表达,分析H.pylori感染和FasL的蛋白在GC发生发展中的相关性.结果 H.pylori感染率和FasL蛋白阳性表达率随着病情的加重而逐渐增高,Dy组及GC组H.pylori感染率比CSG组明显升高(65.8％和75.6％ vs 16.0％)(P＜0.05);IM组、Dy组及GC组FasL蛋白阳性表达率比CSG组明显升高(64.9％、78.9％和92.7％ vs 28.0％)(P＜0.05) ;GC组FasL蛋白阳性表达率比CAG组及IM组明显升高(92.7％vs 60.7％;92.7％ vs 64.9％)(P＜0.05).除CSG外,H.pylori感染与CAG、IM、Dy和GC胃黏膜组织中的FasL蛋白表达具有一致性,差异有统计学意义(P＜0.01).结论 FasL蛋白表达和H.pylori感染对评估胃黏膜癌前病变发展趋势有重要的临床价值,有助于早期发现和诊断GC.     

血吸虫病患者不同胃黏膜病变中Survivin、p53、E-cadherin蛋白表达及临床意义

目的探讨鄱阳湖区域日本血吸虫病患者Survivin、p53、E-cadherin的表达及其临床病理学意义。方法选择鄱阳湖区域确诊为慢性与晚期血吸虫病患者(151例)的胃黏膜标本(其中萎缩性胃炎49例,胃黏膜异形增生30例,不完全性大肠上皮化生34例,胃癌38例)。应用组织芯片和免疫组织化学S-P法检测Survivin、p53、E-cadherin在正常黏膜、癌前病变、胃癌组织中的表达。结果 Survivin蛋白在正常胃黏膜组织壁细胞可见阳性表达,而其他细胞几乎无表达。Survivin蛋白阳性表达率在萎缩性胃炎、不完全性大肠上皮化生、异型增生和胃癌各组分别为51.02%、58.82%、66.67%、86.84%,各组织间比较差异有统计学意义(P<0.05);p53蛋白阳性表达率在正常胃黏膜、萎缩性胃炎、不完全性大肠上皮化生、异型增生和胃癌各组分别为1.32%、16.33%、58.82%、76.67%、92.11%,各组织间比较差异有统计学意义(P<0.05);E-cadherin蛋白在正常胃黏膜表达率为100.00%,在萎缩性胃炎、不完全性大肠上皮化生、异型增生和胃癌各组胃黏膜组织中阳性率分别为83.67%、76.47%、63.33%、26.31%,各组织间比较差异有统计学意义(P<0.05)。Survivin、p53、E-cadherin蛋白表达与胃癌的组织分化程度、浸润程度、淋巴结转移及pTNM分期有关(均P<0.05)。结论 Survivin、p53、E-cadherin蛋白可能参与血吸虫患者胃癌病变的发生发展,可作为较理想的标志物用于胃癌的早期诊断和转移预后的预警。更多     

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.     

Intestinal metaplasia and Helicobacter pylori infection, their relationship and effects of eradication therapy

Intestinal metaplasia is characterized by Goblet cells and Peneth cells in histological examination. It is frequently observed in gastric mucosa with atrophic gastritis and easily diagnosed using Methylene blue stain in endoscopy. Intestinal metaplasia is seemed to occur during the progression of atrophic gastritis. From our prospective endoscopic follow-up study over 8 years, progression of intestinal metaplasia in gastric body is observed in 44.4% out of 27 H. pylori positive patients. Progression of atrophy is also observed in 37.0% of cases. Development of intestinal metaplasia is also assured in other clinical investigations and experimental studies using Mongolian Gerbils. However, reversibility of intestinal metaplasia after H. pylori eradication is under discussion still now. In our study, we can not observe the regression of intestinal metaplasia even 2 years after successful H. pylori eradication.     

幽门螺杆菌根除对不同胃黏膜病变环氧合酶-2表达的影响

目的探讨Hpylori根除对慢性浅表性胃炎和萎缩肠化胃黏膜上皮细胞COX-2表达的影响。方法采用快速尿素酶试验和组织学碱性品红染色法检测胃黏膜Hpylori感染状况;应用免疫组织化学法检测胃黏膜上皮细胞COX-2的表达。结果17例Hpylori阳性慢性浅表性胃炎中11例见不同程度胃黏膜上皮细胞COX-2阳性表达,Hpylori根除后6例COX-2表达消失,2例减弱,2例无改变,1例增强,前后对照差异有显著性(P<0.05)。同时Hpylori根除后12例胃黏膜慢性炎症见不同程度减轻,与COX-2表达变化有较好相关性(P<0.05)。10例Hpylori感染萎缩性胃炎伴肠化生者9例COX-2表达阳性,Hpylori根除后1、2a复查COX-2表达减弱5例,消失2例,1例无变化,1例增强,前后对照差异有显著性(P<0.05),但胃黏膜组织学对照无明显改善。结论根除Hpylori可消除慢性浅表性胃炎胃黏膜上皮细胞COX-2表达,且与慢性炎症程度消退相关。而根除Hpylori虽可减弱萎缩肠化胃黏膜上皮细胞COX-2表达,但不能改善胃黏膜萎缩和肠化状态。     

长春地区慢性胃病患者幽门螺杆菌感染状况调查

目的通过对本地区慢性胃病患者幽门螺杆菌（H.pylori）感染状况调查,了解本地区流行病学特点,为进一步阐明其与慢性胃病发生发展的关系提供理论依据。方法采用ELISA方法测定血清H.pyloriIgG抗体及CagA抗体;采取胃粘膜活检组织进行快速尿素酶试验,调查H.pylori感染情况,分析其与各种疾病的关系。结果1180例慢性胃病患者H.pylori感染率为67.11%,复合性溃疡、十二指肠溃疡、胃溃疡及慢性萎缩性胃炎感染率分别为90.9%、84.57%、83.96%和80.24%。与慢性浅表性胃炎相比差异有显著性。消化性溃疡、慢性萎缩性胃炎、胃癌和胃息肉患者血清Hp-CagA抗体的阳性率明显高于慢性浅表性胃炎（P〈0.05）。结论本地区慢性胃病患者H.pylori感染率高与多数地区的普通人群,H.pylori感染者尤其是CagA阳性者,更易发生慢性萎缩性胃炎、消化性溃疡及胃癌。     

幽门螺杆菌细胞毒素相关蛋白与胃癌的相关性

目的 探讨幽门螺杆菌细胞毒素相关蛋白与胃癌的相关性。方法 采用免疫印迹法检测218例慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)和胃癌(GC)患者血清细胞毒素相关蛋白抗体(CagA)。结果 CagA抗体在218例患者中总检出率为69．27％。在慢性浅表性胃炎、慢性萎缩性胃炎、胃癌患者中CagA抗体阳性率分别为55．43，74．11和90．24％，经x^2检验x^2分割法显示：三组胃疾病阳性率总体间差异有显著性；慢性浅表性胃炎与慢性萎缩性胃炎阳性率比较，差异有显著性；慢性浅表性胃炎与胃癌阳性率比较，差异有非常显著性；慢性萎缩性胃炎与胃癌阳性率比较，差异无显著性。结论 慢性萎缩性胃炎和胃癌的发生与CagA阳性Hp感染有关，定期随访CagA抗体阳性Hp感染特别是已进入慢性萎缩性胃炎阶段的患者，可能有利于胃癌的早期诊断。     

Western blotting of total lysate of Helicobacter pylori in cases of atrophic body gastritis

BACKGROUND: Atrophic body gastritis is considered the first important step in the histogenesis of gastric carcinoma, a multistep process starting from chronic gastritis and progressing through chronic atrophic gastritis, intestinal metaplasia, and dysplasia. Helicobacter pylori is involved in the induction of atrophic body gastritis, but documentation of H. pylori infection is difficult because of the progressive disappearance of the bacterium. Our study aimed to detect past H. pylori infection in patients with atrophic body gastritis. METHODS: We used Western blot analyses of whole bacterial protein lysate of 2 different strains to probe sera from 143 patients. All sera were analyzed by ELISA (Bio-Rad), and results of gastric histology were available for all patients. RESULTS: Among 111 patient sera previously classified as negative for H. pylori infection by ELISA, 106 (95.5%) were positive when assayed by immunoblotting. CONCLUSIONS: Commercial diagnostic reagent sets may fail to detect H. pylori infection. Western blotting of whole bacterial protein extracts could provide the basis of a noninvasive serology tool able to assess previous infection with H. pylori in patients with atrophic body gastritis.     

IL-4 -588C>T polymorphism and IL-4 receptor alpha [Ex5+14A>G; Ex11+828A>G] haplotype concur in selecting H. pylori cagA subtype infections

BACKGROUND: The Th2 cytokine IL-4 might limit H. pylori associated gastric inflammation and favour H. pylori clearance. The aim of the study was to verify whether IL-4 -588C>T SNP, or two SNPs of the gene coding the alpha chain of IL-4 receptor (IL-4RA Ex5+14A>G, IL-4RA Ex11+828A>G) considered singly or as haplotypes, are correlated with H. pylori virulence genes or H. pylori associated diseases. METHODS: We studied 144 patients with non-cardia gastric cancer (NCGC)(41/50 with present or past H. pylori infection), 75 with duodenal ulcer (DU)(66 H. pylori infected) and 171 with gastritis (CG)(107 H. pylori infected). cagA gene was present in 24/28 NCGC, 45/59 DU and 56/107 CG. RESULTS: All SNPs were in Hardy-Weinberg equilibrium. IL-4RA haplotypes frequencies were estimated using Arlequin software. Neither the SNPs nor the IL-4RA haplotype correlated with disease diagnosis, H. pylori infection, degree of mucosal inflammation or intestinal metaplasia. IL-4 -588T allele (OR=3.69, 95% CI:1.34-10.16) and IL-4RA GA haplotype (p<0.05) enhanced the risk for cagA positive infections. IL-4RA GA haplotype correlated with IL-4 protein levels in H. pylori infected gastric mucosa. CONCLUSIONS: IL-4 and IL-4RA gene polymorphisms concur in selecting the H. pylori infecting strain, probably influencing the IL-4 signalling pathway.     

幽门螺杆菌感染与不同胃粘膜病变中基质金属蛋白酶-9表达的关系

目的　探讨基质金属蛋白酶9(MMP 9)在胃癌及不同胃粘膜病变发生过程中的表达,及其与幽门螺杆菌的相互作用。方法　选择2 0 9例病例,包括慢性胃炎2 0例、肠上皮化生18例、轻度不典型增生4 1例、中重度不典型增生76例及胃癌5 4例;HP检测采用Giemsa染色、快速尿素酶试验或14 C尿素呼气试验;SP法检测MMP 9的表达。结果　慢性胃炎粘膜组未见MMP 9表达,肠上皮化生粘膜组MMP 9阳性率为4 4 .4 % ,轻度不典型增生粘膜组MMP 9阳性率为4 8.9% ,中、重度不典型增生粘膜组MMP 9阳性率为71.1% ,胃癌组MMP 9阳性率为83.3% ,明显高于慢性胃炎粘膜组(P <0 .0 1) ,高于不典型增生粘膜组(P <0 .0 1)。MMP 9在不典型增生及胃癌的HP阳性组中的表达率明显高于HP阴性组(P <0 .0 5 )。结论　MMP 9在胃癌中有较高的阳性率,与HP感染密切相关,可作为诊断胃癌的一个参考指标。     

Antigastric autoantibodies inHelicobacter pylori infection: role in gastric mucosal inflammation

The aim of the study was to ascertain whether there is an association between the presence of serum parietal cell autoantibodies (PCA) and: (1) Helicobacter pylori infection; (2) the presence and degree of gastritis and intestinal metaplasia; and (3) the H. pylori infecting strain. Gastric mucosal biopsies were obtained from 49 consecutive patients in order to assess and grade gastritis, make a histological diagnosis, and culture and genotype H. pylori. H. pylori infection was present in 26 patients (group 1), had been present in 17 patients (group 2), and the remaining 6 (group 3) had never had the infection. The infecting strain was cagA positive in 21 of 26 group 1 patients. Positive PCA results were found in 84%, 76%, and 14% of patients in groups 1, 2, and 3, respectively. PCA results were correlated with anti-H. pylori antibody titers (P<0.05). In group 2 patients, PCA were associated with the degree of antral gastritis (Fisher's exact test P<0.05). cagA status was not associated with the presence of PCA (chi2=0.68, NS). The frequency of positive findings for PCA in group 2 was higher in patients with (90%) than in those without (50%) intestinal metaplasia. In conclusion: (1) H. pylori infection is associated with the production of PCA, which, after eradication of the infection, persist and might contribute to the persistent antral chronic gastritis and intestinal metaplasia; (2) the gastric lesions associated with infections sustained by the more-virulent H. pylori strains do not appear to be due to the induction of antigastric autoantibodies.     

胃增生性息肉危险因素分析

目的研究胃增生性息肉与年龄、性别、幽门螺杆菌感染、慢性萎缩性胃炎等危险因素。方法12 454例次胃镜检查,发现胃息肉样病变182例,病理确诊为增生性息肉88例;对照组为经胃镜检查的连续患者496例。幽门螺杆菌检测采用快速尿素酶检查和组织学检查,其中之一阳性为幽门螺杆菌阳性。结果增生性息肉组女性65.91%(58/88),对照组51.61%(256/496),差异有显著性(P<0.05)。增生性息肉组>50岁70.45%(62/88),对照组52.62%(261/496),差异有显著性(P<0.01)。增生性息肉组幽门螺杆菌阳性59%(52/88),对照组46.98%(233/498),差异有显著性(P<0.05)。增生性息肉组肠上皮化生和/或萎缩性胃炎21.59%(19/88),对照组7.46%(37/459)差异有显著性(P<0.01)。结论女性、>50岁、幽门螺杆菌感染、肠上皮化生和/或萎缩性胃炎是胃增生性息肉的危险因素。