胃癌前病变中幽门螺杆菌分布的感染研究

目前不仅公认幽门螺杆菌 (Ｈｐ)的慢性感染对消化性溃疡的形成起重要作用 ,而且很多Ｈｐ感染的慢性胃炎被证实与胃粘膜上皮的增殖和淋巴组织恶变有密切关系 ,所以国际癌症研究会把Ｈｐ列为胃癌的Ⅰ类致癌病原[1] 。Ｈｐ感染可引起慢性活动性胃炎 ,而且会逐步发展导致全胃炎 ,在感染后期会产生慢性萎缩性胃炎 (ＣＡＧ)、肠上皮化生 (ＩＭ ) ,甚至异型增生 (ＤＹＳ) [2 ] ,而这一系列的病变是胃癌形成的高危状态 ,或称癌前病变。本文通过对 486例胃粘膜病变的Ｈｐ感染的检测研究 ,探讨Ｈｐ可能的致癌机制。材料和方法经内镜和病理活检诊断明确…     

幽门螺杆菌感染与胃癌前病变的关系

为探讨幽门螺杆菌（ＨＰ）与胃癌前病变的关系，本文回顾性分析了４５１例因上腹部不适而在本院做胃镜的患者。共检查出ＨＰ阳性２４２例（５３．７％），ＨＰ感染时肠化生及胃粘膜萎缩的发生率分别为１４．９％（３６／２４２）及９．１％（２２／２４２），显著高于无ＨＰ感染的肠化生及萎缩发生率８．１％（１７／２０９）及３．３％（７／２０９）（Ｐ＜０．０５）。ＨＰ感染时发生肠化生及萎缩的平均年龄分别为４６．６±１４．５岁及３９．３±１３．７岁，显著小于无ＨＰ感染时的肠化生及萎缩年龄５６．２±９．２岁及５８．２±８．７岁（Ｐ＜０．０１）。本文结果提示早年感染ＨＰ可使肠化生及萎缩性胃炎发病率升高，故ＨＰ感染可能是胃癌的致病因素之一。     

幽门螺杆菌感染所致胃癌前病变的治疗研究进展

幽门螺杆菌(Hp)的发现至今已有20多年的历程,对于其自身及其相关性疾病的研究也逐步深入,成为众多学者研究的热点,新观点、新发现亦层出不穷.为更好服务于临床,发掘中医药的优势,现将Hp对胃癌前病变(PLGC)的影响综述如下.     

幽门螺杆菌及其根除治疗与胃癌前病变

幽门螺杆菌 (H .pylori)感染与胃癌前病变的发生及演变过程密切相关 ,而其根除治疗在胃癌前病变干预和治疗中的作用倍受争议。该文综述了胃癌前病变中H .pylori的感染状况 ;H .pylori致萎缩、肠化的机制 ;H .pylori对胃癌前病变细胞增殖与凋亡的影响。进一步总结了根除治疗所取得的成果 ,展望了今后研究发展的方向和前景。     

幽门螺杆菌与胃癌前病变的关系

同期检出的胃粘膜病变共302例,其中慢性浅表性胃炎(CSG)132例;慢性萎缩性胃炎(CAG)96例;肠上皮化生(IM)51例;异型增生(DYS)23例。每例于胃窦大小弯侧,胃体大小弯则取粘膜组织4块,分别进行HE染色病理检查和Hp染色的Warthin-starry染色。以镜下见到棕黑色典型Hp菌体为Hp阳性。     

幽门螺杆菌感染与胃癌的关系

目的研究幽门螺杆菌(Hp)感染与胃癌的关系必须研究其与胃癌前病变的关系.方法回顾分析5216例因上消化道症状做目铺患者的Hp检测及胃粘膜病理学检查结果结果Hp总检出率为45.8%,萎缩性胃炎、肠化生及异型增生的Hp检出率显著高于Hp总检出率(P<0.05),上述3种胃癌前病变之间Hp检出率无显著差异,Hp阳性患者3种癌前病变的发生率显著高于Hp阴性患者(P<0.01),萎缩性胃炎和肠化生的发生年龄亦显著提早.Hp阳性患者在3种癌前病变的程度上与Hp阴性患者无显著差异(P>0.05),随着病变程度的加重,Hp检出率逐渐下降;Hp阳性患者的肠化类型与Hp阴性患者无显著性差异(P>0.05).结论Hp感染与胃癌密切相关,Hp感染主要作用于癌前病变的起始阶段.     

幽门螺杆菌感染与胃癌前病变及胃癌的关系

幽门螺杆菌(HELICOBACTER PYLIRI,HP)是上胃肠道疾病的重要致病因子。现就HP感染与胃癌前病变及胃癌的关系综述如下。     

幽门螺杆菌胃内分布与慢性胃炎病变的关系

幽门螺杆菌（Ｈｐ）感染是慢性胃炎的病因之一,是某些胃病的促发因子［１］。Ｈｐ主要定植在胃窦部,随着慢性胃炎的病程进展,Ｈｐ也有从胃窦向胃体、胃底移行的趋势。为此我们对１３４６例Ｈｐ阳性的患者进行观察分析,发现Ｈｐ在胃内定植部位及其密度与胃部病变的发生...     

口腔幽门螺杆菌和胃内幽门螺杆菌感染的关系

幽门螺杆菌(H．pylori)与上胃肠道疾病密切相关，口腔为上消化道入口，有学者提出口腔中亦有H．pylori的生存，并认为口腔H．pylori感染和胃H．pylori感染之间存在一定的相关关系，口腔H．pylori感染可能是胃内H．pylori根除治疗后复发的一个潜在的再感染源。     

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。     

胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin6的表达及其与幽门螺杆菌感染的关系

目的探讨胃黏膜病变演化过程中抗氧化蛋白Peroxiredoxin 6(Prx6)表达水平变化及其与幽门螺杆菌(H.pylori)感染的关系。方法根据组织形态学将104例临床内镜检查活检标本分为慢性浅表性胃炎(33例)、慢性萎缩性胃炎(25例)、肠上皮化生(32例)及异型增生(14例)4组。用免疫组织化学方法检测组织标本中Prx6的表达水平。用快速尿素酶试验及Warthin-Starry银染检测H.pylori感染。结果 Prx6在慢性浅表性胃炎、慢性萎缩性胃炎、肠上皮化生、异型增生组的阳性表达率分别为39.4%(13/33)、80.0%(20/25)、93.8%(30/32)、92.9%(13/14),过表达率分别为15.2%(5/33)、44.0%(11/25)、81.3%(26/32)、85.7%(12/14)。慢性浅表性胃炎、慢性萎缩性胃炎组H.pylori阳性者Prx6阳性表达率显著高于H.pylori阴性者(P<0.05),肠上皮化生组Prx6的表达在H.pylori阳性者和阴性者无显著差异(P>0.05)。结论在胃黏膜病变演化过程中,Prx6的表达随着胃黏膜病变的进展而增加,H.pylori在胃黏膜病变演化的早期阶段促进了Prx6的表达。     

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.     

Effect of Helicobacter pylori infection on Bax protein expression in patients with gastric precancerous lesions

AIM: To investigate the effect of Helicobacter pylori (H pylori) infection on Bax protein expression, and explore the role of H pylori in gastric carcinogenesis. METHODS: H pylori was assessed by rapid urease test and Warthin-Starry method, and expression of Bax protein was examined immunohistochemically in 72 patients with pre-malignant lesions. RESULTS: Bax protein was differently expressed in intestinal metaplasia and gastric dysplasia, and showed 63.99% positivity. The positivity of Bax protein expression in Hpylori-positive gastric precancerous lesions (72.3%) was significantly higher than that in H pylori-negative gastric precancerous lesions (48.0%, X~2=4.191, P<0.05). H pylori infection was well correlated with the expression of Bax protein in gastric precancerous lesions (r=0.978, P<0.01). After eradication of H pylori, the positivity of Bax protein expression significantly decreased in H pylort-positive gastric precancerous lesions (X~2=5.506, P<0.05). In the persisting H pylori-infected patients, the positivity of Bax protein expression was not changed. CONCLUSION: H pylori infection may be involved in the upregulation of Bax gene, which might be one of the mechanisms of H pylori infection-induced gastric epithelial cell apoptosis. H pylori might act as a tumor promoter in the genesis of gastric carcinoma and eradication of H pylori could inhibit gastric carcinogenesis.     

Helicobacter pylori and cytokine gene variants as predictors of premalignant gastric lesions

Gastric cancer remains the third leading cause of mortality from cancer worldwide and carries a poor prognosis,due largely to late diagnosis.The importance of the interaction between Helicobacter pylori(H.pylori)infection,the main risk factor,and host-related genetic factors has been studied intensively in recent years.The genetic predisposition for non-hereditary gastric cancer is difficult to assess,as neither the real prevalence of premalignant gastric lesions in various populations nor the environmental risk factors for cancer progression are clearly defined.For non-cardiac intestinal-type cancer,identifying the factors that modulate the progression from inflammation toward cancer is crucial in order to develop preventive strategies.The role of cytokines and their gene variants has been questioned in regard to non-self-limiting H.pylori gastritis and its evolution to gastric atrophy and intestinal metaplasia;the literature now includes various and non-conclusive results on this topic.The influence of the majority of cytokine single nucleotide polymorphisms has been investigated for gastric cancer but not for preneoplastic gastric lesions.Among the investigated gene variants onlyIL10T-819C,IL-8-251,IL-18RAP917997,IL-22 rs1179251,IL1-B-511,IL1-B-3954,IL4R-398 and IL1RN were identified as predictors for premalignant gastric lesions risk.One of the most important limiting factors is the inhomogeneity of the studies(e.g.,the lack of data on concomitant H.pylori infection,methods used to assess preneoplastic lesions,and source population).Testing the modifying effect of H.pylori infection upon the relationship between cytokine gene variants and premalignant gastric lesions,or even testing the interaction between H.pylori and cytokine gene variants in multivariable models adjusted for potential covariates,could increase generalizability of results.     

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.     

幽门螺杆菌感染在胃癌及癌前病变中的研究

目的　研究胃癌及癌前病变与Hp感染的关系 ,以探讨Hp可能的致癌机制。 方法　经内镜和病理明确诊断的胃癌及癌前病变者共 5 48例 ,包括慢性浅表性胃炎 (CSG) 16 3例、慢性萎缩性胃炎 (CAG) 2 0 7例、肠上皮化生 (IM) 71例 ,异型增生(DYS) 4 5例及胃癌 (GC) 6 2例。每例均活检胃窦大小弯、胃角及胃体大小弯共 5块 ,以WS法检测Hp。结果　癌前病变及胃癌Hp感染均较高 ,CAG(4 2 .5 % ) ,IM(76 .1% ) ,DYS(88.9% )和GC(72 .5 % ) ,与CSG(2 3.9% )有显著性差异 (P <0 .0 5或P <0 .0 1)。随着年龄增大 ,CAG、IM、DYS和GC逐步增多 ,而且≥ 5 6岁年龄组IM、DYS和GC显著多于≤ 40岁组 (P <0 .0 5 ) ,但CSG则相反。肠型胃癌和Hp感染密切相关 (P <0 .0 5 ) ,从胃窦小弯和大弯、胃角及胃体小弯和大弯顺序 ,Hp感染随着CSG、CAG、IM、DYS和GC病变而增高 ,Hp感染部位也在上移 ,尤其在胃体小弯及大弯 ,IM、DYS和GC的Hp感染显著高于CSC部位 (P <0 0 5 )。结论　Hp感染是导致从胃炎→胃萎缩→肠化→异型增生→癌变序列发展的危险因子 ,肠型胃癌和Hp感染密切相关 ,胃镜检查应该多部位取活检作病理及Hp检测 ,尤其是高位     

Helicobacterpylori infection and gastropathy： A comparison between Indonesian and Japanese patients

AIM: To compare the effects of Helicobacter pylori ( H pylori) infection on gastropathy between Indonesian and Japanese patients.METHODS: Biopsy specimens were obtained during upper gastrointestinal endoscopy from 167 subjects (125 Indonesians and 42 Japanese) with uninvestigated symptoms of dyspepsia. The specimens were analyzed for the presence of H pylori using urease analysis, histopathology, and cell culture. The grade and activity of gastritis was assessed using the updated Sydney system.RESULTS: The percentages of Indonesian and Japanese patients who were H pylori-positive at the antrum or body of the stomach were similar (68% and 59.5%, respectively; P = 0.316). Of those who were H pylori-positive, more Japanese patients than Indonesian patients had high levels of polymorphonuclear cells ( P = 0.001), mononuclear cells ( P = 0.013), glandular atrophy ( P = 0.000), and intestinal metaplasia ( P = 0.011) in both the antrum and body of the stomach.CONCLUSION: The grade of gastritis and prevalence of mucosal atrophy and intestinal metaplasia were higher in Japanese patients. The difference between Indonesian and Japanese patients was significant.     

幽门螺杆菌长期感染与胃黏膜炎症和肠上皮化生的关系

目的探讨幽门螺杆菌(Hp)长期感染及根除与胃黏膜炎症和肠上皮化生(IM)的关系。方法随访71例5年前和78例10年前Hp感染者,分析对比其前后Hp感染情况、胃黏膜炎症和IM的变化。结果5年前Hp阳性71例中,现在52例(73.2％)Hp仍呈阳性,19例(26.8％)转阴;10年前Hp阳性的78例中,现在59例(75.6％)Hp仍呈阳性,19例(24.4％)转阴。Hp长期阳性者5年前和现在及10年前和现在慢性炎症严重程度积分分别为1.635±0.376与1.808±0.301(P>0.05)和1.661±0.398与2.232±0.335(P<0.01);IM的发生率分别为17.3％(9/52)与26.9％(14/52)(P>0.05)和11.9％(7/59)与39.0％(23/59)(P<0.01);IM严重程度积分分别为1.444±0.527与1.667±0.442(P>0.05)和1.571±0.534与2.286±0.488(P<0.05)。Hp转阴者5年前和现在及10年前和现在慢性炎症严重程度积分分别为1.684±0.369与1.369±0.426(P<0.05)和1.647±0.389与1.182±0.396(P<0.01);IM的发生率为31.6％(6/19)和52.6％(10/19);IN严重程度积分分别为1.333±0.516与1.167±0.775(P>0.05)和1.600±0.516与1.100±0.316(P<0.05)。结论Hp感染持续时间越长,胃黏膜炎症越严重,IM程度亦越严重且发生率高;根除Hp不仅能减轻胃黏膜的炎症程度和IM程度,而且能防止IM的发生。     

胃黏膜癌前病变中p53、p21^ras蛋白表达与幽门螺杆菌感染的关系

目的观察幽门螺杆菌(Helicobacterpylori)感染及根除H.pylori二年后p53、p21ras在二组胃黏膜上皮细胞的表达,探讨H.pylori在胃癌发生、发展中的作用.方法应用免疫组织化学染色、尿素酶快速试验(RUT)、组织学Warthin-Starry染色.198例H.pylori感染患者,慢性胃炎86例,慢性胃炎伴肠化生67例,慢性胃炎伴异型增生45例;对照组为根除H.pylori 2年后共86例,其中慢性胃炎54例,慢性胃炎伴肠化生32例,慢性胃炎伴异型增生10例.全部病例做p53、p21ras免疫组织化学染色.结果 H.pylori感染组p53、p21 ras 阳性表达率15.7%、18.7%,明显高于H.pylori根除组2.3%、7%,差异显著(P＜0.05);慢性胃炎伴肠化病变中,p53、p21ras在H.pylori感染组阳性表达率17.9%、18.4%均高于H.pylori根除组0%、9.4%,差异显著(P＜0.05)慢性胃炎伴异型增生病变中,p53、p21 ras在H.pylori感染组阳性表达率31.1%、40%均高于H.pylori根除组20%、30.4%,差异显著(P＜0.05);H.pylori 感染组p53、p21ras在慢性胃炎,肠化生,异型增生表达水平依次增高p53、p21ras共同表达阳性37例.结论在胃黏膜癌前病变中p53、p21ras 在H.pylori感染组阳性表达率高于H.pylori根除组,差异显著(P＜0.05);在慢性胃炎,肠化生,异型增生p53、p21ras表达水平在增高;p53、p21 ras表达呈正相关;H.pylori感染在胃癌发生、发展过程中起一定作用,p53、p21ras表达可能是H.pylori致癌的作用机理之一.     

非幽门螺杆菌感染患者上腹部不适的可能机制

目的 探讨非幽门螺杆菌感染患者上腹部不适相关症状的可能机制.方法 收集2006年8月至11月初次行胃镜、组织学检查幽门螺杆菌呈阴性的成人患者232例,2005年9月至2009年8月门诊及住院儿童患者31例(年龄<14岁).对以上患者行胃镜取胃黏膜组织做连续切片,HE染色及WS染色观察组织学改变.结果 成人组患者组织内可观察到微、小动脉腔堵塞和(或)灶性出血病变,其中16例(8.8%)黏膜和(或)黏膜下层见微、小动脉腔部分或完全堵塞,82例(45.6%)仅有黏膜灶性出血,82例(45.6%)两种病变同时存在.微、小动脉腔堵塞病变以移行部检出率最高(65.2%,P=0.159),灶性出血病变以底体部检出率最高(65.6%,P=0.001).微、小动脉腔堵塞病变组烧心症状发生率显著低于无动脉腔堵塞/出血病变组(x2=8.564,P=0.003).儿童组中96.8%(30/31)的患者活检组织中观察到微、小动脉腔堵塞和(或)灶性出血病变.结论 胃微、小动脉堵塞引起的黏膜缺血比较常见,可发生于各个年龄段,可能是导致非幽门螺杆菌感染患者上腹部不适相关症状的重要原因.