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1.
幽门螺杆菌致癌作用的研究   总被引:2,自引:0,他引:2  
房殿春 《胃肠病学》2007,12(10):581-584
摘要幽门螺杆菌(H. pylori)感染,特别是CagA^+株感染,与胃癌的发生密切相关,但其分子机制仍不清楚。对H.pylori致胃黏膜癌变的分子机制进行深入研究,结果显示胃黏膜H.pylori感染可增加胃癌的易感性,导致线粒体DNA微卫星不稳(mtMSI)和线粒体DNA核内整合,使线粒体细胞色素氧化酶(COX)Ⅰ、COXⅡ、COXIImRNA表达下调,Bid和Bax表达上调。提示H.pylori通过线粒体途径影响细胞凋亡,导致细胞增殖和凋亡的失衡,从分子水平揭示了H.pvlori诱导胃癌发生的机制。  相似文献   

2.
目的幽门螺杆菌(Helicobacterpylori,Hp)感染与胃癌的发生关系密切.我们剖析胃癌高发区Hp感染状况及其与胃疾病及胃癌的相关性,旨在为Hp感染及胃癌的综合防治提供依据.方法胃癌高发区16村镇胃癌高危人群3033人,经血清胃蛋白酶原检测及X线初筛出1779例,接受了胃粘膜活检精查.其切片作HE及亚甲兰(MB)染色,观察病理组织学改变及Hp感染情况,同时利用PCR检测Hp.结果Hp总检出率为60.8%.其中男高于女;30岁~59岁组最高(62.4%);山区(64.4%)高于沿海区(56.7%);胃窦(36.2%)高于胃角(32.6%)及胃体(31.2%);以上P<0.01.胃癌Hp检出率为43.8%;各型胃疾病Hp检出率由高至低,前四位依次为胃粘膜糜烂(90.6%)、胃溃疡(87.0%)、中重度浅表性胃炎(79.8%)及萎缩性胃炎(75.3%),上述各组Hp检出率与轻度浅表性胃炎Hp检出率(6.8%)相比,P<0.01.与未检出Hp的组织学基本正常胃粘膜0%相比,异型增生(80.0%)及肠上皮化生(77.7%)的Hp检出率皆明显升高,P<0.01.结论庄河居民Hp感染与胃粘膜糜烂、胃溃疡、中重度浅表性胃炎、萎缩性胃炎等呈明显正相关.庄河不仅胃癌高发且Hp感染亦是高流行.文内尚对有关结果只行了初步探讨,呼吁在我国胃癌高发  相似文献   

3.
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。  相似文献   

4.
为探讨线粒体DNA(mtDNA)5.0kb缺失与充血性心力衰竭(CHF)发病的关系,应用聚合酶链反应(PCR)技术分析72例CHF患者的mtDNA。结果显示,CHF患者mtDNA5.0kb缺失率明显高于对照组(0.254%±0.08%比0.032%±0.01%,P<0.01);CHF组内扩张型心肌病组及冠心病组mtDNA5.0kb缺失率高于风心病及高血压心脏病组(P<0.05)。研究中还发现,随着心功能分级增加,mtDNA5.0kb缺失率增高(P<0.05)。提示mtDNA缺失影响心肌细胞线粒体呼吸功能,心肌能量供应障碍与CHF的发生、发展有关。  相似文献   

5.
目的 探讨线粒体突变及不稳定在胃癌发生、发展中的作用.方法 利用激光显微切割技术分离胃癌组织及其切缘的正常组织,应用变性高效液相色谱DHPLC对胃癌线粒体D-loop调控区D-loop-(CA)n进行突变筛查及测序分析,同时进行线粒体D-loop非编码区(CA)n重复序列的不稳定(mtMSI)检测.结果 胃癌组织样本中D-loop-(CA)n调控区基因突变率为50.8% (31/61),正常组织均未见有序列改变.29.5% (18/61)发生线粒体重复序列(CA)n的不稳定.18例线粒体不稳定(mtMSI)中有16.4%(10/61)同时发生D-loop点突变,有8例同时存在核不稳定(nMSI-H).结论 胃癌mtDNA异常参与了肿瘤的发生、发展.  相似文献   

6.
目的探讨凋亡基因Survivin、Fas在胃癌发生过程中的表达、临床意义及和幽门螺杆菌(Hp)感染的关系。方法采用分子原位杂交分别检测12例正常胃黏膜、22例浅表性胃炎、25例肠上皮化生、37例异型增生及52例胃癌组织中的Survivin-mRNA和Fas-mRNA表达,并检测患者Hp感染状况。结果Survivin-mRNA在肠上皮化生、异型增生组和胃癌组织中的阳性率分别为28.0%、43.2%和69.2%。胃癌组明显高于肠化和异型增生组(P〈0.01;P〈0.05)。胃癌组Fas-mRNA阳性率为36.5%,显著低于对照组和异型增生组(P均〈0.01)。Survivin-mRNA在高分化、中分化和低分化及未分化型胃癌组织中阳性率呈现递增趋势,而且其表达和淋巴结转移、远处转移密切相关。Fas-mRNA阳性率在高、中和低分化及未分化型胃癌患者中呈现递减趋势,且其表达和淋巴结转移密切相关。异型增生患者Survivin-mRNA表达与Hp感染之间呈明显正相关(P〈0.01)。相关回归分析显示胃癌患者各病理分期中Survivin-mRNA与Fas-mRNA表达呈负相关。结论在胃黏膜癌变过程中,Survivin的表达和作用逐渐上调,而Fas的表达和作用逐渐下调,而且在癌前病变组织中Survivin表达和Hp感染有密切关系;在胃癌组织中Survivin和Fas的表达呈负相关。  相似文献   

7.
目的了解大肠癌细胞株(SW480,LOVO,HT29)线粒体DNA的突变,克隆突变的大肠癌线粒体DNA(mtDNA)基因,构建peDNA3.1(+)-mtDNA真核表达重组体,并导入NIH3T3及LST细胞,以探讨线粒体基因突变与肿瘤发生的关系。方法提取大肠癌细胞株(SW480,LOVO,HT29)mtDNA,扩增D—LOOP区,产物用DNA自动测序法进行序列分析。利用DNA重组技术将其定向插入真核表达质粒peDNA3.1(+),并用脂质体法导人NIH3T3及LST细胞。用MitoCa.ptureMitochondrialApoptosisDetectionKit试剂盒染色后用流式细胞仪及荧光显微镜检测转染细胞的凋亡情况。扩增并测序分析转染细胞的D—LOOP区突变特点。结果检测出大肠癌细胞株SW480,LOVO,HT29细胞mtDNAD—LOOP分别有10,9,8个突变位点。转染前后,各组间细胞凋亡无明显变化。转染细胞的核基因组可扩增出目的基因及Neo基因。4株NIH3T3转染细胞mtDNAD-环区分别检测到9,11,8,4个突变点,并相应有3,4,3,2个多态性变化。结论(1)转染突变的大肠癌细胞mtDNA后转染细胞的mtDNA均可发生多处的突变位点。(2)通过转染后突变的外源性的mtDNA可以整合到核基因组内。(3)突变的mtDNA转染LST细胞及NIH3T3细胞后,不影响转染细胞的凋亡改变。(4)mtDNA的突变可能通过影响体细胞mtDNA的突变和通过外源性mtDNA在核内的整合从而影响癌基因或抑癌基因的表达异常,从而参与肿瘤的发生发展。  相似文献   

8.
幽门螺杆菌感染与胃癌的相关性研究   总被引:36,自引:0,他引:36  
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。  相似文献   

9.
幽门螺杆菌长期感染蒙古沙土鼠建立胃癌模型的研究   总被引:24,自引:0,他引:24  
目的:幽门螺杆菌(Hp)长期感染蒙古沙土鼠(MGs)发生胃癌鲜见报道。本实验旨在研究Hp长期定植于MGs导致胃黏膜病变及其致癌性。方法:36只交封闭MGs(雌雄各半)分别接种Hp标准株ATCC43504,或从胃癌患者胃内分离的Hp161株,10只MGs作为对照,接种后第8、20、28和84周分别处死,检查细菌定植及胃黏膜病变情况。结果:绝大多数MGs胃内Hp持续定植,胃黏膜炎症随时间逐渐加重,第84周组织学特征是胃黏膜中-重度胃炎,以淋巴细胞为主的单核细胞弥漫性浸润,黏膜,黏膜下,甚至浆膜下有大量淋巴滤泡浸润,偶见淋巴上皮病变,萎缩,肠化较少见,上皮增生明显,24%(4/17)发生增生性息肉,第84周时18%(3/17)发生高分化腺癌(Hp161组1例,ATCC43504组2例;1雄2雌),结论:单独感染Hp能诱导MGs发生胃癌,并提示可利用不同种属的MGs和不同Hp菌株进行相关研究,首次报道了雌性MGs感染也可发生胃癌。  相似文献   

10.
扩张型心肌病患儿线粒体DNA缺失的研究   总被引:1,自引:0,他引:1  
采用PCR法检测了15例扩张型心肌病(DCM)、13例急性心肌炎(病程<3个月)患儿和10例正常儿童外周血淋巴细胞中线粒体DNA(mtDNA)的缺失情况,以研究mtDNA突变在DCM发病中的作用。结果显示,被检者线粒体均存在5Kb和7.4Kb的mtDNA缺失,但DCM患儿的缺失率显著高于心肌炎患儿和正常儿童(缺失率分别为7.97±3.51%,2.5±1.64%和2.28±1.76%,P<0.05)。提示mtDNA缺失与部分DCM的发病有关。  相似文献   

11.
BACKGROUND: Helicobacter pylori infection has been considered to play significant role in gastric carcinogenesis, but only a minority of people who harbor this organism will develop gastric cancer. H. pylori infection first causes chronic non atrophic gastritis. Chronic non atrophic gastritis may evolve to atrophic gastritis and intestinal metaplasia and finally to dysplasia and adenocarcinoma. AIMS: To estimate the prevalence of H. pylori infection and the precancerous gastric lesions and their relationship, in patients with dyspeptic symptoms who underwent upper gastrointestinal endoscopy at a reference center in the central region of Rio Grande do Sul state, Brazil. METHODS: We analyzed gastric biopsies taken from corpus and antrum of patients who underwent upper gastrointestinal endoscopy for H. pylori detection, between 1994 and 2003. According to Sydney system, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed by histological examination (H-E stain). The histological diagnoses were related to H. pylori infection status. RESULTS: Biopsies from 2,019 patients were included in the study. Patients mean age was 52 (+/-15) and 59% were female. Seventy six percent had H. pylori infection. Normal mucosa, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed in 5%, 77%, 3% and 15%, respectively. The OR for any degree of gastric mucosa lesion in infected patients was 10 (CI95% 6.50 - 17%). The OR for infected patients had chronic non atrophic gastritis was 3 (CI95% 2,2 - 3,4). The OR for infected patients had atrophic gastritis or intestinal metaplasia was less than 1. CONCLUSIONS: The prevalence of H. pylori infection in this population was high (76%) and infected individuals had the probability 10 folds greater than non infected individuals to have any lesion of gastric mucosa. The prevalence of precancerous lesions was 77% for non atrophic chronic gastritis, 3% for atrophic gastritis and 15% for intestinal metaplasia. Infected patients had risk 3 folds greater than non-infected for the occurrence of non atrophic chronic gastritis. H. pylori infection did not show risk for occurrence of atrophic gastritis and intestinal metaplasia, suggesting that other risk factors should be involved in the carcinogenesis process.  相似文献   

12.
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。  相似文献   

13.
EfectofHelicobacterpyloriinfectionongastricepithelialproliferationinprogressionfromnormalmucosatogastriccarcinomaLIUWenZhon...  相似文献   

14.
BACKGROUND/AIMS: The effects of Helicobacter pylori infection on the development of atrophic gastritis and intestinal metaplasia in relation to lifestyle and diet and the effect of the bovine milk on H. pylori adherence to gastric antral mucosa were investigated. METHODOLOGY: H. pylori infection was investigated in 63 patients without endoscopic evidence of gastroduodenal disease. Presence of H. pylori infection was assessed by culture and histologic examination of antral and corpus biopsy samples. Grades of atrophic gastritis and intestinal metaplasia were judged with chromoendoscopy (Congo red-methylene blue test). Adherence of H. pylori was evaluated with scanning electron microscopic examination of antral mucosa in Mongolian gerbils. RESULTS: Cross-sectional analysis of lifestyle and diet showed that a high intake of bovine milk was significantly related to prevention of H. pylori infection and the developments of atrophic gastritis and intestinal metaplasia. H. pylori adherence to the gastric mucosa was inhibited by bovine milk in a dose-dependent manner. CONCLUSIONS: Bovine milk prevents the development of atrophic gastritis and intestinal metaplasia through its defense mechanisms against the attachment of H. pylori to the gastric mucosa.  相似文献   

15.
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.  相似文献   

16.
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.  相似文献   

17.
BACKGROUND: The etiology of gastric cancer has not been clearly delineated. There is some evidence of an association of gastric cancer with Helicobacter pylori-induced chronic gastritis, atrophic gastritis and intestinal metaplasia. Previous studies report a high rate of H. pylori infection and chronic gastritis among Nigerians. METHODS: We retrospectively reviewed 84 tissue specimens with gastric cancer seen in our department over an 18-year period for for the presence of H. pylori infection, chronic gastritis, atrophic gastritis, and intestinal metaplasia in the adjacent non-cancerous gastric mucosa. RESULTS: H. pylori infection was detected in 15 (17.9%) of 84 specimens. Moderate to severe gastritis was found in non-cancerous areas in 77 (91.7%) specimens, and was equally frequent in patients with 'intestinal' and 'diffuse' types of cancer. Atrophic gastritis and intestinal metaplasia were observed in 22 (26.2%) and 35 (41.7%) specimens, respectively, and were more common in 'intestinal' type of gastric cancer. CONCLUSION: Chronic gastritis was seen in the adjacent non-cancerous mucosa in most specimens with gastric cancer. However, its severity did not correlate with the histological subtype of gastric cancer.  相似文献   

18.
OBJECTIVES: Helicobacter pylori is a carcinogen; gastric carcinoma involves a multistep process from chronic gastritis to atrophy, intestinal metaplasia, and dysplasia. The aims of this study were to determine the types of mucosa at different gastric sites in H. pylori-infected and uninfected patients, and whether the presence of antral-type mucosa in the incisura, body, and fundus is associated with gastric atrophy and intestinal metaplasia. METHODS: Two hundred and sixty-eight patients with dyspepsia were enrolled. Eight biopsies (i.e., antrum x3, body x2, fundus x2, and incisura x1) were obtained. One antral biopsy was used for the CLO-test. Three (each from the antrum, body, and fundus) were cultured. The remaining biopsies were examined histologically according to the updated Sydney System after staining with hematoxylin and eosin and Giemsa. A validated serological test was also applied. RESULTS: Overall, 113 (42%) patients were infected with H. pylori. At the incisura, antral-type mucosa was more prevalent in infected than in uninfected patients (84% vs. 18%; odds ratio [OR] = 23.9, 95% confidence interval [CI] 12.5-45.8; p<0.001). Atrophic gastritis and intestinal metaplasia at the incisura was present in 19.5% and 13.3%, respectively, of infected, and 4.5% and 3.2%, respectively, of uninfected patients (both p<0.01). Moreover, atrophic gastritis at the incisura was associated with the presence of antral-type mucosa at the site (termed antralization); the prevalence of atrophic gastritis was 19.5% (24/123) in the presence of antralization, whereas the rate was 2.1% (3/145) without antralization (OR = 11.4, 95% CI 3.4-39.2; p<0.001). Similarly, at the incisura, 16.3% (20/123) of "antralized" cases and 1.4% (2/145) of "unantralized" cases had intestinal metaplasia (OR = 13.8, 95% CI, 3.2-60.7; p<0.001). The association between antralization at gastric body and fundus also appeared to be associated with atrophic gastritis and intestinal metaplasia at these sites. CONCLUSIONS: Atrophic gastritis and intestinal metaplasia occurs predominantly at the gastric antrum and incisura with H. pylori infection. Antralization of the gastric incisura is a common event in H. pylori-infected patients, and appears to be associated with an increased risk of atrophic gastritis and intestinal metaplasia.  相似文献   

19.
目的 探讨幽门螺杆菌 (Hp)感染及慢性萎缩性胃窦炎伴肠上皮化生与CD4 4V6表达程度之间的关系。方法 以单克隆抗体及免疫组化技术等方法对Hp阴性单纯慢性胃炎、Hp阴性萎缩性胃炎伴肠上皮化生、Hp阳性萎缩性胃窦炎伴肠上皮化生、胃窦腺癌的胃镜下活检组织标本进行测定分析。结果 在Hp阴性单纯性胃炎组粘膜上皮未见CD4 4V6表达 ,Hp阴性萎缩性胃窦炎伴肠上皮化生、Hp阳性萎缩性胃窦炎伴肠上皮化生、胃窦腺癌各组CD4 4V6表达程度依次逐渐升高 ,各组之间比较差异有显著性 (P <0 .0 5 )。结论 CD4 4V6的表达可能是上皮细胞癌前病变出现的早期生物学信号 ,肠上皮化生细胞可能诱导CD4 4V6的表达 ,而Hp感染则有促进这种诱导表达的作用。  相似文献   

20.
* Helicobacter pylori gastritis progresses to gland loss and intestinal metaplasia in a considerable proportion of colonized subjects. * The progression to atrophic gastritis is a slow process, occurring with an incidence of 1-2% per year. * The progression of chronic H. pylori gastritis is the same in Africa as in Europe and South America. * This supports the concept of H. pylori as a causative factor of pre-neoplastic conditions of the gastric mucosa; other factors must play a modulating role in the progression to cancer. H. pylori gastritis may progress to atrophic gastritis and lead to the development of intestinal metaplasia, dysplasia and eventually gastric cancer in a minority of subjects. The available data on the kinetics of H. pylori gastritis are limited, but nevertheless very consistent. They suggest that the progression to gland loss or atrophic gastritis among H. pylori-positive subjects occurs at a rate of 1-2% per year. As H. pylori gastritis usually persists for life, a considerable proportion of H. pylori-positive subjects thus eventually show signs of gastric gland loss. The majority of these subjects progress to intestinal metaplasia. Despite these consistent findings in different areas of the world, the incidence of gastric cancer is only moderately related to the prevalence of H. pylori. An example is the so-called African enigma, referring to a low incidence of gastric cancer in certain countries of Africa, despite a high prevalence of H. pylori in all age groups. This is not due to differences in progression to atrophic gastritis; other yet unidentified factors therefore must play a role.  相似文献   

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