幽门螺杆菌感染对患者胃黏膜瘦素含量的影响

目的探讨幽门螺杆菌感染对胃瘦素含量的影响。方法取81例就诊前2周内未行抗H.pylori治疗患者(无糖尿病、糖耐量异常)胃窦和胃体黏膜组织。应用快速尿素酶试验、组织切片Warthin-Starry银染和H.pylori-UreA-PCR技术行H.Pylori诊断;ELISA法测定胃黏膜瘦素含量。结果除胃癌组外,其他各型胃疾患者胃体黏膜瘦素含量H.pylori阳性组均明显高于H.pylori阴性组(P<0.05)。结论H.pylori感染可导致胃体部黏膜瘦素含量升高。胃瘦素可能作为一种应激肽,参与H.pylori相关性胃疾患的发生发展过程。     

幽门螺杆菌对蒙古沙土鼠胃上皮细胞增殖的影响

目的在幽门螺杆菌(H.pylori)长期感染蒙古沙土鼠腺胃模型基础上,探讨H.pylori感染诱致胃癌发生的可能机制。方法采用H.pylori国际标准菌株NCTC11637灌喂蒙古沙土鼠,建立H.pylori长期感染动物模型;用免疫组化及原位杂交方法检测H.pylori感染致胃上皮细胞增殖的改变。结果成功建立了H.pylori长期感染蒙古沙土鼠腺胃模型,其胃粘膜的组织学变化显示,H.pylori感染可致正常胃粘膜发生慢性胃炎→胃萎缩→胃上皮肠化生→胃上皮异型增生的发展过程。H.pylori感染能引起胃窦上皮细胞增殖增加(P<0.05),随着H.pylori感染时间的延长,表皮生长因子(epidermal growth factor, EGF)mRNA及表皮生长因子受体(epidermal growth factor receptor, EGFR)mRNA的阳性信号表达呈逐渐增加的趋势(P<0.05)。结论H.pylori定植致胃窦上皮细胞增殖的异常,对正常胃窦粘膜向不典型增生进展的过程起重要作用;EGF及EGFR在mRNA水平的异常表达可能是H.pylori定植致胃窦上皮细胞增殖异常的重要原因。     

幽门螺杆菌对蒙古沙土鼠胃上皮细胞增殖的影响

目的：在幽门螺杆菌（H.pylori)长期感染蒙古沙土鼠腺胃模型基础上，探讨H.pylori感染诱致胃癌发生的可能机制。方法：采用H.pylori国际标准 株NCC11637灌喂蒙古沙土鼠，建立H.pylori长期感染动物模型，用免疫组化及原位杂交方法检测H.pylori感染致胃上皮细胞增殖的改变。结果：成功建立了H.pylori长期感染蒙古沙土鼠腺胃模型，其胃粘膜的组织学变化显示，H.pylori感染可致正常胃粘膜发生慢性胃炎－胃萎缩－胃上皮肠化生－胃上皮异型增生的发展过程。H.pylori感染能引起胃窦上皮细胞增殖增加（P＜0．05），随着H.pylori感染时间的延长，表皮在子（epidermal growth factor,EGF)mRNA及表皮生长因子受体（epidermal growth factor receptor,EGFR)mRNA的阳性信号表达呈逐渐增加的趋势（P＜0．05），结论：H.pylori定植致胃窦上皮细胞增殖的异常，对正常胃窦粘膜向不典型增生进展的过程起重要作用；EGF及EGFR在mRNA水平的异常表达可能是H.pylori定植致胃窦上皮细胞增殖异常的重要原因。     

胃黏膜相关淋巴组织淋巴瘤内镜特征

目的：探讨胃黏膜相关淋巴组织（MALT）淋巴瘤的内镜特征。方法：回顾性分析13例胃MALT淋巴瘤患者的内镜资料。结果：13例胃MALT淋巴瘤内镜下表现为：①病变累及胃体、窦分别占84.62%、61.54%，多部位病变84.62%，波及十二指肠、贲门分别为23.08%、30.78％。②弥漫性分布69.23%，局限性分布30.77％。③病变形态依次为溃疡型、浸润型、结节型分别占46.15%、30.77%、23.08%。④胃腔变形仅15.38%。⑤伴H.pylori感染率76.92%。⑥内镜确诊率61.54%。结论：内镜下胃MALT淋巴瘤呈病变范围广、病灶多发性、病变多态性、胃腔变形少四大特点，内镜为诊断胃MALT淋巴瘤的有效措施。     

107例食管癌、胃癌病例分析

目的 通过研究食管癌和胃癌的发病特点,提高基层医院食管癌和胃癌的诊断水平.方法 回顾性分析2012年2月至2013年8月成都市新都区中医医院胃镜联合病理活检确诊的107例食管癌和胃癌患者资料,比较其性别、年龄分布及肿瘤发病部位,并统计胃癌患者幽门螺杆菌(helicobacter pylori,Hp)感染情况.结果 男、女患者所占百分率分别为77.57％和22.43％.食管癌、胃癌患者男、女百分比分别为95.83％0、4.17％和62.71％、37.29％,两组性别分布差异有统计学意义(P＜0.001).食管癌和胃癌患者在＜60岁、≥60岁所占比例分别为43.75％、56.25％和22.03％、77.97％,差异有统计学意义(P=0.016).肿瘤部位在食管上段、中段、下段所占比例分别为10.42％、60.41％、29.17％.胃癌患者肿瘤部位在贲门、胃体、胃窦、胃角所占比例分别为23.73％、25.42％、38.98％、11.86％,其Hp检测阳性率为77.97％.结论 男性食管癌、胃癌发病率明显高于女性,大于60岁为高发人群,食管癌和胃癌的最常见发病部位分别为食管中段和胃窦部.Hp感染和胃癌有关.胃镜联合病理活检是诊断食管癌和胃癌的最主要手段.     

广州地区儿童感染幽门螺杆菌iceA基因亚型与胃炎的相关性研究

目的 探讨广州地区儿童感染幽门螺杆菌(H.pylori)的iceA基因亚型与胃炎的关系.方法 105例胃、十二指肠疾病患儿的胃窦处取3块胃黏膜,分别进行快速尿素酶反应、病理检查和聚合酶链反应(PCR).抽提胃黏膜基因组DNA,用3对引物检测H.pylori ureA和iceA基因,分析H.pylori iceA基因亚型与胃炎的关系.结果 105例样本中,快速尿素酶反应、病理检测和聚合酶链反应(PCR)三者均阳性的标本52例,H.pylori iceA1亚型菌株单独检出率78.84%(41/52),H.pylori iceA2亚型菌株单独检出率1.92%(1/52),H.pylori iceA1和iceA2亚型均阳性的检出率3.84%(2/52),iceA1和iceA2亚型均阴性的比率15.38%(8/52),H.pylori iceA1亚型阳性率与其它基因亚型相比较,差异有显著性;感染H.pylori iceA1亚型菌株的患儿中轻度慢性胃炎3例,中度慢性胃炎15例,重度慢性胃炎25例;未感染H.pylori iceA1亚型菌株的患儿中轻度慢性胃炎2例,中度慢性胃炎4例,重度慢性胃炎3例,感染H.pylori iceA1亚型菌株患儿与未感染H.pylori iceA1亚型菌株患儿的胃黏膜病变程度差异有显著性(P＜0.05).结论 H.pylori iceA1亚型是广州地区儿童感染H.pylori的优势基因亚型,H.pylori iceA1菌株容易引起较严重慢性胃炎.     

青年胃癌的临床特征

目的 探讨青年胃癌患者的临床特征,分析影响其预后的因素.方法 回顾性分析上海交通大学医学院附属第九人民医院和复旦大学附属华山医院静安分院2005年1月～2015年12月收治的535例胃癌患者的临床资料,比较分析青年胃癌患者和中老年胃癌患者的临床特征及病理分型特点,探讨可能影响青年患者胃癌的预后因素.结果 青年组中男女比例高于中老年组,最突出的临床表现为上腹痛,中老年组以消瘦、上消化道出血及上腹部疼痛及不适为主,二者差异有统计学意义(P<0.0001);在病变部位方面,青年组多以胃窦为主,同时全胃比例高,而中老年患者胃中上1/3占比高于青年组.H.pylori感染方面:青年组感染率(70.37％,57/81)明显高于中老年组(29.96％,136/454)(P<0.0001);中老年组较青年组有更高的消化性溃疡史(P<0.0001);青年组的Lauren分型弥漫型胃癌的比例高于中老年组.青年组5 a总体生存率低于中老年组(P=0.008).结论 青年组中女性比率高,分布以胃窦为主,有更高的H.pylori感染率、组织分型以弥漫型和混合型为多,5 a总体生存率青年组低于中老年组.     

幽门螺杆菌感染对胃癌细胞糖酵解的影响

目的 探讨幽门螺杆菌(H.pylori)对胃癌细胞糖酵解的影响及分子机制。方法 通过检测胃黏膜上皮细胞GES-1与6种胃癌细胞(MKN28、AGS、HGC27、MGC803、MKN45、NCI-N87)的葡萄糖消耗速率和乳酸产量,确定GES-1和两种胃癌细胞MKN28、AGS为后续研究对象。将GES-1、MKN28和AGS细胞分别与H.pylori(H.pylori-HVS、H.pylori-26695、H.pylori-△cagA)共培养,构建H.pylori急性和慢性感染的细胞模型,将未感染H.pylori的3种细胞设置为对照组。在所有细胞模型中检测葡萄糖消耗、乳酸生成和葡萄糖摄取,并且通过Western blotting检测糖酵解关键酶的蛋白表达水平。结果 与正常胃黏膜上皮细胞GES-1比较,多种胃癌细胞(AGS、HGC27、MGC803、MKN45、NCI-N87)中葡萄糖消耗和乳酸生成上调,差异均有统计学意义(P均<0.001)。与未感染H.pylori的对照组细胞比较,H.pylori急性感染不影响GES-1和两种胃癌细胞MKN28、AGS的葡萄糖摄取和乳酸生成,差异...     

青年胃癌的临床特征

目的 探讨青年胃癌患者的临床特征,分析影响其预后的因素.方法 回顾性分析上海交通大学医学院附属第九人民医院和复旦大学附属华山医院静安分院2005年1月～2015年12月收治的535例胃癌患者的临床资料,比较分析青年胃癌患者和中老年胃癌患者的临床特征及病理分型特点,探讨可能影响青年患者胃癌的预后因素.结果 青年组中男女比例高于中老年组,最突出的临床表现为上腹痛,中老年组以消瘦、上消化道出血及上腹部疼痛及不适为主,二者差异有统计学意义(P<0.0001);在病变部位方面,青年组多以胃窦为主,同时全胃比例高,而中老年患者胃中上1/3占比高于青年组.H.pylori感染方面:青年组感染率(70.37％,57/81)明显高于中老年组(29.96％,136/454)(P<0.0001);中老年组较青年组有更高的消化性溃疡史(P<0.0001);青年组的Lauren分型弥漫型胃癌的比例高于中老年组.青年组5 a总体生存率低于中老年组(P=0.008).结论 青年组中女性比率高,分布以胃窦为主,有更高的H.pylori感染率、组织分型以弥漫型和混合型为多,5 a总体生存率青年组低于中老年组.     

幽门螺杆菌与慢性胃炎病变的关系

0　引言　幽门螺杆菌 ( H elicobacter pylori,Hp)是慢性胃炎的病原菌 .近年来 Hp感染引起胃粘膜病变的作用引起了广泛重视 [1 - 3] .我们对 3 3 14例慢性胃炎的胃粘膜纤维内窥镜活检组织进行了 Hp检测 ,分析 Hp感染在胃粘膜病变形成中的作用 .1　材料和方法1.1　标本来源　取西京医院 1993 /2 0 0 0经纤维内窥镜活检并为病理诊断证实的慢性胃炎 3 3 13 (男 2 182 ,女 113 1)例 .平均年龄 5 3 .1( 2～ 81)岁 .组织学诊断根据 1980年全国胃癌协作组制定的标准 [4 ] .1.2　 Hp检测方法　纤维内窥镜钳取胃粘膜组织 ,取材部位为胃窦、胃体、…     

Relationship of Helicobacter pylori eradication with gastric cancer and gastric mucosal histological changes: a 10-year follow-up study

Background Helicobacter pylori （Hp） is a common and potentially curable cause of gastric mucosa lesion. This study investigated the relationship of Hp infection with histological changes in gastric mucosa and gastric cancer in Hp-positive patients compared with Hp-eradication patients followed up for ten years. Methods From an initial group of 1 006 adults, 552 Hp-positive subjects were randomly assigned to a treatment group （T; n=276） or a placebo group （P; n=276）. In the randomized, double-blind, placebo-controlled, parallel trial, T group subjects received oral doses of omeprazole, amoxicillin and clarithromycin for 1 week; those in the P group received a placebo. One month after treatment ended, a 13C urea breath test was performed, and Hp was undetectable in 88.89% of the T group. All subjects were followed at 1, 5, 8, and 10 years after treatment, with endoscopy and biopsies for histological examination. Results Gastric mucosa inflammation was significantly milder in the T group than that in the P group one year after Hp eradication and this persisted for 10 years. Glandular atrophy and intestinal metaplasia （IM） had deteriorated in both groups during ten years. However, the increased score of glandular atrophy at both the gastric antrum and corpus, and IM only at the gastric antrum, in the P group was more obvious than that in the T group. During the 10 years, 9 patients were diagnosed with gastric cancer （2 in the T group; 7 in the P group; P=0.176）. When mucosal atrophy was absent at the gastric antrum and corpus when entering the study, the incidence of gastric cancer in the P group （n=6） was much higher than that in the T group （n=0, P=0.013）. Conclusions Hp eradication may significantly diminish and delay the development of IM and atrophy gastritis. Hp especially in the early stage of Hp infection. and help halt progression of gastric mucosal inflammation eradication is helpful for reducing the risk for gastric cancer,     

Role of Seroconversion in Confirming Cure of Helicobacter pylori Infection

Context.— The role of serologic testing to confirm cure of Helicobacter pylori infection after antimicrobial therapy is not completely defined. Objective.— To determine the utility of serologic testing in confirming cure of H pylori infection more than 1 year after therapy. Design.— A prospective, before-after interventional trial. Setting.— An outpatient clinical research laboratory in an academic, urban Veterans Affairs medical center. Participants.— Twenty-three otherwise healthy men and women with active H pylori infection demonstrated by gastric biopsy and with positive H pylori serologic findings. Intervention.— A 14-day course of bismuth, tetracycline, and metronidazole. Main Outcome Measures.— Determination of IgG serum antibodies to H pylori at baseline, 1 month, 3 months, and approximately 18 months after completion of therapy compared with serial gastric mucosal biopsy specimens with stains for H pylori and for histologic examination as the criterion standard. Results.— Fifteen (65%) of 23 subjects were cured of their H pylori infection as assessed by gastric biopsy, with elimination of gastritis; median antibody levels declined from 92.5 U/mL at baseline to undetectable levels at 18 months. The other 8 subjects (35%) were not cured and had persistent gastritis at 18 months; median antibody levels declined from 130.6 U/mL at baseline to 89.7 U/mL at 18 months. Sensitivity and specificity of seroconversion (from a positive to negative test result) in detecting cure of H pylori infection were 60% and 100%, respectively. Conclusion.— Undetectable antibody levels beyond the first year of therapy accurately confirm cure of H pylori infection in initially seropositive healthy subjects, with reasonable sensitivity.      

胃黏膜病变演化过程中幽门螺杆菌感染与p53变异和MG-7抗原及核仁组成区相关蛋白表达的关系

目的　从胃黏膜细胞增殖、基因变异、胃癌特异性抗原表达的角度探讨幽门螺杆菌(Hp)感染 ,特别是cagA阳性Hp感染在胃黏膜病变演化中的作用。 方法　根据组织形态学和黏液组织化学检查将 10 9例临床标本分为Ⅰ型肠化、Ⅱ型肠化、Ⅲ型肠化、非典型增生和胃癌 5个组 ;用显微切割 /PCR方法检测标本中的Hp ,并将其分为cagA阳性和cagA阴性两组 ;用免疫组化方法检测 p5 3蛋白、MG 7抗原的表达 ;用组织化学银染检测核仁组成区相关蛋白 (AgNORs)的表达。结果　 (1)P5 3在各组均有表达 ,其中胃癌组P5 3的表达率明显高于其他各组 (P <0 .0 5 )。 (2 )胃癌组MG 7的总表达率与过表达率均明显高于其他各组。在各组胃黏膜病变中 ,Hp阳性与阴性标本MG7表达无明显差异。在各组病变中cagA阳性组与cagA阴性组MG7的表达无明显差异。 (3)Ⅰ型和Ⅱ型肠化→Ⅲ型肠化→非典型增生→胃癌的演变过程中 ,AgNORs平均计数明显增高 (P <0 .0 5 )。各胃黏膜病变组中Hp阳性标本AgNORs计数明显高于Hp阴性标本 (P <0 0 5 )。在Hp阳性的标本中 ,cagA阳性标本AgNORs颗粒计数明显高于cagA阴性标本 (P <0 0 5 )。 结论　Hp感染 ,特别是cagA阳性的Hp感染在胃黏膜病变演化的过程中起重要作用 ,其作用机理与促进黏膜细胞增殖有关 ;p5 3变异和MG 7     

CagA阳性幽门螺杆菌感染与上胃肠道疾病关系的研究

目的探讨CagA阳性幽门螺杆菌(Hp)感染与上胃肠道病变的关系;并观察Hp根除治疗后血清中抗CagAIgG抗体水平的变化.方法808例因上胃肠道症状而接受胃镜检查的病人,同时作Hp检查.对Hp感染者用ELISA方法检测血清中抗CagAIgG抗体;阳性者予含质子泵抑制剂(PPI)三联疗法根除治疗.其中60例根除治疗失败病人和120例根除成功病人在Hp根除治疗结束3个月和6个月时复查血清中抗CagAIgG抗体水平.结果在不同临床疾病中,慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)、胃溃疡(GU)、十二指肠溃疡(DU)和胃癌(GC)感染Hp的病人中抗CagAIgG抗体阳性率分别为55.4%、70.5%、83.2%、90.8%、89.7%.后4组阳性率明显高于CSG组,后3组均明显高于CAG组;在不同程度的胃粘膜病变中,CSG、CAG、肠上皮化生(IM)、非典型增生(Dys)和GC感染Hp的病人中抗CagAIgG抗体的阳性率分别为43.0%、53.8%、77.6%、88.6%、89.7%.IM、Dys和GC组均明显高于CSG和CAG组;60例根除失败者在治疗前及治疗后3个月和6个月时血清中抗CagAIgG水平分别为(72±41)U/ml,(67±36)U/ml和(69±40)U/ml,治疗前后差异无显著意义,无一例转为阴性;120例根除治疗成功者治疗后3个月和6个月血清中抗CagAIgG水平平均由(69±38)U/ml分别下降至(47±30)U/ml和(32±15)U/ml,治疗后与治疗前比较差异均有显著意义,在治疗后3个月和6个月时分别有7.5%(9/120)和19.2%(23/120)的病人抗体转为阴性.结论CagA阳性的Hp可能导致更严重的上胃肠道疾病和更严重的胃粘膜病变;Hp根除治疗后血清中抗CagAIgG抗体水平明显下降,但下降较慢,不宜作为个体监测疗效的指标.     

胃粘膜线粒体DNA核内整合与bcl-2和bax表达的关系

目的　探讨胃癌及其癌前病变组织线粒体DNA核内整合与bcl 2和bax基因mRNA表达的关系。方法　采用原位杂交方法检测线粒体DNA核内整合 ;RT PCR方法检测胃癌及其癌前病变组织bcl 2和bax基因mRNA的表达。结果　胃粘膜肠化 (5 3.3% )和异型增生 (70 % )组bcl 2mRNA表达阳性率显著高于浅表性胃炎组 (10 % ) (P <0 .0 5 ) ,而慢性萎缩性胃炎 (5 0 % )和胃癌 (30 % )组bcl 2mRNA表达阳性率与浅表性胃炎组相比则无显著差异 (P >0 .0 5 ) ;胃粘膜异型增生组bcl 2mRNA表达阳性率显著高于胃癌组 (P <0 .0 5 )。异型增生组baxmRNA表达阳性率 (6 0 % )显著高于浅表性胃炎组 (P <0 .0 5 ) ,而萎缩性胃炎(5 0 % )、肠化 (4 6 .7% )和胃癌 (33.3% )组baxmRNA表达阳性率与浅表性胃炎组 (10 % )相比无显著差异 (P >0 .0 5 )。Hp感染组胃粘膜bcl 2和baxmRNA表达阳性显著高于非Hp感染者 (P <0 .0 5 ) ;bcl 2和baxmRNA表达与HpCagA基因表达没有明显的相关关系 (P >0 .0 5 )。mtMSI(+)组bcl 2和baxmRNA表达阳性率与mtMSI(- )组相比无显著差异 (P >0 .0 5 )。结论　线粒体DNA核内整合可能在部分胃癌的发生中起重要作用 ;线粒体DNA核内整合与bcl 2和baxmRNA的表达无显著相关     

ATP4B在不同程度胃黏膜病变中的表达及其与幽门螺杆菌感染的关系

目的研究ATP4B在胃黏膜病变演化过程中的表达变化。并探讨其与幽门螺杆菌（Hellcobacter pylori,Hp）感染的关系。方法根据组织形态学检查将221例胃镜活检标本分为慢性浅表性胃炎（CSG）、慢性萎缩性胃炎（CAG）、肠上皮化生（IM）和异型增生（Dys）4组;采用免疫组织化学方法检测ATP4B的表达情况;根据胃镜检查时快速尿素酶试验结果确定Hp感染状态。结果ATP4B表达水平随胃黏膜病变演化而降低,在4组的表达率分别为51．4％、15．4％、15．9％及5．0％．CSG组ATP4B表达水平显著高于其他各组（P〈0．05）。CSG组中Hp阳性标本ATP4B的表达率为33-3％,显著低于其在Hp阴性标本中的表达率（59．7％,P〈0．05）;在另外3组中,Hp阳性标本与阴性标本ATP4B的表达率差异无统计学意义（P〉0．05）。结论在胃黏膜病变演化过程中,ATP4B的表达随胃黏膜病变的进展而降低;Hp在胃黏膜病变演化的早期阶段抑制了ATP4B的表达。     

幽门螺杆菌与胃癌发生进程的10年队列研究

目的 探讨幽门螺杆菌（Hp）在胃癌发生进程中的作用。方法 采用整群随机抽样方法,在胃癌高发区山东省临朐县选择14个自然村,对35-64岁的自然人群进行胃镜普查和血清学检验：取胃黏膜活检组织进行病理学诊断,用酶联免疫吸附法检测Hp抗体。随访5年和10年后,分别再对该人群进行胃镜复查。随访期间对观察对象中无论是自然发生还是胃镜复查发现的胃癌病例均进行登记。结果 经10年随访,共获得符合研究条件的观察对象2469名。随访期间有58例发生胃癌,其中1603名Hp感染阳性者中发生44例（2．74％）,866名Hp感染阴性者中发生14例（1．62％）。Hp感染阳性者发生胃癌的危险性显著高于Hp感染阴性者[比值比（OR）=1．871,95％可信区间（CI）：1．012—3．459]。基线正常或浅表性胃炎（SG）组Hp感染阳性者与阴性者向胃癌癌前病变转化和继续发展进度比较,差异无统计学意义（P〉0．05）。而基线萎缩性胃炎（CAG）组Hp感染阳性者胃癌癌前病变的发展速度明显快于阴性者（P〈0．01）;且该组Hp感染阳性者的胃癌发生率（7／615）也明显高于Hp感染阴性者（0／470,P=0．019）。经10年随访,虽然基线肠上皮化生（IM）组和异型增生（DYS）组Hp感染阳性者的胃黏膜病变重于阴性者（分别为P〈0．05,P〈0．01）,但这两组Hp感染阳性者与阴性者的胃癌发生率非常接近：IM组为17／573和7／224（P=0．907）;DYS组为19／368和7／122（P=0．806）。结论 在胃癌的形成过程中,HP是萎缩性胃炎向更高级癌前病变转化和继续发展的重要促进因素,而且在整个胃癌癌前病变的发展过程中均具有促进作用。HP可能不直接引起胃癌,它与其他致癌因素共同作用促进胃癌的发生。HP对正常或仅为浅表性胃炎的胃黏膜可能没有重要的影响,尚需要做进一步研究。     

持续幽门螺杆菌感染对胃黏膜的作用及其转归的影响因素

目的　探讨幽门螺杆菌 (Hp)长期感染对胃黏膜的作用及其转归的影响因素。方法随访 114例 10年前诊断Hp感染的患者 ,分析对比 10年前后其Hp感染情况、胃镜和病理组织学变化。并检测了其中 80例Hp持续感染者血清抗HpCagA IgG和抗HpIgE ,分析它们与Hp长期感染不同转归的关系。结果　 114例患者中 34例 (2 9 8% )Hp转阴 ,80例 (70 2 % )Hp持续阳性。Hp感染持续 10年后消化性溃疡的发生率、胃黏膜慢性炎症程度、肠上皮化生 (IM )和糜烂的发生率均显著增加 ,其IM严重程度显著加剧。而Hp转阴者消化性溃疡的发生率、胃黏膜慢性炎症程度均显著低于 10年前 ,并显著低于Hp持续阳性者。Hp长期感染后发展为消化性溃疡 (PU)者血清抗HpCagA IgG和抗HpIgE阳性率显著高于持续保持慢性浅表性胃炎 (CSG)不变者 ,发生黏膜糜烂和IM者血清抗HpCagA IgG阳性率显著高于不发生黏膜糜烂和IM者 ,均P <0 0 0 5 ,而胃黏膜的慢性炎症程度是否加剧与CagA无关。结论　Hp持续感染可增加消化性溃疡的发生率 ,加剧胃黏膜的炎症程度 ,并促进肠上皮化生的形成和发展 ,根除Hp不仅能减轻胃黏膜的炎症程度 ,而且能阻止肠上皮化生的发生和发展。CagA阳性菌株和产生抗HpIgE的个体 ,其Hp长期感染后病变的转归均较阴性者严重 ,因此 ,对于这类患者应     

Expression of differential nitric oxide synthase isoforms in human gastric mucosa infected with Helicobacter pylori

Objective: To study the relationship between nitric oxide synthase ( NOS) expression in human gastric mu-cosa and Helicobacter pylori (H. pylori) infection. Methods: Gastric mucosa samples were obtained from antrum of 33 patients received gastroendoscopy. H. pylori infection was confirmed by Giems staining and bacteria culture under mi-croaerophilic conditions. Expression of iNOS, eNOS and nitrotyrosine were detected by immunohistochemistry. Results: (1) The positive rate of H. pylori infection was 66. 7% (22/33) . (2) iNOS positive staining in inflammatory cells was detected in 77. 3% (17/22) of samples with H. pylori and 27. 3% (3/11) without H. pylori infection (P < 0.01). (3) eNOS expression in inflammatory cells was found in 77. 3% (17/22) of samples with H. pylori and 18.2% (2/11) without H. pylori infection ( P < 0. 01) . (4) Nitrotyrosine expression in inflammatory cells was observed in 59. 1% ( 13/22) of samples with H. pylori and 54.5%(6/11) without H. pylori infection (P>0.05). (5) Moderate a     

Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial

Context  Although chronic Helicobacter pylori infection is associated with gastric cancer, the effect of H pylori treatment on prevention of gastric cancer development in chronic carriers is unknown. Objective  To determine whether treatment of H pylori infection reduces the incidence of gastric cancer. Design, Setting, and Participants  Prospective, randomized, placebo-controlled, population-based primary prevention study of 1630 healthy carriers of H pylori infection from Fujian Province, China, recruited in July 1994 and followed up until January 2002. A total of 988 participants did not have precancerous lesions (gastric atrophy, intestinal metaplasia, or gastric dysplasia) on study entry. Intervention  Patients were randomly assigned to receive H pylori eradication treatment: a 2-week course of omeprazole, 20 mg, a combination product of amoxicillin and clavulanate potassium, 750 mg, and metronidazole, 400 mg, all twice daily (n = 817); or placebo (n = 813). Main Outcome Measures  The primary outcome measure was incidence of gastric cancer during follow-up, compared between H pylori eradication and placebo groups. The secondary outcome measure was incidence of gastric cancer in patients with or without precancerous lesions, compared between the 2 groups. Results  Among the 18 new cases of gastric cancers that developed, no overall reduction was observed in participants who received H pylori eradication treatment (n = 7) compared with those who did not (n = 11) (P = .33). In a subgroup of patients with no precancerous lesions on presentation, no patient developed gastric cancer during a follow-up of 7.5 years after H pylori eradication treatment compared with those who received placebo (0 vs 6; P = .02). Smoking (hazard ratio [HR], 6.2; 95% confidence interval [CI], 2.3-16.5; P<.001) and older age (HR, 1.10; 95% CI, 1.05-1.15; P<.001) were independent risk factors for the development of gastric cancer in this cohort. Conclusions  We found that the incidence of gastric cancer development at the population level was similar between participants receiving H pylori eradication treatment and those receiving placebo during a period of 7.5 years in a high-risk region of China. In the subgroup of H pylori carriers without precancerous lesions, eradication of H pylori significantly decreased the development of gastric cancer. Further studies to investigate the role of H pylori eradication in participants with precancerous lesions are warranted.