幽门螺杆菌感染与胃癌的关系

为探讨幽门螺杆菌 (Hp)感染与胃癌的关系,对我院 1997～ 1998年期间胃镜检查并经病理证实的 80例胃癌 (胃癌组 ),以及根据性别、年龄、职业配对的 80例慢性浅表性胃炎 (胃炎组 )、 80例十二指肠球部溃疡 (溃疡组 )患者的 Hp感染情况作对照研究,并对不同部位胃癌的 Hp感染情况作一分析。　　一、材料与方法　　1.研究对象：胃癌组 80例中男 61例,女 19例。年龄 26～ 83岁,平均 60.4岁;农民 65例,其它职业 15例。胃炎组 80例和溃疡组 80例均经胃镜检查及活检病理确定,其性别、年龄、职业等均与胃癌配对,有可比性。　　2.活检方法：…     

胃癌与幽门螺杆菌感染的关系

目的:进一步探讨胃癌的发生、发展与HP持续感染的关系。方法:经胃镜检查观察病变的部位和形态,并在病变部位取3块活组织。对病理诊断为胃癌的235例组织再作必良Gimesa染色,以确立HP感染与否。结果:癌肿病变部位HP感染率在胃窦部占58.33％,胃角部占38.33％,贲门部占37.50％,胃体部占16.95％。在控制不同形态胃癌的影响下,不同部位胃癌间HP感染率有非常显著性差异(P<0.01)。癌肿病变形态HP感染率,在早期隆起型占31.11％,中晚期息内型占75.55％,溃疡型占37.39％,弥漫浸润型占26.67％。在控制不同部位胃癌的影响作用下,不同形态胃癌间的HP感染率,有非常显著性差异(P<0.01)。按组织分型,HP感染率在腺癌中占39.0％,粘液癌占60.0％,两组间比较,有显著性差异(P<0.025)。HP感染阳性胃癌与阴性胃癌患者在年龄、性别两组间比较,无显著性差异(P>0.05)。结论:胃窦部中晚期息肉型癌肿可能与HP持续感染关系最为密切。源于胃组织起源不同,粘液癌HP感染率比腺癌为高。胃癌发生年龄、性别与HP感染无明显相关性。     

化工人群幽门螺杆菌感染与胃癌关系的探讨

目的 通过：（１）幽门螺杆菌（ＨＰ）感染的流行病学调查;（２）ＨＰ感染与胃癌前病变的关系;（３）ＨＰ在胃窦癌中的检出率三个方面来评价ＨＰ感染与胃癌的相关性。方法 分别为：（１）随机对南化公司２８４１名健康工人的血清作ＨＰ抗体测定;（２）将胃镜检查的６４８例作ＨＰ检测和病理组织学检查;（３）对５０例胃窦腺癌病理组织学切片鉴定基ＨＰ检出率。结果 化工人群ＨＰ感染率６１．０４％,显著高于本省对照人群（３     

幽门螺杆菌感染的流行病学及其与胃癌的关系

幽门螺杆菌感染的流行病学及其与胃癌的关系王菊梅，胡伏莲（内蒙古巴盟医院内科巴盟０１５０００）自从１９８３年澳大利亚的Ｍａｒｓｈａｌｌ和Ｗａｒｒｅｎ从人胃中发现幽门螺杆菌（ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ，ＨＰ）以来，临床及实验室研究证实ＨＰ在许多...     

幽门螺杆菌感染与胃癌癌前病变的关系初探

本文分析了2563例因上腹部不适而在我院做胃镜检查患者的胃粘膜病理组织学和HP感染的结果,初步探讨HP感染与胃粘膜肠腺化生、萎缩和不典型增生这3种胃癌癌前病变的关系。1 材料与方法1.1 对象12563例均系1994年1月～1996年3月因上腹部不适在我院顺序做胃镜检查患者。其中男1680例,女883例,年龄17～76岁,平均42.3±11.2岁。除外条件:(1)检查前已接受抗HP治疗,(2)胃癌,(3)手术后胃。     

幽门螺杆菌与胃癌的关系

定居于胃粘膜上皮的幽门螺杆菌（ＨＰ），作为非自身免疫性胃炎、胃十二指肠溃疡的病原菌受到广泛的关注和研究。胃癌发生是一个多因素、多步骤的结局。由于慢性胃炎与胃癌的密切关系，引起人们对先前所认识胃癌病因的重新考虑。ＨＰ感染与业已认识的饮食、环境、遗传等因素，交织形成了炎症相关的癌发生模式（ｉｎｆｌａｍｍａｔｉｏｎ－ｒｅｌａｔｅｄｃａｒｃｉｏｎｇｅｎｅｓｉｓ）。关于ＨＰ与胃癌的关系，人们作出了许多研究，希望找到两者之间的因果联系。     

幽门螺杆菌和胃癌的关系

胃癌是消化道最常见的恶性肿瘤,胃癌的发病是多因素多步骤的过程。研究显示,幽门螺杆菌（Hp）感染是诱发胃癌最重要的单一危险因素,世界卫生组织的国际癌症研究机构（IARC／WHO）已将其列为人类胃癌的Ⅰ类致癌原。     

幽门螺杆菌感染与慢性胃炎及胃癌关系研究进展

胡伏莲教授从幽门螺杆菌 (ｈｅｌｉｃｏｂａｃｔｅｒｐｙ ｌｏｒｉ,Ｈｐ)的发现至现在已超过 17年的历史 ,Ｈｐ的研究一直是胃肠病工作者的热门课题。有关Ｈｐ与上胃肠道疾病之间关系受到消化界和微生物学家的极大关注。Ｈｐ的出现使慢性胃炎和消化性溃疡面临着一场发病学和治疗学上的革命。目前已经确认Ｈｐ与上胃肠道疾病中的4种疾病密切相关 :①慢性胃炎 ;②消化性溃疡 ;③胃癌 ;④胃粘膜相关淋巴样组织 (ＭＡＬＴ)恶性淋巴瘤。而Ｈｐ与胃癌关系的研究则是热点中的重点。世界卫生组织已将Ｈｐ列入Ⅰ类致癌因子 ,因而关于Ｈｐ与胃癌的研究…     

幽门螺杆菌与胃癌关系的研究进展

自从Warren和Mashall于1983年首次从胃粘膜中分离出幽门螺杆菌(HP)以来,关于HP及其相关疾病的研究一直方兴未艾.近年来越来越多的研究表明HP与胃癌的发生间存在着密切的关系,本文就这方面的研究进展作一简要综述.1 HP与胃癌的流行病学大量流行病学研究表明HP流行与胃癌的流行有很多相似之处.HP感染者发生胃癌的危险性较非感染者高6倍.就世界范围看,某些发展中国家如秘鲁、哥伦比亚及中国HP感染率较高,其胃癌     

Latest insights into the effects of Helicobacter pylori infection on gastric carcinogenesis

There appears to be the strong association between Helicobacter pylori (H pylori) and gastric cancer. We reviewed the latest evidences about the effects of H pylori infection on gastric carcinogenesis, classified into epidemiology, dynamics of gastric mucosal changes, DNA damages, virulence factors, host factors, and source of gastric malignancy. Through the considerable progress made in research into virulence factors resulting from differences between H pylori strains, such as cagA positivity, as well as into host factors, such as gene polymorphisms, a diverse spectrum of H pylori-associated diseases, including gastric cancer, is beginning to lend itself to elucidation. The impact of the novel hypothesis advanced by Houghton et al proposing bone-marrow derived stem cells (BMDC) as a potential source of gastric malignancy on evolving research remains to be seen with interest. Further progress in research into H pylori eradication as a viable prophylaxis of gastric cancer, as well as into the mechanisms of gastric carcinogenesis, is to be eagerly awaited for the current year and beyond.     

幽门螺杆菌感染在胃黏膜癌变过程中与生长抑素的关系

[目的]分析幽门螺杆菌(Hp)感染在胃黏膜癌变过程中对血清及胃黏膜生长抑素(SS)水平的影响,探讨Hp与SS在胃癌(GC)中的关系。[方法]90例患者随机分为3组,I组为慢性浅表性胃炎(CSG);Ⅱ组为中重度慢性萎缩性胃炎(CAG),伴或不伴肠上皮化生(IM)、轻度至中度不典型增生(ATP);Ⅲ组为GC或重度ATP。采用快速尿素酶试验、Gimsa染色、ELISA法检测Hp,放免法和免疫组化法检测3组血清和胃黏膜组织中SS水平和表达的变化。[结果]Ⅰ、Ⅱ、Ⅲ组血清SS水平分别为(62.28±5.97)、(49.63±5.29)(、25.87±2.64)pg/300μl,3组比较差异有统计学意义(P<0.01)。但各组内Hp感染阳性组与阴性组血清SS水平比较无显著性差异(P>0.05)。免疫组化显示3组SS的阳性表达率比较有统计学意义(P<0.05)。SS在Hp感染阳性组的表达逐渐降低,Ⅲ组中的表达远低于Ⅰ、Ⅱ组,且明显低于Hp阴性组(P<0.05)。[结论]SS在胃黏膜癌变过程表达下降,可能是Hp致胃黏膜癌变的机制之一。     

幽门螺旋杆菌与残胃癌发生的研究进展

残胃癌发病率呈上升趋势,其发生机制与多种因素有关,其中幽门螺旋杆菌感染被认为是重要因素,但尚无肯定的结论.本文就残胃幽门螺旋杆菌感染与残胃癌发生及相关机制作一综述.     

Helicobacter pylori infection,gastrin and cyclooxygenase-2 in gastric carcinogenesis

Gastric cancer is one of the most frequent neoplasms and a main cause of death worldwide, especially in China and Japan. Numerous epidemiological, animal and experimental studies support a positive association between chronic Helicobacter pylori(H. pylori) infec-tion and the development of gastric cancer. However, the exact mechanism whereby H. pylori causes gastric carcinogenesis remains unclear. It has been demon-strated that expression of cyclooxygenase-2(COX-2) is elevated in gastric carcinomas and in their precursor le-sions. In this review, we present the latest clinical and experimental evidence showing the role of gastrin and COX-2 in H. pylori-infected patients and their possible association with gastric cancer risk.     

幽门螺杆菌感染与胃癌局部浸润的相关性

胃癌是一种常见的恶性肿瘤,严重威胁着人类的健康,幽门螺杆菌被国际上确认为胃癌的主要病因之一,且其与胃癌的不良预后相关.本文主要通过探讨幽门螺杆菌与胃癌局部浸润的关系,阐明幽门螺杆菌与胃癌转移的可能机制,为胃癌患者根除幽门螺杆菌治疗提供理论依据.     

胃癌患者中反流性食管炎与幽门螺杆菌感染的相关性分析

目的探讨胃癌患者中反流性食管炎与幽门螺杆菌感染的相关性。 方法选取2015年8月至2017年1月,在新疆维吾尔自治区人民医院就诊的胃癌合并反流性食管炎患者45例与同期在本院就诊的胃癌患者45例,比较两组患者幽门螺杆菌的感染率,并对幽门螺杆菌感染与反流性食管炎进行相关性分析。 结果胃癌合并反流性食管炎组和胃癌患者幽门螺杆菌感染率的发生率分别是22.22%和88.89%,差异有统计学意义（χ²=15.568,P＜0.05）。胃癌合并反流性食管炎组的幽门螺杆菌感染率低于胃癌患者。 结论胃癌患者中幽门螺杆菌感染可能对反流性食管炎发病有一定的保护作用。     

Role of Helicobacter pylori infection in gastric carcinogenesis:Current knowledge and future directions

Helicobacter pylori(H. pylori) plays a role in the patho-genesis of gastric cancer. The outcome of the infection depends on environmental factors and bacterial and host characteristics. Gastric carcinogenesis is a multistep process that is reversible in the early phase of mucosal damage, but the exact point of no return has not been identified. Therefore, two main therapeutic strategies could reduce gastric cancer incidence:(1) eradication of the already present infection; and(2) immunization(prior to or during the course of the infection). The success of a gastric cancer prevention strategy depends on timing because the prevention strategy must be introduced before the point of no return in gastric carcinogenesis. Although the exact point of no return has not been identified, infection should be eradicated before severe atrophy of the gastric mucosa develops. Eradication therapy rates remain suboptimal due to increasing H. pylori resistance to antibiotics and patient noncompliance. Vaccination against H. pylori would reduce the cost of eradication therapies and lower gastric cancer incidence. A vaccine against H. pylori is still a research challenge. An effective vaccine should have an adequate route of delivery, appropriate bacterial antigens and effective and safe adjuvants. Future research should focus on the development of rescue eradication therapy protocols until an efficacious vaccine against the bacterium becomes available.     

Relatedness of Helicobacter pylori populations to gastric carcinogenesis

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that infects half of the human population. The infection is associated with chronic inflammation of the gastric mucosa and peptic ulcers. It is also a major risk factor for gastric cancer. Phylogenetic analysis of global strains reveals there are seven populations of H. pylori, including hpAfrica1, hpAfrica2, hpEastAsia, hpEurope, hpNEAfrica, hpAsia2 and hpSahul. These populations are consistent with their geographical origins, and possibly result from geographical separation of the bacterium leading to reduced bacterial recombination in some populations. For each population, H. pylori has evolved to possess genomic contents distinguishable from others. The hpEurope population is distinct in that it has the largest genome of 1.65 mbp on average, and the highest number of coding sequences. This confers its competitive advantage over other populations but at the cost of a lower infection rate. The large genomic size could be a cause of the frequent occurrence of the deletion of the cag pathogenicity island in H. pylori strains from hpEurope. The incidence of gastric cancer varies among different geographical regions. This can be attributed in part to different rates of infection of H. pylori. Recent studies found that different populations of H. pylori vary in their carcinogenic potential and contribute to the variation in incidence of gastric cancer among geographical regions. This could be related to the ancestral origin of H. pylori. Further studies are indicated to investigate the bacterial factors contributing to differential virulence and their influence on the clinical features in infected individuals.     

太原地区不同临床型胃疾患与幽门螺杆菌感染及其毒力相关基因cagA关系的探讨

目的探讨幽门螺杆菌（Hp）感染、cagA^＋-Hp与胃部疾病严重程度的关系。方法胃镜直视下取102例胃粘膜组织并采血,分离血清。应用Hp-ureA-PCR,ELISA,细菌培养3种方法确定Hp感染例数,用PCR检测cagA-Hp基因。结果102例胃疾患病人,确定Hp感染76例,其中57例检测到cagA-Hp基因,检出率为75.00%。各型胃疾患病人cagA检出率分别为：CSG 52.38%（11/21）,CAG 92.31%（12/13）,GU81.82%（18/22）,GC 80.00%（16/20）。结论1）各种胃部疾病均与Hp感染有关,但单纯的Hp感染不足以解释临床结局的多样性;2）cagA^＋-Hp与胃部疾患的严重程度相关,携带有cagA的Hp可能具有较强的致病性,但其具体的致病机理尚需进一步阐明。     

Causal role of Helicobacter pylori infection and eradication therapy in gastric carcinogenesis

Many epidemiological reports indicate that Helicobacterpylori(H pylori)infection plays an important role ingastric carcinogenesis.Several genetic and epigeneticalterations contribute to the initiation,promotion,andprogression of the cancer cells in a multi-step manner.H pylori is known to induce chronic inflammation in thegastric mucosa.Its products,including superoxides,participate in the DNA damage followed by initiation,andthe inflammation-derived cytokines and growth factorscontribute to the promotion of gastric carcinogenesis.By eradicating H pylori,gastric inflammation can becured; the therapy diminishes the levels not onlyof inflammatory cell infiltration,but also atrophy/intestinal metaplasia in part.A randomized controlledtrial revealed that the eradication therapy diminishedthe gastric cancer prevalence in cases without pre-cancerous conditions.In addition,recent epidemiologicalstudies from Japanese groups demonstrated thatthe development of gastric cancer,especially of theintestinal type,was decreased by successful eradicationtherapy,although these were designed in a non-randomized manner.However,it should be mentionedthat endoscopic detection is the only way to evaluate thedegree of gastric carcinogenesis.We have reported thatthe endoscopic and histological morphologies could bemodified by eradication therapy and it might contributeto the prevalence of gastric cancer development.Considering the biological nature of cancer cellproliferation,it is considered that a sufficiently long-termfollow-up would be essential to discuss the anticancereffect of eradication therapy.