幽门螺杆菌与胃癌相关性研究

［目的］研究幽门螺杆菌（Ｈｐ）与胃癌发生之间的关系。［方法］用美蓝染色对７４１例胃炎性病变和１３１例胃癌病人之胃粘膜活检组织的Ｈｐ感染情况进行检测。［结果］胃癌组和慢性萎缩性胃炎组（ＣＡＧ）Ｈｐ检出率分别为６２．５９％和６１．６０％,明显高于慢性浅表性胃炎组（ＣＳＧ）的３８．６１％（Ｐ＜０．０１）;胃癌组中,伴有癌周粘膜肠化生者Ｈｐ检出率明显高于不伴肠化生者（Ｐ＜０．０５）;在活动性ＣＳＧ和ＣＡＧ中,Ｈｐ检出率分别为８９．４１％和９０．５３％,而在非活动性ＣＳＧ和ＣＡＧ中仅分别为１．７１％和１．２３％,两者差异非常显著（Ｐ＜０．０１）。［结论］提示Ｈｐ感染与胃癌的发生有显著的相关性;Ｈｐ有可能通过引发活动性胃炎、腺体萎缩、上皮肠化生等方式参与胃癌的发生。     

幽门螺杆菌与胃部恶性肿瘤

幽门螺杆菌（Helicobacter pylori,Hp）是非贲门胃腺癌和胃粘膜相关淋巴样组织（MALT）淋巴瘤最重要的危险因子。目前普遍认为Hp根除治疗是肠化生发生之前行之有效的治疗手段。然而单一根除Hp只能一定程度减缓胃癌的发病率。Hp与胃部恶性肿瘤之间的关系尚未明了,Hp的致癌效应涉及Hp与胃上皮细胞粘附、Ⅳ型分泌系统促进代谢物易位导致的胃上皮细胞的信号转导途径改变等方面。本文从流行病学、治疗方法学以及发病机制等方面对幽门螺杆菌与胃部恶性肿瘤的研究近况进行综述。     

Helicobacter pylori Infection and Gastric Mucosal Atrophy in Two Ethnic Groups in Nepal

Serum anti-Helicobacter pylori antibodies and pepsinogens (PGs) have been used as gastric cancer screening and gastric mucosal status markers. Nepal is a low risk country for gastric cancer. However, the mountainous populace in the northern region culturally linked to Tibet as well as Bhutan, a neighboring country, have a high risk of GC. We collected gastric biopsy specimens and sera from 146 dyspeptic patients living in Kathmandu, Nepal. We also examined the sera of 80 volunteers living in the mountainous regions of the Himalayas. The optimal cut-off was calculated for serum biomarkers against the histology. Kathmandu patients (43.8%) were serologically positive for H. pylori infection, which was significantly lower than that for the mountainous (61.3%, P = 0.01). The same results also found in the prevalence of PG-positivity, PG I levels and PG I/II ratios (P = 0.001, P <0.0001 and P = 0.03, respectively). Moreover, the PG I/II ratios were significantly, and inversely correlated with the OLGA score (r = -0.33, P <0.009). The low incidence of gastric cancer in Nepal can be attributed to low gastric mucosal atrophy. However, the mountainous subjects have high-risk gastric mucosal status, which could be considered a high-risk population in Nepal.     

Value of CIM,CLO Test and Multiplex PCR for the Diagnosis of Helicobacter Pylori Infection Status in Patients with Gastritis and Gastric Ulcer

Objective: To assess the value of Current Infection Marker (CIM) test, Campylobacter-Like Organism (CLO) test, and the multiplex polymerase chain reaction test (PCR) for the diagnosis of Helicobacter pylori (H. pylori) infection in a Vietnamese population. Methods: Targeted suitable patients were recruited. CIM test, CLO test and multiplex PCR were used to diagnose for H. pylori infection. Patients were considered positive for H. pylori when at least two of the three tests were positive. The performance of each of the three tests was compared to the H. pylori positive populations as defined. Result: Amongst 201 patients with a mean age of 40.5 (range, 18-74) years, there were 115 females and 86 males. Of the 201 patients, 107 (53.2%) were diagnosed as H. pylori positive according to the defined criteria. The positive patients obtained with CLO test, CIM test and multiplex PCR were 38.3%, 59.2% and 72.1%, correspondingly. The full performance of the three tests as highlighted in order as above were 85.07%, 83.08% and 81.09%, respectively. The positive rate of CLO test was the lowest, with 38.3% positive, but this method was the most accurate, with the accuracy of 85.07%. This suggested that CLO test has the highest specificity among the three. The sensitivity, specificity, positive, negative predictive values and accuracy of the CLO / CIM / multiplex PCR tests were 71.96% / 89.72% / 100%, 100% / 75.53% / 59.57%, 100% / 80.67% / 73.79%, 75.81% / 86.59% / 100%, and 85.07% / 83.08% / 81.09%, respectively. Conclusion: All the three methods have high accuracy for the diagnosis of H. pylori infection in the Vietnamese population with gastritis and gastric ulcers. These tests can be employed in the clinical settings for the Vietnamese population. CLO test should be used in combination with the other tests to reduce false-negative results.     

Association between Gastric Pathology and Hepatitis B Virus Infection in Patients with or without Helicobacter Pylori

Background: In the recent years, hepatitis B virus (HBV) infection has been considered as a risk factor for gastriccancer, but further studies are required to confirm these claim. The present study was aimed to evaluate the correlationbetween gastric pathology (precancerous and cancerous conditions) with HBV infection in Helicobacter pylori (H. pylori)positive or negative patients. Methods: In this cross-sectional study, 728 patients under endoscopy examination in YazdShaheed Sadoughi Hospital between 2017 and 2018 were participated. Histopathological analysis was performed ongastric specimens. Hepatitis B surface antigen (HBsAg) in sera was detected by the enzyme-linked immunosorbent assay(ELISA). The relationship between gastric pathology and HBV infection were explored by logistic regression analysis.Results: Of 728 patients, HBsAg and H. pylori infection were detected in 83 and 408 patients, respectively. Sixty ninepatients were co-infected with H. pylori/HBV. H. pylori infection detected in patients with HbsAg positive significantlymore than those were negative for HbsAg (p=0.029). None of HBV/H. pylori co-infected patients did not have normalgastric tissue. A significant difference was seen in histopathology of gastric tissue between HBsAg positive patientswith and without H. pylori infection (p<0.0001). The HBsAg was associated with histopathology of gastric (OR=21.56,95℅CI=7.070-65.741, p<0.001) and as a risk factor for gastritis (OR=12.457, 95℅CI= 3.007-51.614, P=0.001) but nocancer (OR=2.127, 95℅CI=0.242-18.704, P=0.496). Conclusion: The HBV infection alone is associated with someprecancerous lesions but is not correlated with gastric cancer. It can increase development of premalignant conditionsand carcinoma significantly in H. pylori positive patients.     

幽门螺杆菌感染、p16基因甲基化与胃癌的相关性研究

目的：探讨幽门螺杆菌（Hp)感染、抑癌基因p16 5′-CpG岛甲基化与胃癌的相关性。方法：对57例胃癌患者及30例慢性浅表性胃炎患者（对照组）分别采用快速尿素酶法及Giemsa染色法进行Hp检测,并采用甲基化敏感性限制性内切酶（HpaⅡ、MspⅠ、SacⅡ）酶切后PCR扩增法进行p16基因外显子Ⅰ多位点甲基化状态的检测。结果：57例胃癌患者中,Hp阳性27例（47．4％）,p16基因甲基化18例（31．6％）;Hp阳性胃癌组p16基因甲基化13例（48．2％）Hp阴性胃癌组p16基因甲基化5例（16．75）。对照组30例中,无p16基因甲基化,Hp阳性16例（53．3％）;结果显示胃癌组与对照组Hp感染无显著性差异（P＞0．05）。2组p16基因甲基化比较有显著性差异（P＜0．05）,Hp阳性胃癌组与Hp阴性胃癌组比较,p16基因甲基化有显著性差异（P＜0．05）。幽门螺杆菌感染可诱发抑癌基因p16 5 ′-CpG岛出现甲基化,可能是幽门螺杆菌与参致癌的机制之一。     

慢性胃病伴肠上皮化生、胃癌与幽门螺旋杆菌感染的关系

目的探讨慢性胃病伴肠上皮化生、胃癌与幽门螺旋杆菌（helicobacter pylore,HP）感染的关系。方法采用warthin—strarry银染色方法,对380例慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡组织及胃癌的癌旁组织进行HP检测．应用（alcianblue—PH2．5-periodic—schiff,AB—PAS）、（high-iron—diamine-alcianblue—PH2．5,HID-AB）黏液组织化学方法,区别慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡组织及胃癌的癌旁组织伴有肠上皮化生的类型。结果总例数380例。HP阳性率为69．74％。慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡组织及胃癌的癌旁组织伴肠上皮化生的HP感染率分别为77．78％、85．71％、100．00％、80．95％。慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡及胃癌的癌旁组织伴肠上皮化生AB—PAS染色阳性率分别为86．84％、91．43％、93．33％、100．00％;HID—AB染色阳性率分别为34．21％、42．86％、53．33％、85．71％。癌旁组织的肠上皮化生中,78．57％为不完全大肠型,慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡伴肠上皮化生中,不完全小肠型比例分别为52．63％、54．28％、53．33％;不完全大肠型比例分别为28．95％、31．43％、20．00％。结论HP感染与慢性胃病伴肠上皮化生及胃癌的发生密切相关。癌旁组织的不完全大肠型肠上皮化生与胃癌的发生密切相关;慢性胃病组织当中的小灶状不完全大肠型上皮化生具有潜在发生癌变的可能性。     

DNMT3a rs1550117 Polymorphism Association with Increased Risk of Helicobacter pylori Infection

Background: DNA methyltransferase-3a (DNMT3a) plays significant roles in embryogenesis and the generationof aberrant methylation in carcinogenesis. This study aimed to investigate associations between single nucleotidepolymorphisms (SNPs) of the DNMT3a gene and risk of Helicobacter pylori infection, gastric atrophy and gastriccancer. Methods: The subjects comprised 447 patients with gastric cancer; 111 individuals with gastric atrophyand 961 healthy controls. Two SNPs (rs1550117 and rs13420827) of the DNMT3a gene were genotyped by Taqmanassay. DNMT3a expression was analyzed in cancer tissues from 89 patients by tissue microarray technique. Oddsratio (ORs) and 95% confidence intervals were calculated by multivariate logistic regression. Results: Amonghealthy controls, risk of H.pylori infection was significantly higher in subjects with the rs1550117 AA genotype,compared to those with GG/AG genotypes of DNMT3a [OR=2.08, (95%CI: 1.02-4.32)]. However, no significantcorrelation was found between the two SNPs and risk of developing gastric atrophy or gastric cancer. In addition,no increase in DNMT3a expression was observed in the gastric cancer with H.pylori infection. Conclusions:This study revealed that DNMT3a rs1550117 polymorphism is significantly associated with an increased risk ofH. pylori infection, but did not support any evidence for contributions of DNMT3a rs1550117 and rs13420827to either gastric atrophy or gastric cancer. The biological roles of DNMT3a polymorphisms require furtherinvestigation.     

Helicobacter pylori Infection and the Risk of Colorectal Adenoma and Adenocarcinoma: an Updated Meta-analysis of Different Testing Methods

Background and Aims: Helicobacter pylori infection may be associated with an increased risk of colorectalcarcinoma. However, as most studies on this subject were relatively small in size and differed at least partially intheir designs, their results remain controversial. In this study, we aimed to carry out a meta-analysis to evaluatethe potential association of H. pylori infection with colorectal adenoma and adenocarcinoma risk, covering all ofthe different testing methods. Methods: We conducted a search in PubMed, Medline, EBSCO, High Wire Press,OVID, and EMBASE covering all published papers up to March 2013. According to the established inclusioncriteria, essential data were then extracted from the included studies and further analyzed by a systematicmeta-analysis. Odds ratios were employed to evaluate the relationship between H. pylori infection and therisk of colorectal neoplasms. Results: Twenty-two studies were included, and the odds ratio for the associationbetween H. pylori infection and colorectal cancer was 1.49 (95% confidence interval 1.30-1.72). No statisticallysignificant heterogeneity was observed. Publication bias was ruled out. Conclusion: The pooled data suggest H.pylori infection indeed increases the risk of colorectal adenoma and adenocarcinoma.     

Sirt1 Gene Expression and Gastric Epithelial Cells Tumor Stage in Patients with Helicobacter pylori Infection

Introduction: The World Health Organization has categorized Helicobacter pylori as a carcinogen for gastriccancer, which causes human mortality worldwide. A number of studies have shown that H. pylori affects cell signalingin gastric epithelial cells and changes the expression of some proteins such as proinflammatory cytokines. Bacterialinfections may alter sirt1 and sirt2 genes expression in inflammatory tissues and cancer cells. In this study, sirt1 andsirt2 genes expression in gastric cancers was surveyed with reference to H. pylori status. Methods: Stomach biopsieswere collected from 50 gastric cancer patients, 25 H. pylori-positive and 25 H. pylori-negative as determined by theurea rapid test. Tumor grade was determined by a pathologist. After total RNA extraction from gastric cancer biopsysamples and cDNA synthesis, sirt1 and sirt2 genes expression levels were determined by Real Time PCR and ΔΔCTmethods. Results: There was no statistically significant link between H. pylori infection and sirt1 (P<0.899) and sirt2(P<0.169) genes expression in gastric epithelial cells. However, pathologic findings showed that there is a statisticallysignificant relationship between sirt1 gene expression and the tumor grade (P<0.024). Discussion: A statisticallysignificant association was found between sirt1 gene expression and tumor grade of gastric cancers that could be dueto effects on progression of cancer cells infected with H. pylori.     

Synergistic Promoting Effects of Helicobacter pylori Infection and High-salt Diet on Gastric Carcinogenesis in Mongolian Gerbils

Helicobacter pylori ( Hp ) infection and high-salt diet administration are both considered to be important factors in gastric carcinogenesis in man. To investigate the interaction of these two factors on gastric carcinogenesis, an experimental study of the carcinogenesis model was performed. Mongolian gerbils were treated with 20 ppm of N -methyl- N -nitrosourea (MNU) in their drinking water for alternate weeks for a total of 5 weeks' exposure (groups 1, 2, 3 and 4) or were maintained as controls (groups 5, 6, 7 and 8). At week 11, the animals were inoculated with Hp (groups 1, 2, 5 and 6) or the vehicle alone (groups 3, 4, 7 and 8), and after week 12, animals were fed a 10% high salt diet (groups 1, 3, 5 and 7) or the control diet (groups 2, 4, 6 and 8). At week 50, the incidence of adenocarcinomas in group 1 (32.1%, 6 well-differentiated, 2 poorly-differentiated adenocarcinomas, and one signet-ring cell carcinoma) was significantly higher than in groups 3 (0%) ( P <0.005) and 4 (0%) ( P <0.01). The incidence of adenocarcinomas in group 2 (11.8%, one well-differentiated adenocarcinoma, and one signet-ring cell carcinoma) was also higher than in groups 3 and 4. A high-salt diet enhanced the effects of Hp infection on gastric carcinogenesis, and these two factors acted synergistically to promote the development of stomach cancers. Moreover, Hp infection promoted gastric carcinomas more than the high-salt diet.     

幽门螺杆菌感染与胃癌的关系

探讨幽门螺杆菌感染与胃癌的关系。方法在世界癌最高发区之一－福建省长乐市进行１：１配对病例对照研究,用ＥＬＩＳＡ方法检测血清抗Ｈｐ的ＩｇＧ抗体。结果研究对象中Ｈｐ阳性总检出率为６３．６８％,病例和对照Ｈｐ感染率的差异无显著意义。结论Ｈｐ感染与长期摄入鱼露,少吃新鲜蔬菜和不良饮食习惯等因素相互作用,胃癌发生的危险性增高。     

Risk of Gastric Cancer in Children with Helicobacter pylori Infection

Background: Helicobacter pylori (H. pylori) is the most common chronic infectious agent in the stomach.Most importantly, it may lead to atrophy, metaplasia and cancer. The aim of this study was to investigate theincidence of H. pylori infection and to detect early mucosal changes that may lead to malignant degenerationin children. Materials and Methods: Children who underwent upper gastrointestinal endoscopy were included.Familial history of gastric cancer was noted. Endoscopic examinations were performed by a single pediatricgastroenterologist. A minimum of three biopsy samples were collected during endoscopy. The patients wereaccepted as H. pylori infected if results of biopsies and rapid urease test were both positive. Biopsies wereevaluated for the presence and degree of chronic inflammation, the activity and severity of gastritis, glandularatrophy and intestinal metaplasia. Results: A total of 750 children (388 boys, 362 girls) were evaluated in ourstudy, with a mean age of 10.1 years. A total of 390 patients (52%) were found to be infected with H. pylori.Among the H. pylori infected patients, 289 (74%) were diagnosed to have chronic superficial gastritis, 24 (6.2%)had gastric atrophy. Most strikingly, intestinal metaplasia was observed in 11 children, all were in the H. pyloripositive group. There was no difference in the mean of age, gender and socioeconomic class between H. pyloriinfected and non-infected groups. The frequency of gastric cancer in family members (4 in number) was higherin patients with H. pylori infection. No gastric cancer case was reported from the parents of non-infected children.The worst biopsy parameters (atropy and metaplasia) were improved after H. pylori eradication on controlendoscopy. Conclusions: The current study shows a higher prevalence of familial history of gastric cancer in H.pylori infected children. Intestinal metaplasia was also higher in the infected children. Eradication of H. pyloriinfection for this risk group may prevent subsequent development of gastric cancer.     

Gastric cancer, Helicobacter pylori infection and other risk factors

Gastric cancer incidence is declining. However, it is too early to consider this neoplastic disease as rare and the worldwide mortality rate still remains high. Several risk factors have been identified for non-cardia gastric cancer and primary prevention is feasible since most of the risk factors can be removed. Helicobacter pylori eradication treatment reduces but does not abolish gastric cancer risk. Indeed, gastric cancer is a multifactorial disease and removing one factor does not therefore prevent all cases. Endoscopic surveillance is still needed, especially in subjects at higher risk. The definition of high-risk patients will be the future challenge as well as identifying the best surveillance strategy for such patients.     

上消化道癌高低发区幽门螺旋杆菌感染与胃癌

目的：研究江苏上消化道癌高发区淮安市、低发区邳州市幽门螺旋杆菌（Ｈｐ）感染与胃癌发生的关系。方法：用酶联免疫法及乳胶凝集法检测７９例胃癌、７７例食管癌、１５６例患者亲属和１００名一般居民对照者血浆中Ｈｐ抗体,结果：低发区胃癌患者组Ｈｐ感染率（６６．６７％）显著高于发区（３８．６４％）,两地区其他组之间Ｈｐ感染率无显著差异,低发区ＨＰ感染者胃癌的危险性显著升高（ＯＲ３．６１,９５％ＣＩ１．０１－１２     

Genotyping of Peroxisome Proliferator-Activated Receptor gamma in Iranian Patients with Helicobacter pylori Infection

Helicobacter pylori (H. pylori) infection as a serious problem in both adults and children can induce chronicgastritis, peptic ulcer disease (PUD), and possibly gastric cancer. The aim of the current study was to surveyantibiotic resistance and also to determine influence of PPARγ polymorphism in patients with H. pylori infection.During an 11-month-period, 98 H. pylori isolates were collected from 104 biopsy specimens. In vitro susceptibilityof H. pylori isolates to 4 antimicrobial agents metronidazole, clarithromycin, amoxicillin and tetracycline wereassessed by quantitative method according to European Committee on Antimicrobial Susceptibility Testing(EUCAST) guideline. PPARγ polymorphism was determined using polymerase chain reaction-restrictionfragment length polymorphism assay. The frequency of H. pylori infection in our study was 94.2%. In vitrosusceptibility data showed that highest level of resistance was related to metronidazole (66.3%), and the majorityof H. pylori isolates were highly susceptible to amoxicillin and tetracycline (94.9% and 96.9%, respectively).Genotypic frequencies were 25.5% for CC (Pro12Pro), 40.8% for GC (Pro12Ala) and 33.7% for GG (Ala12Ala).In our study, CG genotype had highest distributions among infected patients with H. pylori. The study suggeststhat the PPAR-γ Pro12Ala polymorphism could be evaluated as a potential genetic marker for susceptibility togastric cancer in the presence of H. pylori infection.     

Helicobacter pylori vacA d1 Genotype Predicts Risk of Gastric Adenocarcinoma and Peptic Ulcers in Northwestern Iran

Background: There is a close relationship between Helicobacter pylori (H pylori)-specific factors and differentgastroduodenal diseases. The present study aimed to investigate the prevalence of vacA d1, d2 genotypes in theH pylori isolates from patients with gastric adenocarcinoma, peptic ulcer disease (PUD) and gastritis in EastAzerbaijan region, where the incidence of gastric cancer (GC) is high. Strains isolated from this area are likelyto be of European ancestry. Materials and Methods: In this study, genotyping of the vacA d region of 115 isolatesobtained from patients with different gastrodoudenal diseases was accomplished by PCR methods. In additionto PCR amplification of H pylori 16S rDNA, rapid urease tests or histological examination were used to confirmthe presence of H pylori in biopsy specimens. Data were collected and analyzed using SPSS version 19. Results:Of the total of 83 H pylori isolates, 36 (43.4%) contained the d1 allele and 47 (56.6%) were subtype d2. Theresults of the multiple linear/logistic regression analysis showed high correlation between allele d1 and gastricadenocarcinoma or PUD. Conclusions: This study suggests that the H pylori vacA d1 genotype helps predict riskfor gastric adenocarcinoma and PUD in East Azerbaijan, Iran.     

Gastric cancer development after the successful eradication of Helicobacter pylori

Gastric cancer (GC) develops as a result of inflammation-associated carcinogenesis due to Helicobacter pylori (H. pylori) infection and subsequent defects in genetic/epigenetic events. Although the indication for eradication therapy has become widespread, clinical studies have revealed its limited effects in decreasing the incidence of GC. Moreover, research on biopsy specimens obtained by conventional endoscopy has demonstrated the feasibility of the restoration of some genetic/epigenetic alterations in the gastric mucosa. Practically, the number of sporadic cases of primary/metachronous GC that emerge after successful eradication has increased, while on-going guidelines recommend eradication therapy for patients with chronic gastritis and those with background mucosa after endoscopic resection for GC. Accordingly, regular surveillance of numerous individuals who have received eradication therapy is recommended despite the lack of biomarkers. Recently, the focus has been on functional reversibility after successful eradication as another cue to elucidate the mechanisms of restoration as well as those of carcinogenesis in the gastric mucosa after H. pylori eradication. We demonstrated that Congo-red chromoendoscopy enabled the identification of the multi-focal distribution of functionally irreversible mucosa compared with that of restored mucosa after successful eradication in individuals at extremely high risk for GC. Further research that uses functional imaging may provide new insights into the mechanisms of regeneration and carcinogenesis in the gastric mucosa post-eradication and may allow for the development of useful biomarkers.     

Risk of gastric cancer development after eradication of Helicobacter pylori

Helicobacter pylori (H. pylori) infection is the most important risk factor for gastric cancer (GC) development through the Correa’s gastric carcinogenesis cascade. However, H. pylori eradication alone does not eliminate GC, as pre-neoplastic lesions (atrophic gastritis, intestinal metaplasia and dysplasia) may have already developed in some patients. It is therefore necessary to identify patients at high-risk for gastric cancer after H. pylori eradication to streamline the management plan. If the patients have not undergone endoscopy with histologic assessment, the identification of certain clinical risk factors and non-invasive testing (serum pepsinogen) can predict the risk of atrophic gastritis. For those with suspected atrophic gastritis, further risk stratification by endoscopy with histologic assessment according to validated histologic staging systems would be advisable. Patients with higher stages may require long-term endoscopic surveillance. Apart from secondary prevention to reduce deaths by diagnosing GC at an early stage, identifying medications that could potentially modify the GC risk would be desirable. The potential roles of a number of medications have been suggested by various studies, including proton pump inhibitors (PPIs), aspirin, statins and metformin. However, there are currently no randomized clinical trials to address the impact of these medications on GC risk after H. pylori eradication. In addition, most of these studies failed to adjust for the effect of concurrent medications on GC risk. Recently, large population-based retrospective cohort studies have shown that PPIs were associated with an increased GC risk after H. pylori eradication, while aspirin was associated with a lower risk. The roles of other agents in reducing GC risk after H. pylori eradication remain to be determined.     

Investigation of Association between oipA and iceA1/iceA2 Genotypes of Helicobacter pylori and Gastric Cancer in Iran

Background: H pylori is the main causative agent of Gastric cancer and chronic gastritis. Genetic diversityof H. pylori has major contribution in its pathogenesis. We investigated the prevalence of oipA and iceA1/iceA2positive strains of H. pylori among patients with gastric cancer and gastritis. Materials and Methods: Samplingperformed by means of endoscopy from 86 patients. DNA was extracted from tissue samples using DNA extractionkit. PCR assay was performed and products were monitored by Agarose Gel Electrophoresis. Results: UreaseTest and 16S rRNA PCR did not show significant differences in detection of H. pylori. The frequency of iceA1allele in patients with gastric cancer was significantly higher than those with gastritis (p<0.05). However, therewas no significant difference in prevalence of oipA and iceA2 genes among the two groups of patients (p>0.05).Conclusions: The iceA1 gene, but the oipA and iceA2 genes , is associated with H. pylori-induced gastric cancer.However, confirmatory studies must be performed in future.