根除幽门螺杆菌对胃黏膜炎症变化的人群随访研究

目的 观察胃癌高发区中幽门螺杆菌(Hp)阳性者根除Hp5年后胃黏膜组织的炎症变化,以探讨。Hp感染与胃黏膜组织炎症及胃癌的关系。方法 对胃癌高发区山东省烟台市成年人群随机抽样1006例,做内镜、快速尿素酶试验及胃窦、胃体部黏膜组织学检查,将Hp阳性者随机分为治疗组(奥美拉唑20mg、克拉霉素500mg、阿莫西林1000mg)及对照组,2组入选者分别于1年后、5年后进行内镜复检,本研究是将5年后复查胃镜及相同部位胃黏膜组织病理检查与5年前结果进行比较并做χ^2检验。结果 552例Hp阳性者随机分为治疗组及对照组各276例,5年后Hp持续阴性者161例,持续阳性者198例。2组结果统计显示：(1)入选前2组胃窦部炎症及活动度发生率与体部相比差异无显著性,P值分别为0．105及0．084,但萎缩及肠化生发生率明显高于体部,P值均为0．000;(2)根除Hp 5年后胃窦、胃体部炎症及活动度均明显减轻,P值均为0．000;(3)根除Hp5年后胃窦部肠化生减轻或未进展,而Hp持续阳性组肠化生发生率明显增加,P=0．032;(4)根除Hp 5年后窦、体部萎缩改善差异无显著性,两组比较P值分别为0．223及0．402。结论 根除Hp可使胃慢性炎症及活动度明显减轻,窦部肠化生得到显著控制,溃疡病发病明显减少;持续Hp感染可使萎缩及肠化生呈进行性加重。     

根除幽门螺杆菌对胃黏膜癌前病变的影响的Meta分析

目的探讨根除幽门螺杆菌（Hp）对萎缩性胃炎、肠化生等癌前病变的逆转效用。方法全面检索1984年至2008年底国内外生物医学期刊发表的根除Hp对胃黏膜癌前病变影响的临床研究文献及学术会议的交流论文,共6个随机对照试验524例患者进入本系统评价。采用胃黏膜组织学评分、组织学变化作为观察指标。结果（1）Hp根除组胃黏膜萎缩程度改善率显著高于对照组（OR=0．27,95％CI0．17～0．46,P=0．000）;但胃黏膜肠化生改善率在Hp根除组和对照组之间无显著差异（OR=0．55,95％CI0．28～1．08,P=0．082）;（2）Hp根除组Hp根除后胃窦部、胃体、胃底部黏膜的活动性炎症、慢性炎症以及萎缩评分均显著低于对照组（P〈0．01）,但各部位黏膜的肠化生评分改善在Hp根除组和对照组之间无显著差异（P〉0．05）。结论本Meta分析表明,根除Hp可改善慢性萎缩性胃炎的萎缩程度,活动性炎症和慢性炎症程度,但是对胃黏膜肠化生的改善不明显。     

幽门螺杆菌感染与胃癌的相关性研究

目的：为了研究幽门螺杆菌（Hp）感染与胃癌及肠化类型的关系。方法：对胃癌高发区1333例普查人群的胃活检组织和30例胃癌手术标本病理切片做Warthin－starry染色，对慢性萎缩胃炎伴肠化生、慢性浅表胃炎伴肠化生、癌旁肠化生用粘液组化方法染色分型。结果：Hp感染与十二指肠球部溃疡高度相关，与胃溃疡、慢性浅表活动性胃炎、早期胃癌显著相关，与单纯萎缩性胃炎、萎缩胃炎伴肠化生、胃增生性息肉亦相关（P均＜0．05）；进展期胃癌的Hp感染率与慢性非活动性胃炎相比较，差异无显著性（P＞0．05）；各型胃癌中以腺癌Hp检出率高（75．4％），与粘液细胞癌Hp检出率（30％）相比较，差异有非常显著性（P＜0．01）。各型肠化生之间的Hp检出率比较，差异无显著性（P均＞0．05）。结论：Hp感染与胃癌有相关性。     

根除幽门螺杆菌对胃窦黏膜萎缩和肠上皮化生逆转影响的前瞻性研究

目的 探讨根除幽门螺杆菌(Hp)对逆转胃窦黏膜萎缩和肠上皮化生(肠化生)病理改变的作用.方法 对行胃镜检查的门诊患者,于胃窦处取黏膜活检行病理学检查,并确定Hp感染状态.将Hp感染的慢性胃炎伴胃窦黏膜萎缩或(和)肠化生患者作为入选对象并分为两组,一组行Hp根除治疗,为Hp根除组(48例);另一组未行抗Hp治疗,为对照组(38例).分别在1年和5年后对两组患者进行胃镜随访,并在同一部位取材,根据2次病理结果的不同分为逆转和未逆转两种情况.结果 胃窦黏膜萎缩逆转率在Hp根除组显著高于对照组(37.1%比12.0%).5年后Hp根除组的胃窦黏膜萎缩逆转率显著高于1年后,45岁以下者显著高于45岁以上者.而在对照组中,胃窦黏膜萎缩逆转和随访的时间及年龄无明显关系.在2次随访中,肠化生逆转率在Hp根除组和对照组间差异均无统计学意义(P>0.05).结论 根除Hp尚不能逆转胃窦黏膜肠化生,但对逆转胃窦黏膜萎缩有作用,这种作用与随访观察时间及患者的年龄有关.因此,对有Hp感染的胃窦黏膜萎缩者应及早行根除Hp治疗.     

联合培菲康根除幽门螺杆菌对胃黏膜组织学变化的研究

目的 探讨培菲康联合四联疗法根除幽门螺杆菌(Hp)的疗效及对慢性胃炎胃黏膜病理变化和癌前病变的影响.方法 取我院门诊和住院病人102例,采用随机、对照方法分两组,即对照组(A组)及治疗组(B组).A组予四联根除Hp治疗10 d,B组在对照组基础上加培菲康0.42 g tid(与抗生素至少间隔2h)持续服2周.入院时行胃镜及病理检查,于四联服药结束至少4周后复查Hp.随访观察1年后复查Hp和胃镜及病理,分析两组Hp根除率和Hp根除后及未根除患者胃黏膜病理变化情况.结果 治疗组Hp根除率高于对照组,分别为92.2％和74.5％,两组根除率相比差异有统计学意义(P＜0.05).两组不良反应发生率差异有统计学意义(P＜0.05).两组胃黏膜炎症均减轻,但以治疗组明显.两组萎缩、肠化程度亦有减轻,但差异无显著性.而Hp未根除组慢性炎症程度、活动性炎症明显增加,萎缩、肠化程度亦增加,与Hp根除组比较差异有显著性.结论 益生菌(培菲康)联合四联疗法可提高Hp根除率;根除Hp感染可减轻胃黏膜炎症,阻止萎缩和肠化的发生发展.     

胃窦部幽门螺杆菌清除对萎缩性胃炎病理改变的影响

目的通过对幽门螺杆菌（Hp）相关的萎缩性胃炎病人Hp清除治疗前后胃窦部黏膜病理改变的分析，来确定Hp对其炎症程度、活动性（中性粒细胞浸润）、腺体萎缩和肠上皮化生的影响。方法106例Hp相关的萎缩性胃炎患者接受Hp清除治疗，对其治疗前后胃窦部黏膜的病理变化进行分析，分析标准按96悉尼系统评定。结果在62例治疗成功组中，治疗后胃黏膜的炎症程度及活动性较治疗前明显减轻，但腺体萎缩及肠上皮化生未减轻。在44例治疗失败组中，治疗前后胃黏膜的炎症程度、活动性、腺体萎缩及肠化均没有变化。且随着Hp感染时间的延长，腺体萎缩和肠化还可加重。结论Hp的清除治疗可使萎缩性胃炎患者胃黏膜的炎症程度及活动度减轻，对此类病人应行Hp清除治疗。     

根除幽门螺杆菌对消化性溃疡合并胃炎及胃泌素的影响

目的 :评估胃舒散联合呋喃唑酮、阿莫西林对消化性溃疡 (PU)患者Hp根除的效果及其对溃疡合并胃炎、血清胃泌素(Gas)的影响。方法 :77例Hp阳性十二指肠溃疡组 (DU ,52例 )和胃溃疡组 (GU ,2 5例 )患者 ,均服用胃舒散 2 .0g(含铋 0 .1 2g) ,呋喃唑酮0 .1g,阿莫西林 0 .5g ,各 3次 /d ,2周后再继服胃舒散 4周。治疗前及疗程结束 1月后进行内镜检查并对胃窦、胃体胃炎予以内镜下评分。采用放射免疫法于治疗前及结束 1月、6月后检测胃泌素水平。结果 :DU组与GU组溃疡愈合率分别为 1 0 0 %和 92 % ,Hp根除率分别为 90 .3 %和 84.0 % ,二组比较差异均无显著性 (P >0 .0 5)。将根除Hp的 47例DU和 2 1例GU患者分为 2组 ,治疗前 2组胃窦胃炎的评分差异无显著性 (P >0 .0 5) ;GU组胃体胃炎的评分显著高于DU组 (P <0 .0 0 1 ) ;血浆中胃泌素含量 (DU组 39.4± 1 3 .6pg/ml;GU组38.4± 1 2 .3pg/ml)均显著高于正常对照值 (2 8.5± 1 0 .6pg/ml,P <0 .0 5)。Hp根除 1月后 ,2组患者胃窦胃炎与胃体胃炎的评分均显著下降 ,与治疗前自身比较 ,差异有统计学意义 (均P <0 .0 0 1 )。DU组Hp根除治疗 1月后 ,胃泌素水平显著下降到 32 .7± 1 0 .5pg/ml (P <0 .0 5)。GU组Hp根除 1月后 ,胃泌素水平有所下降 ,但与治疗前相比 ,差     

唾液幽门螺杆菌抗原检测与慢性胃炎活动性及癌前病变关系的研究

目的 评价唾液幽门螺杆菌（Helicobacterpylori，Hp）抗原与慢性胃炎活动性以及胃黏膜癌前病变肠上皮化生与不典型增生的相关性。方法 应用酶联免疫吸附法（ELISA），对2004年6月至2005年6月浙江大学医学院附属第二医院消化内科246例接受胃镜检查患者的唾液标本进行幽门螺杆菌抗原检测，分别比较不同胃病患者唾液中Hp抗原的阳性检出率。结果 慢性活动性胃炎组唾液中Hp抗原阳性检出率为74．29％（26／35）．明显高于慢性非活动性胃炎组46．92％（99／211）（P〈0．05）。慢性胃炎组患者唾液中Hp抗原的阳性检出率为45.98％（80／174），慢性胃炎伴轻度肠上皮化生（肠化）组唾液中Hp抗原阳性检出率为52.63％（20／38），慢性胃炎伴中重度肠化组唾液中Hp抗原阳性检出率为68．18％（15／22），慢性胃炎伴不典型增生组唾液中Hp抗原阳性检出率为83．33％（10／12），结果显示．慢性胃炎伴中重度肠化或不典型增生组与慢性胃炎组相比，差异有统计学意义（P〈0．05）。结论 唾液中存在高Hp检出率现象，1：3腔可能为Hp的重要寄居地．1：3腔内Hp感染程度与胃炎活动程度及部分胃黏膜癌前病变有关，慢性活动性胃炎或伴中重度肠化或不典型增生患者口腔内Hp检出率明显增高，口腔内Hp是否需行根除治疗，值得今后进一步研究探讨。     

根除幽门螺杆菌对胃癌患病率及胃黏膜组织学变化的八年随访研究

目的观察胃癌高发区中幽门螺杆菌(Hp)阳性患者根除Hp后8年的胃癌患病率及胃黏膜组织学变化,探讨Hp感染与胃黏膜组织学变化的关系。方法1996年在胃癌高发区山东烟台市自然人群中整群抽样选择1006例成年人(年龄35～75岁,入组时无胃癌患者)。将Hp阳性患者552例随机分为治疗组(T组,276例)和安慰剂组(P组,276例),采用随机、双盲、安慰剂对照平行试验方法,T组给予奥美拉唑、羟氨苄青霉素和克拉霉素口服治疗1周,P组给予安慰剂对照。停药1个月后行13C尿素呼气试验(13CUBT),T组Hp根除率为89%。再按Hp状况重新分为Hp根除组(246例)和Hp阳性组(306例),分别于1、5、8年后进行内镜复查。将8年后复查胃镜及相同部位胃黏膜组织病理检查与8年前结果进行比较。结果①8年随访共发现7例胃癌患者,Hp根除组1例,Hp阳性组6例,两组胃癌患病率按人年计算:Hp根除组为1/1968人年、Hp阳性组为6/2448人年。用泊松分布比较,两组胃癌患病率差异有统计学意义(P<0.05)。②5年随访时两组胃癌患病率及死亡共6例,Hp根除组1例,Hp阳性组5例,两组胃癌患病率按人年计算:Hp根除组为1/1230人年,Hp阳性组为5/1530人年。用泊松分布比较,两组胃癌患病率差异无统计学意义(P>0.05)。③Hp根除8年后,患者胃体部萎缩进展缓慢,而Hp阳性组患者胃体部萎缩发生率明显增加,两组相比差异有统计学意义(P<0.01)。根除Hp8年后胃窦部萎缩肠化改变两组间差异无统计学意义(P>0.05)。结论Hp感染可增加胃癌发病率,根除Hp有利于减少胃癌发生,并可使胃体部萎缩进展缓慢。持续Hp感染可使萎缩及肠化呈进行性加重。     

幽门螺杆菌感染对十二指肠溃疡和功能性消化不良患者胃G细胞功能的影响

目的探讨幽门螺杆菌(Helicobacterpylori,Hp)感染及溃疡灶对胃窦部G细胞功能的影响。方法活动性十二指肠溃疡(DU)77例根据Hp情况分为A组Hp根除组51例,男37例,女14例,年龄为(35．2±12．6)岁;B组Hp持续阳性12例,男9例,女3例,年龄为(34．5±10．3)岁;C组Hp阴性14例,男9例,女5例,年龄为(37．5±11．8)岁。D组为Hp根除的功能性消化不良(FD)25例,男15例,女10例,年龄为(38．1±12．6)岁。治疗前后检查内镜,取胃窦黏膜观察G细胞数量(ABC法免疫组化)、胃泌素基因表达(32P-dATP掺入RT-PCR),血浆胃泌素采用RIA测定。结果各组G细胞数量比较,差异无显著性(P>0．05)。治疗前各DU组(A、B、C组)胃泌素基因表达水平高于FD组(D组)(P<0．01)、Hp阳性DU组(A、B组)与Hp阴性DU组(C组)相似(P>0．05)。治疗后各DU组(A、B、C组)胃泌素基因表达、血浆胃泌素水平有下降趋势,但差异无显著性(P>0．05),而FD组水平均低于根除前(P<0．05)。治疗前FD组胃泌素水平与DU组相似(P>0．05),Hp根除后胃泌素水平低于各DU组(P<0．001)。血浆胃泌素水平与胃泌素基因表达水平正相关(P<0．05)。结论Hp感染不影响胃G细胞数量,但可促进胃泌素基因表达和胃泌素释放,Hp根除后胃泌素水平降低;溃疡灶可使胃泌素过度释放。     

幽门螺杆菌根除对门脉高压性胃病患者预后的影响

目的:探讨幽门螺杆菌(Helicobacter pylori,H pylori)根除对门脉高压性胃病(portal hypertension gastric disease,PHGD)患者疗效．方法:106例PHGD患者,均为H pylori阳性,随机分为:对照组 50例,仅服用奥美拉唑;H pylori根除组56例,口服奥美拉唑和克拉霉素及阿莫西林,试验结束时所有患者均行胃镜复查及14C 呼气试验．结果:试验前46例患者(45．8％)内镜检查发现糜烂性胃炎,试验结束后H pylori根除组50例患者H pylori阴性(95．9％),对照组3例转阴(6．1％),两组H pylori根除率差异显著(P<0．01)．H pylor根除组16例失效,对照组有7例失效,两者相比差异显著(29．8％ vs 14．3％,P<0．05)．对照组患者胃体萎缩及胃体肠化较H pylori根除组明显增多．结论:H pylori根除可降低质子泵抑制剂(PPI)治疗PHGD的疗效,但H pylori根除对PHGD患者胃体糜烂及胃体肠化有防治作用.     

Eradication of Helicobacter pylori infection reverses E-cadherin promoter hypermethylation

BACKGROUND: E-cadherin methylation is important in gastric carcinogenesis. Reversing hypermethylation may halt the carcinogenic process. We have previously reported that Helicobacter pylori infection is associated with E-cadherin methylation in chronic gastritis patients. AIM: To examine if eradication of H pylori could reverse E-cadherin methylation. METHODS: Patients with dyspepsia and positive for H pylori infection, with a mucosal biopsy showing chronic active gastritis, were randomised to receive H pylori eradication therapy (group 1, n = 41) or no treatment (group 2, n = 40), and were followed up prospectively. Gastric mucosae were taken for methylation assay at week 0 (before treatment) and week 6 (after treatment). Archived specimens of intestinal metaplasia with H pylori infection (n = 22) and without (n = 19) were retrieved for methylation analysis. Methylation was assessed using methylation specific polymerase chain reaction and sequencing. RESULTS: Methylation at E-cadherin was detected in 46% (19/41) and 17% (7/41) of patients at weeks 0 and 6, respectively, in group 1 (p = 0.004); 78.9% (15/19) of specimens were unmethylated after eradication of H pylori. Mucosal biopsy showed chronic inactive gastritis in 35 patients, intestinal metaplasia in one, and normal mucosa in five at week 6. Methylation was detected in 47.5% (19/40) and 52.5% (21/40) of patients at weeks 0 and 6, respectively, in group 2 (P = 0.5). Gastric mucosal biopsy showed persistent chronic active gastritis in all cases. Methylation frequency did not differ in H pylori positive or negative intestinal metaplastic specimens (72.7% v 63%; p = 0.5). CONCLUSION: H pylori eradication therapy could reverse methylation in patients with chronic gastritis. This demonstrates an environmental effect on methylation.     

幽门螺杆菌感染对胃黏膜病理变化的影响

背景：幽门螺杆菌(H．pylori)感染已被公认为慢性胃炎和消化性溃疡的重要危险因素，根除H．pylori能加速消化性溃疡的愈合，但其对胃黏膜病理变化的影响尚有待进一步探索。目的：了解根除H．pylori对慢性胃炎胃黏膜病理变化和癌前状态的影响。方法：采用多中心随机对照临床试验和回顾性队列研究，样本选自胃癌高发区：上海郊区的金山区和奉贤区。共纳入360例经内镜检查证实有H．pylori感染的慢性胃炎伴或不伴十二指肠溃疡患者，随机分为两组。治疗组用三联疗法(质子泵抑制剂或Hz受体阻滞剂加两种抗生素)治疗，对照组单纯慢性胃炎患者予西沙必利、十二指肠溃疡患者予西米替丁治疗。在第1年和第4年末随访胃镜，根据H．pylori是否根除将患者分为两组：H．pylori阳性组和H．pylori阴性组。所有胃黏膜活检标本由两位病理科医师统一复读。结果：至第4年末，有120例患者完成全部随访，其中H．pylori持续根除组54例，阳转组5例；H．pylori持续未根除组45例，阴转组16例。持续根除组第1年随访时，活动性炎症比例减少(P＜O．05)；第4年随访时，慢性炎症和肠化程度以及活动性炎症比例减少(P＜O．05)。持续未根除组第1年随访时，慢性炎症程度增加(P＜O．05)；第4年随访时，慢性炎症和肠化程度以及活动性炎症比例增加(P＜O．05)，萎缩程度较第1年随访时增加(P＜O．05)。结论：根除H．pylori可以减轻慢性胃炎的炎症程度，防止肠化的发生和发展。     

Effects of Helicobacterpylori eradication on atrophic gastritis and intestinal metaplasia： A 3-year follow-up study

AIM: To investigate the effect of H pylori eradication on atrophic gastritis and intestinal metaplasia (IM). METHODS: Two hundred and fifty-nine patients with atrophic gastritis in the antrum were included in the study, 154 patients were selected for H pylori eradication therapy and the remaining 105 patients served as untreated group. Gastroscopy and biopsies were performed both at the beginning and at the end of a 3-year follow-up study. Gastritis was graded according to the updated Sydney system. RESULTS: One hundred and seventy-nine patients completed the follow-up, 92 of them received H pylori eradication therapy and the remaining 87 H pylori-infected patients were in the untreated group. Chronic gastritis, active gastritis and the grade of atrophy significantly decreased in H pylori eradication group (P<0.01). However, the grade of IM increased in H pylori -infected group (P<0.05). CONCLUSION: H pylori eradication may improve gastric mucosal inflammation, atrophy and prevent the progression of IM.     

乙、丙型肝炎病毒及幽门螺杆菌在慢性肝炎、肝硬化患者胃黏膜的表达

目的 探讨乙、丙型肝炎病毒(HBV、HCV)的泛嗜性及幽门螺杆菌(Helicobacter pylori)感染的关系。方法 选择慢性乙型肝炎(慢肝)28例、乙型肝炎后肝硬化(肝硬化)44例,共72例作为观察组,无肝病的胃病患者30例作为对照组。受检者常规胃镜检查,取胃窦幽门周围3cm以内活体组织3块,除普通病理检查外,分别做乙型肝炎病毒表面抗原(HBsAg)、乙型肝炎病毒核心抗原(HBcAg)、丙型肝炎病毒抗原(HCVAg)检测及快速尿素酶、品红染色和免疫组化法检测H.pylori抗原(HPAg)。结果 慢肝组有不同程度的胃黏膜慢性炎症者达92.9％(26/28)、肝硬化组为95.5％(42/44)。排除年龄影响因素外,慢肝组以单纯慢性炎症为多,而肝硬化组以伴萎缩和肠化者多。72例慢性肝病者中有51例胃黏膜HBVAg阳性,其中HBsAg、HBcAg双阳性31例。肝硬化组HBsAg或HBcAg表达及HBsAg、HBcAg双阳性者均高于慢肝组(P均<0.05)。51例慢性肝病胃黏膜中有33例占64.7％有HCVAg表达;其中22例占52.4％与HBsAg或(和)HBcAg同时表达。在慢肝和肝硬化组有炎症的胃黏膜中H.pylori阳性率分别为67.9％(20/26)、69.0％(29/42),与对照组相比无显著差别。慢性肝病H.Pylori阳性、阴性者胃黏膜HBV抗原表达率分别为69.8％(37/53)、73.7％(14/19),亦无统计学差异(P>0.05)。结论 (1)HBV、H     

萎缩性胃炎患者幽门螺杆菌根除后表皮生长因子及其受体的变化

目的　研究幽门螺杆菌 (Helicobacterpylori,H .pylori)感染对胃黏膜表皮生长因子受体 (epidermalgrowthfactorreceptor ,EGFR)、血清表皮生长因子 (epidermalgrowthfactor,EGF)水平的影响。方法　对 60例H pylori检测阳性的慢性萎缩性胃炎患者进行根除治疗 ,在治疗前及疗程结束 3个月后分别进行胃镜检查 ,并采用免疫组化及放射免疫法测定H pylori根除前后胃黏膜EGFR和血清EGF含量。 3 0例H pylori检测阴性且胃镜检查无明显异常者作为正常对照组。结果　 60例H pylori检测阳性的CAG患者的胃黏膜EGFR阳性率及血清EGF水平均高于正常对照 ,其差异有显著性 (P <0 0 5 ,P <0 0 1)。有 3 1例在根除治疗 3个月后进行了复查 ,其中 2 4例H pylori得到成功根除。 2 4例H pylori得到根除的CAG患者 ,根除后血清EGF水平明显下降 (P <0 0 1) ,而EGFR阳性率无改变 (P >0 0 5 )。结论　H pylori感染引起胃黏膜EGFR阳性率及血清EGF水平增加 ,根除H pylori后血清EGF可恢复至正常水平 ,而胃黏膜EGFR阳性率在短期内没有明显改变     

Apparent Reversal of Early Gastric Mucosal Atrophy after Triple Therapy for Helicobacter pylori

Helicobacter pylori may be difficult to detect in individuals with intestinal metaplasia or atrophic gastritis, even though bacteria may persist in the mucosa in low numbers, maintaining elevated serum H. pylori antibody levels. We report a patient with marked, endoscopically visible gastric mucosal changes and focal changes of histological atrophic gastritis, who was negative for H. pylori on urease test, culture, and histology, but had positive H. pylori serology. When treated with triple therapy and reassessed at 6 months, his H. pylori antibody titer fell to low/negative levels, abnormal mucosa was replaced by a velvety, normal lining, and the previous evidence of histological atrophic gastritis was no longer detectable.     

Expression of gastric cancer—associated MG7 antigen in gastric cancer,precancerous lesions and H.pylori—associated gastric diseases

AIM: To investigate the relationship between the antigen MG7 antigen expression and gastric cancer as well as precancerous condition; to study the relationship between the MG7 antigen expression and H. pyloriinfection in benign gastric lesions in order to find out the effect of H. pylori infection on the process of gastric cancer development.METHODS: The level of MG7 antigen expression was determined by immunohistochemical method in 383 gastric biopsied materials. The intestinal metaplasia was determined by histochemistry method. The H. pyloriinfection was determined by HE stain, PCR and ELISA in 291 specimens, among which only 34 cases of H. pylori-associated gastric lesions were followed up.RESULTS: The positive rate of MG7 expression in normal gastric mucosa, intestinal metaplasia, dysplasia and gastric cancer increased gradually in ascending order (P＜0.01). The positive rate of MG7 antigen expression in type Ⅲ intestinal metaplasia of gastric mucosa was higher than that of type Ⅰand Ⅱ intestinal metaplasia, being highly significant (P＜0.05).The positive rate of MG7 antigen expression in superficial gastritis, atrophic gastritis and gastric cancer increased gradually (11.9 %, 64.8 %, 91.2 %, P＜0.01). There was no significant difference between H.pylori-negative and H. pyloripositive intestinal metaplasia, atrophic gastritis and dysplasia of gastric epithelium in the positive rate of MG7 antigen expression. There was no expression of MG7 antigen in H. pylori-negative superficial gastritis. The positive rate of MG7 expression in H. pylori-positive superficial gastritis was 20.5 %, and the difference between them was significant (P＜0.05). During following up, one of the three H. pylori negative cases turned positive again, and its MG7 antigen expression turned to be stronger correspondingly. 3 of 31 H. pyloripositive cases were detected as early gastric cancer, among which one with "+++" MG7 antigen expression was diminished after H. pylori eradication.CONCLUSION: MG7 antigen expression is highly specific in gastric cancer and can be used as a good marker for screening of gastric cancer; type Ⅲ intestinal metaplasia, atrophic gastritis and dysplasia should be followed up and MG7 antigen expression has high clinical value in the dynamic follow-up study; although the positive -MG7 in positiveH. pylorisuperficial gastritis show benign morphology in features, there is still the potential risk of developing into gastric cancer, hence special attention should be paid to those showing increasing MG7 antigen expression.     

Effect of Helicobacter pylori infection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis.

BACKGROUND: Helicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability. AIM: To evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression. METHODS/SUBJECTS: Morphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients with H pylori negative chronic gastritis, 53 with H pylori positive chronic gastritis, and 11 with gastric cancer. RESULTS: All patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pylori infection. Atrophy was present in three of 10 patients with H pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients with H pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whom H pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged. CONCLUSIONS: Chronic H pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication of H pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.     

Hp相关性胃疾病与胃肠化生、不典型增生的关系

目的探讨Hp感染与肠化生、不典型增生等胃癌前期病变的关系.方法693例胃病患者,分慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)、胃溃疡(GU)及十二指球部溃疡(DU)等四组,胃镜下观察粘膜病变、溃疡部位及性质,胃镜下取材,常规HE染色后观察组织学改变、Giemsa染色后观察Hp感染程度,统计分析Hp感染与肠化生、不典型增生等的关系.结果四组胃疾病中,Hp感染程度与肠化尘程度差异显著(P＜0.01),DU组的Hp感染率高于其它组(P＜0.01),CAG组的胃肠化生率最高(P＜0.05);Hp阳性标本中,CAG组的胃肠化及不典型增生最高(P＜0.01)Hp阴性标本中,CAG组的胃肠本的胃肠化和不典型增生发生率与Hp阴性标本的发生率有显著差异(P＜0.05).结论Hp与CAG并存时,癌前病变发生率最高,其次为GU;建议在临床上,抗Hp治疗和对CAG、GU的治疗同时进行,并内镜随访.