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。     

幽门螺杆菌与胃液素关系的探讨

幽门螺杆菌(Hp)感染后血清胃液素增高是由于Hp感染使胃内pH增高所致。为探讨这一问题,我们于1991年5月起对此进行了观察,报告如下。 1 对象和方法 本组男性59例,女性9例。年龄最小23岁,最大97岁,平均42.3岁。胃镜诊断为十二指肠溃疡(DU)、胃溃疡(GU)、浅表性胃炎(CSG)、萎缩性胃炎(CAG)及疣状胃炎     

幽门螺杆菌与慢性胃病的相关性

目的了解幽门螺杆菌(Hp)在慢性胃炎(CG)和消化性溃疡(PU)患者中的感染情况及其相关性.方法对1245例胃病患者的Hp感染情况及其相关性进行分析研究.其中男887例,女358例;年龄12岁～84岁,平均36.4岁;慢性浅表性胃炎(CSG)585例,慢性萎缩性胃炎(CAG)420例,胃溃疡(GU)152例,十二指肠溃疡(DU)43例,复合性溃疡(CPU)45例.结果 Hp阳性检出率为34.1%.CSG,CAG,GU,DU和CPU阳性检出率分别为30.8%,36%,34.9%,32.6%和55.6%.其中伴胆汁反流者Hp阳性检出率为25.7%,伴肠化者Hp阳性检出率为31.4%.结论 Hp的存在与否与CG和PU无明显相关性,其相关性还需要临床进一步研究确定.     

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,口腔可能为Hp的重要寄居地,口腔内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。     

十二指肠溃疡与萎缩性胃炎相关性研究

背景:愈来愈多的迹象表明胃溃疡(GU)与胃癌发生的危险性增加相关,而十二指肠溃疡(DU)则与胃癌的发生负性相关.目的:研究DU与萎缩性胃炎的相关性.方法:对DU、GU和复合性溃疡(CU)患者胃窦、胃窦胃体交界处和胃体黏膜以及慢性胃炎(CG)患者胃窦黏膜活检标本进行组织学检查,统计各自胃黏膜的萎缩、肠化、慢性炎症、活动性和幽门螺杆菌(H.pylori)感染的发生率及其严重程度.结果:DU患者胃窦、胃窦胃体交界处和胃体黏膜的萎缩发生率分别为54.2%、9.5%和12.4%,肠化发生率分别为18.9%、2.5%和1.5%.其胃窦黏膜肠化的发生率明显低于相应的GU、CU或CG者.3种消化性溃疡和CG患者均存在胃窦部慢性炎症,且消化性溃疡患者胃体部炎症的发生率较高,其胃炎活动性以胃窦部为主,且均较CG者高(P<0.05).DU、GU和CU患者胃窦部Ⅰ型肠化的发生率分别为68.1%、43.8%和45.0%;而其Ⅲ型肠化的发生率则分别为6.4%、25.0%和20.0%(P<0.05).结论:DU患者的胃窦部可有灶性萎缩和肠化发生,其胃窦黏膜肠化发生率和Ⅲ型肠化的发生率最低,这可能是DU患者罹患胃癌危险性较低的原因之一.     

慢性胃炎和溃疡病患者幽门螺杆菌定量检测意义

为探讨 1 4 C-尿素酶呼气试验 ( 1 4 C- UBT)方法定量检测幽门螺杆菌 ( Hp)感染与慢性胃炎、消化性溃疡的关系 ,我们回顾性分析了 62例 Hp感染的患者 ,现将结果报告如下。资料与方法 :胃镜及病理组织学确诊为 Hp感染的 62例患者 ,男性 3 3例 ,女性 2 9例 ;年龄 18～ 79岁。其中慢性浅表性胃炎 ( CSG组 ) 16例 ,慢性萎缩性胃炎 ( CAG组 ) 14例 ,胃溃疡 ( GU组 ) 17例 ,十二指肠溃疡 ( DU组 ) 15例。方法 :对所有研究对象用 1 4 C- UBT方法进行 Hp感染的定量检测。清晨空腹以约 2 0 m l凉开水送服 0 .75微居里 (μci) 1 4 C-尿素胶…     

胃癌中幽门螺杆菌感染与原癌基因c—met表达及预后研究

目的　研究幽门螺杆菌(Hp)感染的胃癌(GC)组织中c-met表达及(Hp)感染对胃癌预后的影响。方法　经病理证实,不同病变胃粘膜145例以免疫组化检测c-met基因表达,以W-S法及快速尿素酶试验检测(Hp)感染。结果　在浅表性胃炎(CSG)、萎缩肠化生胃炎(CAG+IM)、异型增生(DYS)、早期GC和进展期GC中,c-met基因表达率分别为25.53%,51.28%,61.54%,66.67%和68.42%,CAG+IM、DYS、GC均显著高于CSG(P＜0.05)。肠型胃癌c-met阳性表达与(Hp)感染密切相关。CAG+IM,DYS和GC组c-met阳性表达(Hp)感染者明显高于阴性组。(Hp)阳性者5年生存期显著短于(Hp)阴性者。结论　(Hp)感染和c-met表达与胃粘膜增殖和恶化有关,前者也与胃癌预后有关。     

大鼠幽门螺杆菌感染慢性萎缩性胃炎模型的研究

目的 建立Hp相关CAG大鼠模型,探讨Hp与胃粘膜损伤因子在CAG中的致病作用.方法 采用二级、体质量90 g～110 g、♂Wistar大鼠60只,随机分为Hp感染CAG模型组,单纯Hp感染组,单纯胃粘膜损伤CAG模型组与对照组.采用灌胃接种Hp菌株(SSl),30 g/L水杨酸钠灌胃,5 mmol/L去氧胆酸钠溶液、50 mL/L乙醇交替自由饮用及饥饱失常的方法建立Hp相关CAG模型.Hp末次接种12 wk后处死所有动物,检测Hp感染情况及粘膜固有层厚度、粘膜表面上皮层厚度,壁细胞计数和肠化、不典型增生等病变.结果 Hp感染CAG模型组及单纯Hp感染组Hp阳性.Hp感染CAG模型组出现以淋巴细胞浸润为主的慢性炎症,粘膜固有层厚度,胃窦(68±4)/μm,胃体(315±40)μm,粘膜表面上皮层(71±7)μm,PAS阳性层厚度(81±7)μ与正常组(99±16)μm,(407±33)μm,(101±11)μan,(121±14)μm比较明显变薄(P＜0.01),壁细胞计数(34.9±1.1)/腺管明显减少,正常组为(51.1±2.4)/腺管(P＜0.01),无明显肠化及不典型增生.单纯Hp感染组大鼠亦出现较明显的慢性炎症与活动性炎症,粘膜固有层厚度,壁细胞计数与正常组比较无明显变化.结论 Hp感染大鼠CAG模型的病因、病理与人类CAG病变相似,Hp相关CAG大鼠模型获得了初步成功.可作为Hp相关CAG发病机制及药物筛选较合适的动物模型.单纯Hp感染12 wk内无胃粘膜萎缩病变形成.     

肠化生、胃癌组织中幽门螺杆菌感染与ras基因表达

螺杆菌(Hp)感染引起慢性活动性胃炎、萎缩性胃炎、肠腺化生、不典型增生,最终导致肠型胃癌的链状改变虽被公认,但并非Hp高感染率的地区胃癌的发生率一定升高.胃癌的发生、发展是癌基因的突变与抑癌基因失活逐渐演变的复过程,而癌基因突变与抑癌基因失活并非Hp单一因素,而是多因素参与的结果.通过病理染色、快速尿素酶试验检测Hp感染,免疫组织化学染色检测P21蛋白,了解在肠化生、胃癌组织中Hp感染与ras基因表达之间的关系.     

幽门螺杆菌与胃黏膜细胞凋亡的关系

[目的]探讨幽门螺杆菌(Hp)感染时胃黏膜组织一氧化氮(NO)水平及其与细胞凋亡的关系.[方法]应用快速脲酶法及PCR法对132例胃病患者胃黏膜进行Hp检测,其中Hp阳性75例,Hp阴性57例;病理学分型采用悉尼分型法;用亚硝基还原法检测血清中NO水平及荧光染色法检测胃黏膜细胞的凋亡情况.[结果]Hp阳性组血清NO水平高于Hp阴性组(P＜0.01),在Hp阳性患者中,血清NO水平胃癌(GCA)＞萎缩性胃类(CAG)＞浅表性胃炎(CSG)(P＜0.01).凋亡指数(AI)的比较:Hp阳性组高于Hp阴性组(P＜0.01),CAG＞CSG(P＜0.01),GCA与CSG之间比较差异无统计学意义.[结论]Hp感染与胃黏膜的萎缩、肠化生等癌前病变的关系密切;Hp诱导产生的NO与GCA的形成发展密切相关.对NO水平的调控可望成为治疗癌前病变,阻止GCA形成的有效措施.     

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and Hpylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pyloripositivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylorinegativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylon positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.     

Comparison of He/icobacter py/ori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylineosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.     

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.     

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.     

幽门螺杆菌相关性胃病的细胞增殖和凋亡

目的 观察幽门螺杆菌（Hp)及其CagA基因对细胞增殖和凋亡的影响,进而探讨Hp增加胃癌发生危险性的机制。方法 研究对象为慢性浅表性胃炎（CSG）、慢性萎缩性胃炎（CAG）、慢性萎缩性胃炎伴肠上皮化生（CAGIM）、不典型增生（DYS）、胃癌（GC）患者127例及正常对照组（NS）14例。应用ki-67免疫组化技术评价幽门窦上皮细胞增生,用切口末端标记法（TUNEL）检测胃上皮细胞凋亡,应用聚合酶链反应（PCR）技术检测Hp的CagA基因。结果 Hp阳性患者的增殖指数（LI）和凋亡指数（AI）显著高于Hp阴性者或正常对照（P＜0．05和P＜0．01）。CSGHp阳性的LI和AI明显高于Hp阴性者（P＜0．01）,而其余四种胃病Hp阳性患者（P＜0．05）。Hp阳性或阴性CSG、NS组的AI与LI呈正相关,GC患者的AI与LI呈负相关。LI和AI与胃粘膜炎症程度无明显关系。结论 Hp诱导胃粘膜上皮细胞过度增殖和凋亡主要发生在Hp感染的早期,CagA^ Hp与CagA^－Hp促增殖和凋亡作用的能力明显不同,Hp感染通过引起增殖和凋亡比例的失调,最终促进肿瘤发生。     

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     

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.     

幽门螺杆菌感染和端粒酶活性以及c-myc、p16基因的表达在胃黏膜癌变中的相关性研究

幽门螺杆菌(H.pylori)是胃癌的主要致病因子,H.pylori、端粒酶和肿瘤相关基因的关系在胃黏膜癌变发生过程中研究很少。目的:观察H.pylori感染和端粒酶活性以及c-myc、p16基因在胃癌中的关系。方法:通过胃镜活检和外科手术获取171例胃组织标本,快速尿素酶试验和H.pylori培养确定有无H.pylori感染;酶联免疫法检测H.pylori感染患者的血清CagA-IgG水平;聚合酶链反应.酶联免疫吸附测定(PCR-ELISA)法检测端粒酶活性;免疫组化法检测c-myc、p16基因的表达。结果:胃癌(GC)组端粒酶表达率显著高于其他各组(P<0.01);慢性萎缩性胃炎(CAG)伴中、重度肠化(IM)组端粒酶和c-myc表达率显著高于CAG伴轻度IM组(P<0.05);而慢性浅表性胃炎(CSG)和CAG伴轻度IM组p16表达率显著高于CAG伴中、重度IM、异型增生(Dys)和GC组(P<0.05)。在CAG伴轻、中、重度IM组中,H.pylori阳性组端粒酶活性比阴性组高:无论有无H.pylori感染,胃癌组端粒酶活性都非常高。在CAG伴中、重度IM、Dys和GC组中,H.pylori阳性亚组c-myc表达显著高于阴性亚组(P<0.01),而在ECAG伴中、重度IM和Dys组中,H.pylori阳性亚组p16基因表达显著低于阴性亚组(P<0.01)。结论:H pylori感染很可能主要通过c-myc基因的激活和p16基因的失活以及其他基因的变化来诱导CAG伴中、重度     

Anti-Helicobacter pylori immunoglobulin G （IgG） and IgA antibody responses and the value of clinical presentations in diagnosis of H.pylori infection in patients with precancerous lesions

AIM: To determine the prevalence of Helicobacter pylori(H. pylon) infection, the serum anti-H, pylori immunoglobulin G (IgG) and IgA antibody responses, and the value of clinical presentations in diagnosis of H. pylori infection in patients with gastric atrophy, intestinal metaplasia and dysplasia.METHODS: H. pylori infection was detected by histology in 209 patients with mild chronic atrophic gastritis (CAG, n=76),severe CAG (n=22), mild intestinal metaplasia (IM, n=22),severe IM (n=58), or dysplasia (DYS, n=31). Serum anti-H. pylori IgG and IgA were double sampled and evaluated by enzyme-linked immunoadsordent assays. 35 clinical presentations were observed and their relationship with H.pylori infection was analyzed by the k-means cluster method.RESULTS: Both IgG and IgA levels in H. pylori positive patients were significantly higher than those negative for H.pylori(P&lt;0.001-0.01). The prevalence of H. pyloriwas highest in severe IM (84.5%), and lowest in mild CAG (51.3%)(P&lt;0.01). They were similar in severe CAG (68.2%), mild IM (72.7%), and DYS (67.7%). In H. pyloripositive patients,the IgG levels in severe CAG were significantly higher than those in mild CAG (P&lt;0.01). In H. pylorinegative patients,both IgG and IgA levels increased remarkably in severe IM,compared to those in mild IM (P&lt;0.01-0.05). H. pyhri infection exhibited no association with patient‘s gender (62.1% inmales; 71.7% in females) and age (r=0.0814, P=0.241).The diagnostic accuracy based on 35 clinical presentations was 65.7%. It could be improved by 5.7% when only the assemblage of digestive symptoms were engaged, or by 8.6% when the pathogenic factors, general status and grossoscopy were combined. The diagnostic accuracy could be decreased when only the general symptoms were engaged, or when the pathogenic factors were accompanied with some common digestive symptoms.CONCLUSION: H. pylori infection is a major risk factor for the process from atrophy, IM to DYS of gastric mucosa.Serum IgG and IgA are good indicators to evaluate this progress with a certain arrearage. Investigation on the effective assemblages of clinical presentations may provide a better understanding in the pathogenesis, diagnosis and treatment for H. pyloriinfection.