Helicobacter pylori

Helicobacter pylori infection is a major cause of peptic ulcer disease, and its detection and eradication are now an important part of gastroenterology. Effective regimes are available which will eliminate the organism in about 90% of cases in developed countries.     

Helicobacter pylori.

Since 1983, rapid advances in the knowledge of Helicobacter pylori have given new insights into the pathogenesis of upper gastrointestinal diseases. Several methods are now available for the diagnosis of the infection. Antimicrobial therapy has emerged as a new and effective treatment for peptic ulcer disease in a proportion, as yet to be determined, of patients in the Caribbean.     

幽门螺杆菌感染与胃癌

自1983年发现幽门螺杆菌(Helicobacter pylori．H．pylori)以来，大量流行病学资料显示，Hp感染与胃癌的发生密切相关。1994年世界卫生组织国际癌症研究机构(IARC)将幽门螺杆菌(Helicobacter pylori．Hp)列为人类胃癌第1类致癌原。Hp与胃癌关系的研究更加受到重视。目前认为HD感染为胃癌发生的始发因素，而综合因素     

幽门螺杆菌与胃癌

幽门螺杆菌(Hp)感染与胃癌的发生密切相关，其分子机制非常复杂，可能通过多个途径的调节而发生。动物模型的建立为阐明Hp感染在胃癌发生中的作用奠定了基础。本文就近年来该领域流行病学、动物模型、分子发病机制等研究作一综述。     

Helicobacter pylori and gastric diseases

Helicobacter pylori (H. pylori) infection is a pathogenic agent of gastric diseases, but their mechanisms are unclear. Effects of ammonia, tumor necrosis factor (TNF), and anti-Lewis autoantibodies induced after H. pylori infection on the development of gastric diseases were investigated. Ammonia disturbed the collagen metabolism in the ulcer base. Soluble TNF receptors regulate the action of TNF. The involvement of anti-Lewis autoantibodies in the development of peptic ulcer might be unlikely. Moreover, H. pylori-specific IgA in gastric juice and TNFalpha gene polymorphism in persons infected with H. pylori were studied. According to H. pylori-specific IgA titer in gastric juice, persons were divided into two histologically and endoscopically different states of disease. TNFA -857 single nucleotide polymorphism (SNP) may be associated with rugal hyperplastic gastritis and gastric carcinomas without severe atrophy. However, complete elucidation of pathogenic mechanisms of H. pylori-induced gastric diseases requires further research.     

Helicobacter pylori in children

The clinical manifestations of Helicobacter pylori (formerly Campylobacter pylori) infection in children overlap with those encountered in adults but there are some important differences. The aim of this review is to describe the range of manifestations of this infection in children, together with means of diagnosis and treatment.     

Transmission of Helicobacter pylori

Helicobacter pylori is found predominantly in human gastric mucosa. Transfer of the bacterium remains an open topic, but it is likely that infection is usually acquired at a young age, particularly where lower socio-economic conditions prevail. Transmission via an external source such as water supply is a possibility but, in general, infection is probably passed from person to person. Arguments for and against faecal-oral, oral-oral and gastric-oral transmission have been presented, but the dominance of one of these routes is still to be determined.     

幽门螺杆菌的耐药性分析

目的:分析幽门螺杆菌(Hp)菌株对阿莫西林、克拉霉素、甲硝唑、呋喃唑酮的耐药情况,并探讨Hp对克拉霉素耐药与23S rRNA基因点突变的关系.方法:分离培养Hp,药敏纸片法进行药敏实验,按酚-氯仿法提取Hp的DNA,PCR方法扩增23S rRNA基因中的片段,用限制性片段长度多态性(PCR-RFLP)检测克拉霉素耐药菌株的点突变.结果:Hp菌株对阿莫西林、克拉霉素、甲硝唑、呋喃唑酮的耐药率分别为9.3%、18.6%、53.5%、0%;8个克拉霉素耐药的Hp菌株有7个存在23S rRNA基因的A2143G点突变,进行PCR-RFLP的29个敏感菌株均无23S rRNA的点突变.结论:Hp菌株对甲硝唑耐药率高,对克拉霉素、阿莫西林和呋喃唑酮敏感;23S rRNA基因A2143G点突变与Hp对克拉霉素的耐药相关.     

幽门螺杆菌感染与非甾体类抗炎药

目的探讨幽门螺杆菌感染与非甾体类抗炎药的关系.方法将本院收治的110例连续服用非甾体类抗炎药治疗4～12周的患者行胃镜及病理组织学检查,经检查将110例患者分为幽门螺杆菌感染组和非感染组,分析非甾体类抗炎药与幽门螺杆菌感染的关系.结果幽门螺杆菌感染组45例,非甾体类抗炎药相关性胃病发生率17.78%(8/45),幽门螺杆菌感染组65例,非甾体类抗炎药相关性胃病发生率18.46%(12/65).结论幽门螺杆菌感染并不加剧非甾体类抗炎药相关性胃病的发生.     

Helicobacter pylori: pathogen and symbiont

There are puzzles in defining the exact role of Helicobacter pylori infection in humans. The bacterium, which is associated with human disease of the upper gastrointestinal tract, may otherwise exist as a commensal with probable symbiotic association in some human hosts. Although virulence associated genes have been detected in some strains which explain their pathogenicity, their pathogenic effect and subsequent clinical manifestations seem to vary in different human populations or geographical locations. Some human hosts remain predominantly asymptomatic in spite of the "virulent" H. pylori strain(s) they harbour. There are probable benefits of H. pylori colonisation of the human gastric mucosa. Thus the recommendation of eradication therapy in patients with known peptic ulcer disease may be more advantageous than the "test and treat policy", which suggests treatment of uninvestigated dyspeptic patients, who may not have any lesions.     

幽门螺杆菌L型及其致病性

目的：对幽门螺杆菌L型的生物学特性与致病性进行研究。方法：在体外用羧苄西林诱导幽门螺杆菌形成L型以研究其生物学特性，分别取幽门螺杆菌原菌与L型感染实验小鼠以测定其生物学特性与致病性。取136份胃癌与30份慢性胃炎患者标本进行组织学检查和细菌分离。结果：体外诱导的L型与原菌在特性上差别很大，但仍能以免疫酶染色与PCR法识别，实验动物感染，在体内的L型呈圆球体，大多在胃与十二指肠黏膜引起间质性炎症，一只腺脏并见有恶性病变，临床胃癌标本检查见L型亦呈圆球体状，77.3%患者幽门螺杆菌抗原阳性。慢性胃炎胃液分离，除见有幽门螺杆菌外，并有多种细菌和L型存在。结论：幽门螺杆菌L型形态多变，其中以圆球体多见于病原部位。且导致间质性和肿瘤的形成。但与慢性胃炎的关系尚有待进一步研究。     

幽门螺杆菌耐药性对其根除治疗影响的研究

目的了解幽门螺杆菌（Hp）耐药菌株以及患者性别、年龄和不同临床疾病对Hp根除治疗的影响,阐明Hp根除治疗失败的主要原因。方法对因上胃肠道症状而来北京大学第一医院胃镜室接受胃镜检查的Hp培养阳性患者,采用E-试验法测定Hp菌株对甲硝唑及克拉霉素的最低抑菌浓度（MIC）。对所有人选患者采用兰索拉唑、甲硝唑和克拉霉素的三联7d疗法进行Hp根除治疗。结果共有157例患者进入本研究,并完成了治疗。Hp对甲硝唑和克拉霉素的耐药率分别为：45．9％（72／157）和18．5％（29／157）。157例接受治疗患者的Hp根除率为61．8％（97／157）,Hp根除率在不同性别、年龄及不同临床疾病患者之间差异均无统计学意义（均P〉0．05）;甲硝唑敏感菌株和耐药菌株的根除率分别为89．4％（76／85）和29．2％（21／72）（P〈0．01）。克拉霉素敏感菌株和耐药菌株的根除率分别为72．7％（93／128）和16．0％（4／29）（P〈0．01）。结论Hp对抗生素耐药是导致Hp根除治疗失败的主要原因。     

特发性血小板减少性紫癜患者幽门螺杆菌尿素酶B检测及抗幽门螺杆菌治疗效果分析

目的分析特发性血小板减少性紫癜（ITP）患者的幽门螺杆菌（Hp）感染情况,探讨抗Hp治疗对Hp感染阳性ITP患者的疗效。方法 ITP组45例,正常对照组32例,利用双抗夹心ELISA法检测两组Hp感染情况,对Hp感染阳性的ITP患者在治疗ITP的同时加用抗Hp治疗,与ITP组中Hp阴性病例治疗后的血小板数进行比较。结果 ITP组及正常对照组的Hp检出阳性率分别为66.7%与43.8%,ITP组Hp阳性率明显较高（P〈0.05）;25例Hp阳性的ITP患者经抗Hp治疗后,转阴21例的血小板数明显高于ITP组中Hp阴性组（P〈0.05）;Hp根除后的21例中,有12例血小板计数明显上升或恢复正常。结论 ITP患者Hp感染阳性率高于正常人;抗Hp治疗可以提高Hp感染的部分ITP患者血小板数量;Hp感染可能与ITP发病有关。