Helicobacter pylori in dental plaque and stomach of patients from Northern Brazil

AIM: To establish whether virulence factor genes vacA and cagA are present in Helicobacter pylori (H. pylori) retrieved from gastric mucosa and dental plaque in pa-tients with dyspepsia. METHODS: Cumulative dental plaque specimens and gastric biopsies were submitted to histological exami-nation, rapid urease test and polymerase chain reac-tion (PCR) assays to detect the presence of cagA and vacA polymorphisms.RESULTS: Detection of H. pylori from dental plaque and gastric biopsy samples was greater by PCR com-pared to histological examination and the rapid ure-ase test. DNA from H. pylori was detected in 96% of gastric mucosa samples and in 72% of dental plaque samples. Sixty-three (89%) of 71 dental plaque sam-ples that were H. pylori-positive also exhibited identical vacA and cagA genotypes in gastric mucosa. The most common genotype was vacAs1bm1 and cagA positive, either in dental plaque or gastric mucosa. These viru-lent H. pylori isolates were involved in the severity of clinical outcome.CONCLUSION: These pathogenic strains were found simultaneously in dental plaque and gastric mucosa, which suggests that gastric infection is correlated with the presence of H. pylori in the mouth.

Role of dental plaque,saliva and periodontal disease in Helicobacter pylori infection

Helicobacter pylori (H. pylori) infection is one of the most common bacterial infections in humans. Although H. pylori may be detected in the stomach of approximately half of the world’s population, the mechanisms of transmission of the microorganism from individual to individual are not yet clear. Transmission of H. pylori could occur through iatrogenic, fecal-oral, and oral-oral routes, and through food and water. The microorganism may be transmitted orally and has been detected in dental plaque and saliva. However, the role of the oral cavity in the transmission and recurrence of H. pylori infection has been the subject of debate. A large number of studies investigating the role of oral hygiene and periodontal disease in H. pylori infection have varied significantly in terms of their methodology and sample population, resulting in a wide variation in the reported results. Nevertheless, recent studies have not only shown that the microorganism can be detected fairly consistently from the oral cavity but also demonstrated that the chances of recurrence of H. pylori infection is more likely among patients who harbor the organism in the oral cavity. Furthermore, initial results from clinical trials have shown that H. pylori-positive dyspeptic patients may benefit from periodontal therapy. This paper attempts to review the current body of evidence regarding the role of dental plaque, saliva, and periodontal disease in H. pylori infection.

Study of Helicobacter pylori genotype status in saliva,dental plaques,stool and gastric biopsy samples

AIM:To compare genotype of Helicobacter pylori(H.pylori) isolated from saliva,dental plaques,gastric biopsy,and stool of each patient in order to evaluate the mode of transmission of H.pylori infection.METHODS:This cross-sectional descriptive study was performed on 300 antral gastric biopsy,saliva,dental plaque and stool samples which were obtained from patients undergoing upper gastrointestinal tract endoscopy referred to endoscopy centre of Hajar hospital of Shahrekord,Iran from March 2010 to February 2011.Initially,H.pylori strains were identified by rapid urease test(RUT) and polymerase chain reaction(PCR) were applied to determine the presence of H.pylori(ureC) and for genotyping of voculating cytotoxin gene A(vacA) and cytotoxin associated gene A(cagA) genesin each specimen.Finally the data were analyzed by using statistical formulas such as Chi-square and Fisher's exact tests to find any significant relationship between these genes and patient's diseases.P < 0.05 was considered statistically significant,RESULTS:Of 300 gastric biopsy samples,77.66% were confirmed to be H.pylori positive by PCR assay while this bacterium were detected in 10.72% of saliva,71.67% of stool samples.We were not able to find it in dental plaque specimens.The prevalence of H.pylori was 90.47% among patients with peptic ulcer disease(PUD),80% among patients with gastric cancer,and 74.13% among patients with none ulcer dyspepsia(NUD) by PCR assay.The evaluation of vacA and cagA genes showed 6 differences between gastric biopsy and saliva specimens and 11 differences between gastric and stool specimens.94.42% of H.pylori positive specimens were cagA positive and all samples had amplified band both for vacA s and m regions.There was significant relationship between vacA s1a/m1a and PUD diseases(P = 0.04),s2/m2 genotype and NUD diseases(P = 0.05).No statically significant relationship was found between cagA status with clinical outcomes and vacA genotypes(P = 0.65).The evaluation of vacA and cagA genes showed 6 differences between gastric biopsy and saliva specimens and 11 differences between gastric and stool specimens,CONCLUSION:Regard to high similarity in genotype of H.pylori isolates from saliva,stomach and stool,this study support the idea which fecal-oral is the main route of H.pylori transmission and oral cavity may serve as a reservoir for H.pylori,however,remarkable genotype diversity among stomach,saliva and stool samples showed that more than one H.pylori genotype may exist in a same patient.

Multiple genetic alterations and behavior of cellular biology in gastric cancer and other gastric mucosal lesions:H.pylori infection,histological types and staging

AIM To investigate the expression of multiplegenes and the behavior of cellular biology ingastric cancer（GC）and other gastric mucosallesions and their relations to Helicobacter pylori（H.pylori）infection,tumor staging andhistological subtypes.METHODS Three hundred and twenty-sevenspecimens of gastric mucosa obtained viaendoscopy or surgical resection,and ABCimmunohistochemical staining were used todetect the expression of p53,p16,Bcl-2 andCOX-2 proteins.H.pylori was determined byrapid urea test combined with pathologicalstaining or14C urea breath test.Cellular image analysis was performed in 66 patients withintestinal metaplasia（IM）and/or dysplasia（Dys）.In 30 of them,both cancer and theparacancerous tissues were obtained at the timeof surgery.Histological pattern,tumor staging,lymph node metastasis,grading ofdifferentiation and other clinical data werestudied in the medical records.RESULTS p16 expression of IM or Dys wassignificantly lower in positive H.pylori chronicatrophic gastritis（CAG）than those withnegative H.pylori（CAG:54.8% vs 88.0%,IM:34.4% vs 69.6%,Dys:23.8% vs 53.6%,allP【0.05）,Bcl-2 or COX-2 expression of IM orDys in positive H.pylori cases was significantlyhigher than that without H.pylori（Bcl-2:68.8%vs23.9%,90.5% vs 60.7%;COX-2:50.0% vs10.8%,61.8% vs 17.8%;all P【0.05）.Themean number of most parameters of cellularimage analysis in positive H.pylori group wassignificantly higher than that in negative H.pylori group（Ellipser:53±14,40±12μm,Area1:748±572,302±202 μm2,Area2:3050±1661,1681±1990 μm2,all P【0.05;Ellipseb:79±23,58±15 μm,Ratio1:22%±5%,13%±4%,Ratio2:79%±17%,53%±20%,all P【0.01）.There was significant correlation between Bcl-2and histologic pattern of gastric carcinoma,andbetween COX-2 and tumor staging or lymph nodemetastasis（Bcl-2:75.0% vs 16.7%;COX-2:76.0% vs 20.0%,79.2% vs 16.7%;allP【0.05）.CONCLUSION p1l6, Bcl-2, and COX-2 but not p53 gene may play a role in the early genesis/ progression of gastric carcinoma and are associated with H. pylori infection. p53 gene is relatively late event in gastric tumorigenesis and mainly relates to its progression. There is more cellular-biological behavior of malignant tumor in gastric mucosal lesions with H. pylori infection. Aberrant Bcl-2 protein expression appears to be preferentially associated with the intestinal type cancer. COX-2 seems to be related to tumor staging and lymph node metastasis.

Can eradication rate of gastric Helicobacter pylori be improved by killing oral Helicobacter pylori ?

AIM:To evaluate the influence of oral Helicobacter pylori(H.pylori)on the success of eradication therapy against gastric H.pylori.METHODS:A total of 391 patients with dyspepsia were examined for H.pylori using the saliva H.pylori antigen test(HPS),13C-urea breath test(UBT),gastroscopy,and gastric mucosal histopathological detection.Another 40 volunteers without discomfort were subjected to HPS and13C-UBT,and served as the control group.The 233 patients who were13C-UBT+were enrolled in this study and divided into 4 groups.Patients who were HPS-and13C-UBT+(n=53)received triple therapy alone.Those who were both HPS+and13CUBT+(n=180)were randomly divided into 3 groups:(1)the O+G+t group which received triple therapy alone(n=53);(2)the O+G+tm group which received both triple therapy and mouthrinse treatment(n=65);and(3)the O+G+tmp group which received triple therapy,mouthrinse,and periodontal treatment(n=62).The HPS and13C-UBT were continued for 4 wk after completion of treatment,and the eradication rate of gastric H.pylori and the prevalence of oral H.pylori in the 4 groups were then compared.RESULTS:The eradication rates of gastric H.pylori in the O-G+t group,the O+G+tm group,and the O+G+tmp group were 93.3%,90.0%,and 94.7%respectively;all of these rates were higher than that of the O+G+t group(78.4%)[O-G+t group vs O+G+t group(P=0.039);O+G+tm group vs O+G+t group(P=0.092);O+G+tmp group vs O+G+t group(P=0.012);O+G+tm group vs O-G+t group(P=0.546);O+G+tmp group vs O-G+t group(P=0.765);O+G+tm group vs O+G+tmp group(P=0.924)].The eradication of gastric H.pylori was significantly improved using the combination of triple therapy,mouthrinse,and periodontal treatment.The eradication rates of gastric H.pylori in the peptic ulcer group,chronic atrophic gastritis group and control group were higher than in the duodenitis group and the superficial gastritis group.The prevalence rates of oral H.pylori in the O-G+t group,O+G+t group,O+G+tm group and O+G+tmp group following treatment were 0%,76.5%,53.3%,and 50.9%,respectively[O-G+t group vs O+G+t group(P<0.0001);O+G+tm group vs O+G+t group(P=0.011);O+G+tmp group vs O+G+t group(P=0.006);O+G+tm group vs O-G+t group(P<0.0001);O+G+tmp group vs O-G+t group(P<0.0001);O+G+tm group vs the O+G+tmp group(P=0.790)].Both mouthrinse and periodontal treatment significantly reduced the prevalence of oral H.pylori.CONCLUSION:Mouthrinse treatment alone or combined with periodontal treatment can,to some extent,reduce the prevalence of oral H.pylori and improve the eradication rate of gastric H.pylori.

Study of T-lymphocyte subsets,nitric oxide,hexosamine and Helicobacter pylori infection in patients with chronic gastric diseases

Chronic gastritis ( CG ) and peptic ulcer ( PU ) are frequently-occurring diseases. It is now well recognized that Helicobacter pylori (Hp) is a major factor that leads to CG and PU[1-8] In order to study the relationship among T lymphocyte subsets, NO, Hexosamine and Hp infection in patients with chronic gastric diseases, the levelsof blood T lymphocyte subsets, plasma NO and hexosamine in gastric mucosa were measured respectively in 30 patients with CG and 32 patients of PU + CG.

Seroepidemiology of Helicobacter pylori infection among asymptomatic Chinese children

INTRODUCTIONIncreasing data has demonstrated that Helicobacterpylori(H.pylori),a spiral gram negativebacterium,colonized in human stomach,can causetype B gastritis,is strongly associated withgastric and duodenal ulceration,and has beenimplicated in the causation of gastric carcinomaand mucosa-associated lymphoid tissue(MALT)lymphomas.It has been reported that there

Development of early gastric cancer 4 and 5 years after complete remission of Helicobacter pyloriassociated gastric low-grade marginal zone B-cell lymphoma of MALT type

AIM: To report 3 of 120 patients on the German MALT lymphoma trial with H. pylori associated gastric MALT lymphoma who developed early gastric cancer 4 and 5 years, after complete lymphoma remission following cure of H. pylori infection. PATIENTS AND RESULTS: Three patients (two men, 74 and 70 years; one women, 77 years) with H. pylori-associated low-grade MALT lymphoma achieved complete lymphoma remission after being cured. Surveillance endoscopies were performed twice a year in accordance to the protocol. Four years after complete lymphoma remission in two patients, and after 5 years in the other, early gastric adenocarcinoma of the mucosa-type, type IIa and type IIc, respectively, was detected, which were completely removed by endoscopic mucosa resection. In one patient, the gastric cancer was diagnosed at the same location as the previous MALT lymphoma, in the other patients it was detected at different sites of the stomach distant from location of the previous MALT lymphoma. The patients were H. pylori negative during the whole follow-up time. CONCLUSION: These findings strengthen the importance of regular Long-term follow-up endoscopies in patients with complete remission of gastric MALT lymphoma after cure of H. pylori infection. Furthermore, gastric adenocarcinoma may develop despite eradication of H. pylori.

Treatment outcome of localized Helicobacter pylori-negative low-grade gastric MALT lymphoma

AIM: To investigate treatment outcome of Helicobacter pylori (H.pylori )-negative low-grade gastric mucosaassociated lymphoid tissue (MALT) lymphoma.METHODS: In this study,we retrospectively reviewed the clinical outcome and clinicopathologic factors of stage Ⅰ E H.pylori -negative low-grade gastric MALT lymphoma cases from August 1998 to June 2009.RESULTS: A total of eleven patients with H.pylori -negative low-grade gastric MALT lymphoma were enrolled in the study and received anti-H.pylori eradication treatment and/or radiotherapy or excisional therapy.Complete remission (CR) of gastric MALT lymphoma was achieved in all patients.The time to CR was 1-66 mo (median,1 mo).CONCLUSION: Eradication therapy may be offered as an initial treatment option even in cases of localized H.pylori -negative gastric MALT lymphoma.

穴位埋线辅助四联疗法治疗脾胃虚弱型慢性萎缩性胃炎伴Hp感染临床研究

目的:观察穴位埋线辅助四联疗法治疗脾胃虚弱型慢性萎缩性胃炎(CAG)伴幽门螺杆菌(Hp)感染的临床疗效。方法:选取112例脾胃虚弱型CAG伴Hp感染患者,采用随机数字表法分为对照组(予四联疗法治疗)和观察组(予穴位埋线辅助四联疗法治疗)各56例。治疗结束后,2组均随访5个月。比较2组临床疗效、胃黏膜功能指标[胃泌素17(G-17)、胃蛋白酶原Ⅰ(PGⅠ)]、健康调查简表(SF-36)评分、中医证候积分、病理评分、不良反应发生率及复发率。结果:总有效率观察组96.43%,高于对照组80.36%(P<0.05)。治疗后3个月,2组血清G-17、PGⅠ水平均较治疗前升高(P<0.05),观察组上述2项指标水平均高于对照组(P<0.05)。治疗后1个月、3个月,2组SF-36评分均较治疗前升高(P<0.05),观察组SF-36评分均高于同期对照组(P<0.05)。治疗后3个月,2组中医证候积分均较治疗前降低(P<0.05),观察组中医证候积分低于对照组(P<0.05)。治疗后5个月,2组病理评分均较治疗前下降(P<0.05),观察组病理评分低于对照组(P<0.05)。不良反应发生率观察组8.93%,与对照组3.57%比较,差异无统计学意义(P>0.05)。治疗后5个月,复发率观察组1.85%,低于对照组15.56%(P<0.05)。结论:穴位埋线辅助四联疗法治疗脾胃虚弱型CAG伴Hp感染,可减轻患者的临床症状,改善胃黏膜功能,提高生活质量,降低复发率,且安全性好。

Apoptosis,proliferation and p53 gene expression of H.pylori associated gastric epithelial lesions

AIM: To study the relationship between Helicobacter pylori (H. pylori) and gastric carcinoma and its possible pathogenesis by H. pylori. METHODS: DNEL technique and immunohistochemical technique were used to study the state of apoptosis, proliferation and p53 gene expression. A total of 100 gastric mucosal biopsy specimens, including 20 normal mucosa, 30 H. pylori-negative and 30 H. pylori-positive gastric precancerous lesions along with 20 gastric carcinomas were studied. RESULTS: There were several apoptotic cells in the superficial epithelium and a few proliferative cells within the neck of gastric glands, and no p53 protein expression in normal mucosa. In gastric carcinoma, there were few apoptotic cells, while there were a large number of proliferative cells, and expression of p53 protein significantly was increased. In the phase of metaplasia, the apoptotic index (AI, 4.36%+/-1.95%), proliferative index (PI, 19.11%+/-6.79%) and positivity of p53 expression (46.7%) in H. pylori-positive group were higher than those in normal mucosa (P【0.01). AI in H. pylori-positive group was higher than that in H. pylori-negative group (3.81%+/-1.76%), PI in H. pylori-positive group was higher than that in H. pylori-negative group (12.25%+/-5.63%, P【0.01). In the phase of dysplasia, AI (2.31%+/-1.10%) in H. pylori-positive group was lower (3.05%+/-1.29%) than that in H. pylori-negative group, but PI (33.89%+/-11.65%) was significantly higher (22.09+/-8018%, P【0.01). In phases of metaplasia, dysplasia and gastric cancer in the H. pylori-positive group, AIs had an evidently graduall decreasing trend (P【0.01), while PIs had an evidently gradual increasing trend (P【0.05 or P【0.01), and there was also a trend of gradual increase in the expression of p53 gene. CONCLUSION: In the course of the formation of gastric carcinoma, proliferation of gastric mucosa can be greatly increased by H. pylori, and H. pylori can induce apoptosis in the phase of metaplasia, but in the phase of dysplasia H. pylori can inhibit cellular apoptosis. And H. pylori infection can strengthen the expression of mutated p53 gene.

Detection of H.pylori DNA in gastric epithelial cells by in situ hybridization

AIM: To investigate the presence of H.pylori DNA within gastric epithelial cells in patients with H.pylori infection and its possible carcinogenic mechanism. METHODS: Total 112 patients, with pathologically confirmed chronic superficial gastritis, chronic atrophic gastritis, intestinal metaplasia, atypical hyperplasia or gastric cancer were studied. Among them, 28 were H.pylori negative and 84 H.pylori positive. H.pylori DNA in gastric epithelial cells was detected by GenPoint catalyzed signal amplification system for in situ hybridization. RESULTS: In the H.pylori positive group, zero out of 24 chronic superficial gastritis (0.0%), four out of 25 precancerous changes (16.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the nucleus of gastric epithelial cells, the positive rates of H.pylori DNA in the nucleus of gastric epithelial cells were progressively increased in chronic superficial gastritis, precancerous changes and gastric cancer groups (chi(2)=12.56, P=0.002); One out of 24 chronic superficial gastritis (4.2%), eleven out of 25 precancerous changes (44.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the cytoplasm of gastric epithelial cells (chi(2)=10.86, P=0.004). In the H.pylori negative group, only one patient with gastric cancer was found H.pylori DNA in the nucleus of gastric epithelial cells; Only two patients, one patient with precancerous changes and another with gastric cancer, showed H.pylori DNA in the cytoplasm of gastric epithelial cells. Furthermore, H.pylori DNA must have been in the cytoplasm as long as it existed in the nucleus of gastric epithelial cells. CONCLUSION: H.pylori DNA exists both in the nucleus and the cytoplasm of gastric epithelial cells in patients with H.pylori infections. The pathological progression from chronic superficial gastritis, precancerous changes to gastric cancer is associated with higher positive rates of H.pylori DNA presence in the nucleus of gastric epithelial cells.

Low grade gastric mucosa associated lymphoid tissue lymphoma:Treatment strategies based on 10 year follow-up

AIM:To deduce strategic guidelines of gastric mucosa associated lymphoid tissue lymphoma (MALTOMA) by evaluating the long-term outcome of patients in respect to various treatment modalities. METHODS:A total of 55 patients with MALTOMA from May 1992 to August 2002 were retrospectively reviewed. RESULTS:Complete remission was obtained in 24 (82.8%) of 29 patients treated with anti Helicobacter pylori (Hpylori) regimen only.The duration to reach complete remission was 12 months (85 percentile,2-33 months).Five patients showed complete remission with radiation therapy (26-86 months).Two of them were Hpyloritreatment failure cases. CONCLUSION:Hpylorieradication is an effective primary treatment option for low grade MALTOMA and radiation therapy could be considered in patients with no evidence of Hpyloriinfection or who do not respond to Hpylorieradication therapy 12 months after successful eradication.

幽门螺杆菌在口腔中的特征性分布

目的 :研究幽门螺杆菌 (Helicobacterpylori,Hp)在慢性胃炎患者口腔中的分布。 方法 :依据Hp尿素酶C基因和细胞毒素相关基因 (cagA)设计引物建立PCR方法 ,从 32例慢性胃炎患者口腔内多部位采集标本 ,检测和鉴定牙菌斑 (每人采集 6个牙的龈上和龈下菌斑 )、含漱液、舌背黏膜、颊黏膜及腭黏膜表面中的Hp。 结果 :32例患者中有 2 9例 (90 6 % )从口腔内牙菌斑、含漱液、舌背黏膜、颊黏膜及腭黏膜至少一处检测出Hp ,其中 2 8例 (87 5 % )从胃和口腔内同时检出Hp ,口腔内各部位标本中Hp检出率依次为牙菌斑 84 4 % ,口腔含漱液 5 6 2 % ,舌背黏膜 4 3 8% ,颊黏膜 2 8 1% ,腭黏膜 9 4 % ;在 384份牙菌斑中 ,磨牙的牙菌斑Hp的检出率高于前牙 (33 2 %vs 2 1 9% ,P <0 0 1) ;而上下牙的牙菌斑Hp的阳性率差异无显著性 (2 9 7%vs 2 9 2 % ,P >0 0 5 ) ;在PD >4mm的牙周袋 ,菌斑Hp检出率显著高于PD <4mm的袋 (P <0 0 5 ) ,龈下菌班Hp的阳性率显著高于龈上菌斑 (P <0 0 1)。 结论 :口腔多部位存在Hp ,牙菌斑中居多 ,并呈一定的分布规律 ;口腔Hp可能是胃Hp感染的重要来源。

2种牙菌斑控制法对胃黏膜幽门螺杆菌再感染的影响研究

目的比较2种牙菌斑控制法对胃黏膜幽门螺杆菌(H.pylori)再感染率的影响,探讨H.pylori相关性胃病患者行菌斑控制的必要性及有效方法。方法将148例胃炎和消化性溃疡患者随机分为试验一组(54例)、试验二组(55例)和对照组(39例),经消化内科抗H.pylori系统治疗并碳13尿素呼气试验证实H.pylori被根除后,试验一组行日常菌斑控制,试验二组除日常菌斑控制外增加牙菌斑的口腔专业处理,对照组未行上述处理。半年后行碳13尿素呼气试验检查确定各组胃黏膜H.pylori的感染率。结果试验一组中5例患者因停用含漱液漱口被淘汰,试验二组中8例患者因未严格执行牙菌斑控制被淘汰。试验一组、试验二组、对照组患者H.pylori的感染率分别为67.3%、19.1%、82.1%。统计分析表明,试验二组患者H.pylori的感染率低于对照组、试验一组(掊2=33,P<0.05;掊2=31.06,P<0.05),试验一组患者H.pylori的感染率与对照组之间无统计学差异(掊2=2.43,0.1<P<0.25)。结论牙菌斑是胃H.pylori再感染的重要来源,H.pylori相关性胃病患者应控制牙菌斑,以专业牙菌斑处理加药物含漱为佳。

Pyrosequencing检测口腔与胃中的幽门螺杆菌16SrDNAV1区基因序列

目的通过Pyrosequencing检测口腔与胃幽门螺杆菌16SrDNAV1区序列基因片段分析,以进一步验证口—口传播的的假设。方法选择18例患有慢性中度牙周炎且胃镜活检Hp感染阳性患者及其中10例患者的家属。提取患者胃、牙菌斑和含漱液共74例样本中的DNA,PCR扩增阳性后pyrosequecing检测16SrDNAV1区序列基因片段。结果患者胃和口腔Hp及其家属口腔Hp的序列相比较,有0～1个碱基不同。结论口腔中的Hp与胃内Hp16SrDNAV1区基因型比较95.8%～100%的同源性,口腔可能为Hp的聚集地。口腔Hp可能与胃Hp感染的复发或再感染有关。

胃粘膜相关淋巴组织型淋巴瘤形态学研究

目的：研究胃粘膜相关淋巴组织（ＭＡＬＴ）型淋巴瘤及其与胃粘膜套细胞淋巴瘤和滤泡性淋巴瘤的鉴别诊断。方法：应用ＨＥ染色和免疫组化ＡＢＣ法检测胃ＭＡＬＴ型淋巴瘤，内镜作幽门螺杆菌（ＨＰ）培养或尿素试验检测ＨＰ感染。结果：３１例胃ＭＡＬＴ型淋巴瘤中低度恶性２７例，高度恶性４例。细胞类型以ＣＣＬ型最常见。免疫表型以ＩｇＭ为主，缺乏ＩｇＤ。３１例中２８例有ＨＰ感染（占９０．５２％）。结论：①低恶ＭＡＬＴ型淋巴瘤常见到淋巴上皮病变，滤泡性克隆化和反应性滤泡，具有诊断和鉴别诊断价值。②高恶ＭＡＬＴ型淋巴瘤伴有低恶成分。

幽门螺杆菌感染与胃黏膜增殖及与胃癌预后的关系

目的 :探讨增殖细胞核抗原 (PCNA)在幽门螺杆菌 (HP)感染的不同胃黏膜增殖性病变演进中的表达情况及其相互关系 ,并着重探讨HP感染对胃癌预后的意义。方法 :对 14 5例经病理证实的不同胃黏膜病变用免疫组化方法检测PCNA标记指数 (LI) ,Warthin Starry(W S)法检测HP感染。结果 :在浅表性胃炎 (CSG)、萎缩肠化性胃炎 (CAG +IM)、异型增生 (DYS)、早期胃癌和进展期胃癌中 ,PCNA LI为 2 4 0 0± 17 88,4 6 5 9± 18 15 ,6 0 5 9± 2 0 2 6 ,5 7 92± 15 15 ,71 0 8± 2 1 2 5。在IM、DYS、胃癌组织均高于CSG(P <0 0 5 )。PCNA阳性表达与胃癌组织类型、浆膜浸润和淋巴结转移密切相关 ,而且Bor rmannIV高于早期胃癌 (P <0 0 5 )。PCNA阳性表达与肠型胃癌HP感染有关。CAG +IM、DYS和GC组PCNA阳性表达中HP感染者高于阴性者。胃癌HP阳性者 5年存期短于HP阴性者。结论 :PCNA基因表达与胃黏膜增殖和恶化有关。HP感染和胃黏膜增殖和恶化有关 ,HP感染与胃癌预后有关。

幽门螺杆菌诱导胃粘膜上皮细胞凋亡与Bax蛋白的表达

目的观察幽门螺杆菌(Hp)感染诱导胃粘膜上皮细胞凋亡与Bax 蛋白表达的关系,探讨 Hp 诱导胃粘膜上皮细胞凋亡的机制。方法采用脱氧核糖核酸末端转移酶介导的缺口末端标记(TUNEL)技术原位观察和比较73例慢性胃炎患者胃粘膜上皮细胞凋亡情况,对其中50例 Hp 阳性患者 Hp 根除前后胃粘膜上皮细胞凋亡的变化进行检测;并采用免疫组织化学染色检测 Bax 蛋白表达变化。结果 Hp 阳性患者胃粘膜上皮细胞凋亡指数为12.8%,明显高于 Hp 阴性者(3.6%)(t=6.64,P<0.01);Hp 根除后胃粘膜上皮细胞凋亡指数(4.4%)较治疗前明显降低(12.5%,t=5.39,P<0.01),而持续阳性者凋亡指数无明显降低,Hp阳性患者胃粘膜上皮细胞 Bax 蛋白表达率为62.3%,显著高于Hp 阴性者(35.0%,x^2=4.36,P<O.05);Bax 蛋白表达阳性的 Hp 阳性患者在 Hp 根除后 Bax 阳性细胞密度显著减少(t=3.18,P<0.01),而 Hp 未被根除者 Bax 阳性细胞密度无明显变化。结论 Hp 感染可诱导胃粘膜上皮细胞凋亡,这可能是 Hp 参与胃癌发生的重要机制之一;Hp 感染可促进 Bax 蛋白表达增加,这可能是 Hp 感染诱导胃粘膜上皮细胞凋亡的机制之一。

胃病患者口腔中的幽门螺杆菌

目的 通过多聚酶链反应(PCR) 检测胃病患者口腔中的幽门螺杆菌( Hp) 。方法 从13 例有上消化道症状经内镜检查证实的胃病患者采集胃粘膜、口腔含漱液和6 个牙位的龈上及龈下菌斑,应用PCR 检测标本中的Hp 。同时用酶联免疫法(ELISA) 检测静脉血、唾液、龈沟液中抗Hp 特异性IgG 抗体。结果 PCR 检测胃粘膜均为Hp 阳性。6 例患者(46 .2 % ) 的含漱液和11 例患者(84 .6 % ) 的至少一份菌斑样本中检测出Hp 。龈下菌斑中Hp 的检出率(38 .5 % ) 显著高于龈上菌斑(19 .2 % )(P< 0 .01) 。此外, 从患者静脉血、唾液、龈沟液中均可检测到抗Hp 特异性IgG 抗体。结论 本研究结果表明龈沟或牙周袋可能是口腔Hp