Heterogeneity of cag genotypes and clinical outcome of Helicobacter pylori infection

Helicobacter pylori infecting strains may include colony subtypes with different cytotoxin-associated gene (cag) genotypes. We sought to determine whether the cag heterogeneity of infecting strains is related to the clinical outcome of infection. Gastric biopsies for culture and histologic study were taken from 19 patients infected with cagA-positive strains (6 with duodenal ulcer, 8 with atrophic gastritis, and 5 with nonatrophic gastritis). For each biopsy, DNA was extracted from 10 single colonies and from a sweep of colonies. Polymerase chain reaction (PCR) for cagA and cagE (both located in the right half of cag) and virB11 (located in the left half of cag) was performed. Random amplified polymorphic DNA PCR (RAPD-PCR) and sequencing of glmM PCR product were performed to verify strain identity of colonies with different cag genotypes. In all patients, PCR from sweeps were positive for cagA, showing that all specimens contained cagA-positive H. pylori subtypes. In 11 patients, PCR products from all colonies were positive for cagA, cagE, and virB11, but in 8 patients, PCR products from varying numbers of colonies were negative for 1 or more cag genes. RAPD-PCR and sequencing of glmM PCR product confirmed the strain identities of colonies with different cag genotypes. We detected cag deletions in 6 of 8, 2 of 5, and 0 of 6 patients with atrophic gastritis, nonatrophic gastritis, and duodenal ulcer, respectively (P = .02). In conclusion, changes in cag genotype in single colony isolates from subjects infected with cagA-positive H. pylori strains are more common in atrophic than in nonatrophic gastritis or duodenal ulcer. These findings are consistent with host-induced (acid secretion?) adaptive changes in cag genotype during infection.     

Helicobacter pylori strain-specific differences in genetic content, identified by microarray, influence host inflammatory responses

Helicobacter pylori enhances the risk for ulcer disease and gastric cancer, yet only a minority of H. pylori-colonized individuals develop disease. We examined the ability of two H. pylori isolates to induce differential host responses in vivo or in vitro, and then used an H. pylori whole genome microarray to identify bacterial determinants related to pathogenesis. Gastric ulcer strain B128 induced more severe gastritis, proliferation, and apoptosis in gerbil mucosa than did duodenal ulcer strain G1.1, and gastric ulceration and atrophy occurred only in B128+ gerbils. In vitro, gerbil-passaged B128 derivatives significantly increased IL-8 secretion and apoptosis compared with G1.1 strains. DNA hybridization to the microarray identified several strain-specific differences in gene composition including a large deletion of the cag pathogenicity island in strain G1.1. Partial and complete disruption of the cag island in strain B128 attenuated induction of IL-8 in vitro and significantly decreased gastric inflammation in vivo. These results indicate that the ability of H. pylori to regulate epithelial cell responses related to inflammation depends on the presence of an intact cag pathogenicity island. Use of an H pylori whole genome microarray is an effective method to identify differences in gene content between H. pylori strains that induce distinct pathological outcomes in a rodent model of H. pylori infection.     

Analysis of the vacA,cagA, cagE,iceA, and babA2 genes in Helicobacter pylori from sixty-one pediatric patients from the Midwestern United States

This study was designed to characterize H. pylori from pediatric gastric biopsy specimens in terms of several genes (vacA, cagA, cagE, iceA1, iceA2, and babA2) proposed to be involved in the pathogenesis of this organism. Many of these genes have been studied in adult H. pylori isolates, however, these genes have not been well characterized in H. pylori from children. Using PCR we observed that 44% of the H. pylori in our biopsies shared two common genotypes (vacA s1b m1, cagA, cagE, iceA2 +/- babA2). While 26% of the H. pylori had unique genotypes. The cag pathogenicity island associated genes, cagA and cagE, were found together in 64% or our H. pylori, while 84% were iceA2 positive. The presence of the babA2 gene has been proposed to be associated with a higher risk of H. pylori related diseases, however, we found that only 36% of our H. pylori contained this gene.     

幽门螺杆菌细胞毒素相关蛋白A、细胞毒素相关蛋白E、细胞空泡毒素A基因型与上消化道疾病的关系

目的分析幽门螺杆菌(Hp)的细胞毒素相关蛋白A(cagA)、细胞毒素相关蛋白E(cagE)、细胞空泡毒素A(vacA)基因型与上消化道疾病的关系。方法选取112例上消化道疾病患者,对其胃黏膜组织中Hp菌株的cagA、cagE、vacA基因型进行检测和分析。结果所有患者胃黏膜样本中的Hp菌株均为cagA基因和cagE基因阳性表达,阳性率均为100%。患者的vacAs1/m~2表型的阳性率最高,分别为54.1%和60.5%,其次为vacAs1/mlb表型和vacAs1/m~-表型,阳性率分别为13.2%~21.1%。消化性溃疡患者和慢性胃炎患者的Hp基因各表型的阳性率的差异均无统计学意义(P0.05)。结论上消化道疾病患者胃黏膜组织中的Hp菌株呈现cagA、cagE、vacAs1/m~2等基因亚型的优势表达,说明这些毒力因子表型在Hp引发和促进上消化道疾病的过程中具有重要的作用,但与上消化道疾病类型缺乏相关性。     

H. pylori infection: bacterial virulence factors and cytokine gene polymorphisms as determinants of infection outcome

The gram negative bacterium H. pylori infects the human stomach worldwide, invariably causing mucosal inflammation. In the majority of cases, H. pylori-associated gastritis remains the only clinical manifestation of the infection, which might cause, otherwise, peptic ulcer, gastric adenocarcinoma. or MALToma. The balance between the bacterial virulence machinery and the host response to the infection determines the different clinical outcomes. The main bacterial virulence factors comprise adhesins (BabA, SabA), the vacuolating cytotoxin VacA, and the products of cag pathogenicity island. The pattern of cytokine production in response to the infection is one of the main host determinants involved in limiting the infection outcome to gastritis or in favoring peptic ulcer or cancer onset. The polymorphisms of some cytokine genes (IL-1beta IL-1RN, TNF-alpha, IFN-gamma) have been correlated with H. pylori-associated gastric adenocarcinoma or peptic ulcer, possibly because they influence the amount of cytokine production in response to H. pylori infection. This review focuses on the role of H. pylori virulence genes and on host cytokines' genes polymorphisms in determining clinical outcome to H. pylori infection.     

Association between Helicobacter pylori genotypes and gastric disorders in relation to the cag pathogenicity island

Helicobacter pylori is a bacterium associated with upper gastrointestinal diseases in humans. However, only a small proportion of infected people become sick. Although several studies have tried to establish an association between known virulence markers and clinical outcomes, in many cases the results have been conflicting. The aim of this study was to investigate the importance of virulence markers to predict clinical outcome in Brazil. Mixed infections by genetically unrelated strains detected by vacA genotyping were found in 18% of the patients. The cagA and cagE genes and the vacAs1 genotype were associated with the development of peptic ulcer disease (PUD). The cagAvacAs1m1 genotype was associated with PUD and duodenal ulcer (DU). Conversely, jhp947 was not associated with DU or PUD, indicating that this gene is not a universal virulence marker. These results also show that a high proportion of the patients were simultaneously infected by cag-positive and cag-negative H. pylori types. This finding suggests the existence of a dynamic equilibrium between the loss and gain of the cag pathogenicity island, probably depending on the physiologic conditions of the patient's stomach. To the best of our knowledge, this is the first study that has documented this finding in Brazil.     

广州地区消化道疾病患者中H.pylori ureA和vacA s1基因及cagA基因亚型分布

目的 分析研究广州地区消化道疾病患者中H.pylori ureA、vacA s1基因和cagA基因亚型(ABC、ABD、ABAB、AAD等)的分布状况及其与胃黏膜病理检测结果间的相关性.方法 随机选取227例消化道疾病患者的胃黏膜标本,分别来自病理组织学检测无病理改变者46例,慢性胃炎130例,消化性溃疡29例,萎缩性胃炎15例,胃癌7例.并用实时荧光定量PCR检测H.pylori ureA基因、vacA s1基因,用PCR扩增cagA羧基端EPIYA基序所在区,然后测序确定其亚型.以保守基因ureA的存在判断H.pylori感染.结果 227例消化道疾病患者中,有50.7% (115/227)的患者H.pylori阳性,其中,vacA s1基因阳性91.3%(105/115),cagA基因阳性78.3%(90/115).4种cagA-EPIYA亚型分布为,ABC 17.8%(16/90)、ABD 78.9%(71/90)、AAD 2.2%(2/90)、ABAB 1.1%(1/90).无病理改变组中H.pylori 阳性32.6%(15/46),vacA s1基因阳性28.3%(13/46),cagA基因阳性26.1%(12/46);慢性胃炎组H.pylori 阳性48.5%(63/130),vacA s1基因阳性43.8%(57/130),cagA基因阳性36.2%(47/130);溃疡组H.pylori 阳性72.4%(21/29),vacA s1基因阳性65.5%(19/29),cagA基因阳性55.2%(16/29);萎缩性胃炎组H.pylori 阳性66.7%(10/15),vacA s1基因阳性66.7%(10/15),cagA基因阳性66.7%(10/15);胃癌组H.pylori阳性85.7%(6/7),vacA s1基因阳性85.7%(6/7),cagA基因阳性71.4%(5/7).H.pylori在不同胃黏膜病理组的分布差异有统计学意义(χ2=16.72;P<0.01),溃疡、萎缩性胃炎、胃癌组中H.pylori的分布明显高于无病理改变与炎症组(χ2=16.02;P<0.01).但在H.pylori阳性患者中,强毒力因子vacA s1基因(χ2=2.00;P=0.74)、cagA基因(χ2=3.44;P=0.49)及cagA-EPIYA亚型(χ2=3.66;P=0.45)在无病理改变、炎症、溃疡、萎缩性胃炎及胃癌组中的分布差异均无统计学意义.结论 广州消化道疾病患者中H.pylori的感染与胃黏膜病理改变显著相关,而广州地区消化道疾病患者中H.pylori高毒力亚型的强致病性并不明显,需扩大标本量,再细化疾病种类进一步分析高毒力H.pylori对胃肠道疾病发生的影响.

Abstract：

Objective To detect the distribution of H.pylori ureA, vacA s1 gene and cagA subtype(ABC, ABD, ABAB, AAD, et al) in patients with digestive diseases in Guangzhou and investigate the relationship with the pathological findings of gastric mucosa.Methods A total of 227 randomly selected gastric mucosa from patients with digestive diseases were enrolled in the research, including 46 without pathological changes, 130 with chronic gastritis, 29 with peptic ulcer, 15 with atrophic gastritis and 7 with gastric cancer.Real-time PCR assay were used to detect Helicobacter pylori ureA gene and vacA s1 gene.EPIYA motifs in the 3′ region of cagA were amplified by conventional PCR followed by subtype sequencing. The conserved gene ureA was used to detect H.pylori infection.Results Among the 227 patients with digestive diseases, 50.7% (115/227) patients were H.pylori positive, in which 91.3%(105/115) carried vacA s1 and 78.3% (90/115) carried cagA. Four types of cagA-EPIYA subtype were detected, including ABC 17.8%(16/90), ABD 78.9%(71/90), AAD 2.2%(2/90) and ABAB 1.1%(1/90).In the non-pathological change group, 32.6% (15/46) were H.pylori positive, in which 28.3% (13/46) carried vacA s1 and 26.1% (12/46) carried cagA;in chronic gastritis group, it was 48.5% (63/130), 43.8% (57/130) and 36.2% (47/130), respectively;in ulcer group, it was 72.4% (21/29), 65.5% (19/29) and 55.2% (16/29), respectively;in atrophic gastritis group, it was 66.7% (10/15), 66.7% (10/15) and 66.7% (10/15), respectively;in gastric cancer group, it was 85.7% (6/7), 85.7% (6/7) and 71.4% (5/7), respectively.The distribution of H.pylori among the 4 groups had statistical significance (χ2=16.72;P<0.01). H.pylori was more prevalent in ulcer, atrophic gastritis and cancer group than in inflammation group and non-pathological change group (χ2=16.02;P<0.01).In patients infected by H.pylori, there was no significant difference in the distribution of vacA s1 gene as high virulence factors among non-pathological change, inflammation, ulcer, atrophic gastritis and cancer group (χ2=2.00;P=0.74), as well as cagA (χ2=3.44;P=0.49) and EPIYA subtypes (χ2=3.66;P=0.45).Conclusions H.pylori infection is significantly associated with the pathological change of gastric mucosa for patients with digestive diseases in Guangzhou, while the relationship with the pathogenicity of H.pylori with high virulence genotype is not significant.More samples and diseases reclassification are needed to make an advanced analysis of the effect of H.pylori with high virulence in gastrointestinal diseases development.     

cagA vacA alelles and babA2 genotypes of Helicobacter pylori associated with gastric disease in Brazilian adult patients

Helicobacter pylori is an important human pathogen that causes chronic gastritis and is associated with development of peptic ulcer disease and gastric malignancies. The vacuolating cytotoxin (vacA), cagA gene, and babA2 gene are important virulence factor involving gastric diseases. Eighty-nine Helicobacter pylori-positive gastric biopsies were analyzed by polymerase chain reaction and Southern blotting for H. pylori detection and genotyping with primer pairs from each virulence gene. Fifty-three strains (59%) were common vacA genotype s1/m1, and only 14 (16%) were s2/m2, 12% of strains was found to have multiple infection. The cagA presence was detected in 48% (43 strains) and babA2 gene was detected in 44% of our H. pylori strains. We observed high percentage of s1/m1 strains with chronic gastritis and peptic ulcer and a significant correlation between cagA presence with the s1 allele and babA2 gene with chronic gastritis.     

长春地区慢性胃病患者幽门螺杆菌感染状况调查

目的通过对本地区慢性胃病患者幽门螺杆菌（H.pylori）感染状况调查,了解本地区流行病学特点,为进一步阐明其与慢性胃病发生发展的关系提供理论依据。方法采用ELISA方法测定血清H.pyloriIgG抗体及CagA抗体;采取胃粘膜活检组织进行快速尿素酶试验,调查H.pylori感染情况,分析其与各种疾病的关系。结果1180例慢性胃病患者H.pylori感染率为67.11%,复合性溃疡、十二指肠溃疡、胃溃疡及慢性萎缩性胃炎感染率分别为90.9%、84.57%、83.96%和80.24%。与慢性浅表性胃炎相比差异有显著性。消化性溃疡、慢性萎缩性胃炎、胃癌和胃息肉患者血清Hp-CagA抗体的阳性率明显高于慢性浅表性胃炎（P〈0.05）。结论本地区慢性胃病患者H.pylori感染率高与多数地区的普通人群,H.pylori感染者尤其是CagA阳性者,更易发生慢性萎缩性胃炎、消化性溃疡及胃癌。     

不同消化性疾病患者幽门螺杆菌毒力基因类型及意义研究

目的分析用不同消化性疾病来源的幽门螺杆菌(Hp)毒力基因的检测结果及其意义。方法收集该院胃镜室于2015年1月至2016年7月采集的628例患者胃活检标本,分离培养Hp,检测其携带的毒力基因,并探讨Hp与慢性萎缩性胃炎(CAG)、慢性浅表性胃炎(CSG)、消化性溃疡(PUD)的相关性。结果 628份胃活检标本中成功分离出214株Hp,选取其中172株提取DNA,发现Hp携带cagA、vacA、dupA、iceA、oipA、luxS多种毒力基因,其中vacA s1m1是CSG的危险因素,vacA s1m2与iceA1+/iceA2+提高PUD的发生率,dupA+提高十二指肠溃疡危险度。结论不同消化性疾病与Hp感染密切相关,dupA可考虑作为Hp致十二指肠溃疡的标记基因,vacA s1m2与iceA1+/iceA2+增加了发生PUD的危险性。     

High prevalence of VacA, CagA protein expression and presence of cag pathogenicity island in Japanese Helicobacter pylori isolates

VacA, CagA proteins and cag pathogenicity island (PAI) were reported to be major virulence factors of Helicobacter pylori. By using specific antibodies, the expression of VacA and CagA was evaluated in Japanese isolates, together with vacuolating assay. To characterize the status of not only cagA, but entire cag PAI, H. pylori isolates were evaluated for cagA and 13 other cagPAI genes by Southern blot. VacA and CagA proteins were expressed in 87% and in 90%, respectively. Vacuolating assay was positive in 84% isolates. Most strains had all cag PAI genes and the only 6% were cag PAI deleted despite of retaining cagA gene. The majority of Japanese isolates were positive for VacA, CagA proteins and cag PAI, and the high prevalence of infection with virulence strains may contribute to the characteristics of H. pylori infection in Japan.     

Eradication of Helicobacter pylori in Japan]

Twenty five years has passed since the re-discovery of Helicobacter pylori. Many people have studied on this organism since that time. Some mechanisms about gastric mucosal inflammation have been clarified, and pathogenesis of peptic ulcer formation and gastric cancer have been solved. H. pylori infection is related to chronic gastritis, peptic ulcer, gastric carcinoma, and MALToma. In 1998, it was reported that gastric cancer occurred in H. pylori infected mongolian gerbils. In Japan, the prevalence of peptic ulcer and gastric cancer is very high. Therefore, the treatment for H. pylori infection is necessary to prevent occurrence of these diseases. To treat H. pylori infection, various regimen have been tried. Triple therapy with PPI and two antibiotics is recommended for cure of H. pylori infection in European and US guidelines. Some guidelines for management of H. pylori infection and regimen were shown in this part.     

诱导胃上皮细胞白细胞介素-8分泌的幽门螺杆菌基因型

目的：分析临床分离的幽门螺杆菌的cag致病岛的差异和不同激素抑制剂对幽门螺杆菌诱导人胃上皮细胞白细胞介素－8（IL－8）分泌的影响。方法：分别用临床分离的不同基因型的cagA^ cagE^ 、cagA^ cagE^-、cagA^-cagE^ 、cagE^-幽门螺杆菌与人胃上皮细胞MGC－803共同培养，IL－8分泌用酶联免疫吸附试验进行检测，比较蛋白激酶A、C、G和蛋白酪氨酸激酶的抑制剂对幽门螺杆菌诱导胃上皮细胞IL－8分泌的影响。结果：cagA^ cagE^ 基因型幽门螺杆菌不能增加胃上皮细胞IL-8的分泌。蛋白激酶A、C、G的抑制剂不能阻断幽门螺杆菌增加胃上皮细胞IL－8的分泌，而蛋白酪氨酸激酶的抑制剂阻断了幽门螺杆菌增加胃上皮细胞IL－8的分泌。结论：cagA^ cagE^ 基因型幽门螺杆菌显著增加了胃上皮细胞IL－8的分泌并且依赖于蛋白酪氨酸激酶的磷酸化。     

Helicobacter pylori induces beta3GnT5 in human gastric cell lines, modulating expression of the SabA ligand sialyl-Lewis x

Chronic Helicobacter pylori infection is recognized as a cause of gastric cancer. H. pylori adhesion to gastric cells is mediated by bacterial adhesins such as sialic acid-binding adhesin (SabA), which binds the carbohydrate structure sialyl-Lewis x. Sialyl-Lewis x expression in the gastric epithelium is induced during persistent H. pylori infection, suggesting that H. pylori modulates host cell glycosylation patterns for enhanced adhesion. Here, we evaluate changes in the glycosylation-related gene expression profile of a human gastric carcinoma cell line following H. pylori infection. We observed that H. pylori significantly altered expression of 168 of the 1,031 human genes tested by microarray, and the extent of these alterations was associated with the pathogenicity of the H. pylori strain. A highly pathogenic strain altered expression of several genes involved in glycan biosynthesis, in particular that encoding beta3 GlcNAc T5 (beta3GnT5), a GlcNAc transferase essential for the biosynthesis of Lewis antigens. beta3GnT5 induction was specific to infection with highly pathogenic strains of H. pylori carrying a cluster of genes known as the cag pathogenicity island, and was dependent on CagA and CagE. Further, beta3GnT5 overexpression in human gastric carcinoma cell lines led to increased sialyl-Lewis x expression and H. pylori adhesion. This study identifies what we believe to be a novel mechanism by which H. pylori modulates the biosynthesis of the SabA ligand in gastric cells, thereby strengthening the epithelial attachment necessary to achieve successful colonization.     

Helicobacter pylori associated antral gastritis in peptic ulcer disease patients and normal healthy population of kashmir, India

Aim: To study the association of Helicobacter pylori infection with chronic antral gastritis in peptic ulcer disease patients and healthy population of Kashmir.Methods: 50 peptic ulcer patients (duodenal ulcer = 46, gastric ulcer = 2 and combined duodenal and gastric ulcer = 2) and 30 asymptomatic healthy volunteers were included in this study. Peptic ulcer was diagnosed on endoscopic examination. 4-6 punch biopsies were taken from gastric antrum in all the individuals and in case of gastric ulcer an additional biopsy was taken from the edge of the ulcer to exclude its malignant nature. Helicobacter pylori (H. pylori) organism was diagnosed using three different test methods, viz. Histology (using Giemsa Stain), Microbiology (Gram Stain) and Biochemistry (using one minute Endoscopy Room Test). Histological diagnosis of H. pylori was taken as the "gold standard" for the presence of H. pylori organism. Histological diagnosis of gastritis was made using Hematoxylin and Eosin Stain and the gastritis was classified as active chronic gastritis and superficial chronic gastritis.Results: Out of 30 peptic ulcer disease patients with associated antral gastritis, 27 (90%) were positive for H. pylori on histological examination (13 superficial chronic gastritis and 14 active chronic gastritis) whereas out of 8 healthy volunteers with histological evidence of chronic antral gastritis, H. pylori was observed in 7 individuals (87.50%) (4 active chronic gastritis and 3 superficial chronic gastritis).Conclusion: A highly significant association between H. pylori infection with chronic antral gastritis both in peptic ulcer disease patients and healthy volunteers of Kashmir was found in this study. Association between H. pylori infection and chronic gastritis was 90% in peptic ulcer group and 87.50% in healthy population (P<0.005).     

Gastric mucosal immunity induced by H. pylori infection

H. pylori infection induces various humoral and cellular immunities in gastric mucosa. Some reports indicate predominant CD4+ cells infiltrate in H. pylori infected gastric mucosa, and these cells express the T helper 1 phenotype. Local humoral immunity is also induced. Gastric plasma cells produce anti-H. pylori antibodies, however, their protective immunity is not enough to eradicate bacteria in human. We found heat shock protein 60 kDa (hsp60) may be closely associated with pathogenesis in MALT lymphoma. IgG1 antibodies to hsp60 were significantly correlated with the antibodies to H. pylori whole cell in patients with MALT lymphoma. CD40-CD40L dependent B cell proliferation was induced by cytokine and/or hsp60 stimulations in those patients. Cytotoxicity of gastric epithelial cells which is associated with host immunity induced by H. pylori infection is still unclear. We found that lymphocytes from patients with peptic ulcer showed cytotoxicity to gastric cell line HGC-27 in vitro. Cytotoxicity was enhanced by cytokine stimulus to T-lymphocytes and by heat stress and/or patients' antibodies treatment of HGC-27 cells. The pathogenicity of H. pylori may involve not only bacterial virulence factor but also host immunity. Studies of mucosal local immunity will help explain the mechanisms of H. pylori induced gastrodoudenal diseases.     

Virulence gene of H. pylori

H. pylori is a well-recognized pathogen that infects up to 50% of humans in the world. H. pylori lives for decades in the hostile environment of the human stomach. H. pylori is closely associated with histologic gastritis, gastric ulceration, duodenal ulceration, gastric cancer and MALT lymphoma. These various clinical outcomes are considered by 1) different virulence, 2) host response, 3) other environmental factors, and their interactions. Since the whole genome was sequenced in 1997, the virulence genes have been investigated in molecular genetic aspects. The cag pathogenicity island (cagPAI) is a complex of virulence genes, which code approximately 30 proteins. The cagPAI acquired by horizontal transfer and is coding for type 4 secretion machinery system. Via this system, many virulence gene products or other interactive proteins are transferred into the host cells.     

Helicobacter pylori infection and GERD

Helicobacter pylori (H. pylori) is an important pathogen that is known to be associated with gastritis, peptic ulcer diseases, and gastric cancer. The association between H. pylori infection and gastro-esophageal reflux disease (GERD) is, however, uncertain. Recent studies indicate that the prevalence of H. pylori is significantly lower in patient with GERD from East Asia than in patients from Western Europe and North America, and that H. pylori might protect against GERD. The frequency of hypochlorhydria might due to atrophic gastritis induced by H. pylori infection is associated with the low prevalence of GERD in Japan.     

PCR and RFLP analysis for identification and typing of Helicobacter pylori strains isolated from gastric biopsy specimens

Helicobacter pylori (H. pylori) infection is the most common gastrointestinal tract infection which plays an important role in the ethiopathogenesis of peptic ulcer and gastritis. In recent years, molecular biological methods have been presented for detection of H. pylori in addition to histopathological and microbiological methods. Among these methods, polymerase chain reaction (PCR) and following restriction fragment length polymorphism analyses (RFLP) are highly sensitive methods for diagnosis and follow up of patients. In this present study our aim was to amplify H. pylori urease A and B genes by PCR and perform RFLP analysis. Gastric biopsy specimens from 17 female and 18 male patients were included in the study. Amplified PCR products were subjected to RFLP analysis and typing of the bacteria in pre and posttreatment specimens were performed. H. pylori urease A and B gene amplification was observed in 32 pretreatment samples and in 8 of 21 posttreatment specimens. As a result, PCR is a sensitive method to determine the H. pylori infection. RFLP, which is another effective method in order to demonstrate the reinfection of H. pylori.     

胆汁反流和幽门螺杆菌感染在胆汁反流性胃炎和消化性溃疡发病中的作用

目的探讨胆汁反流和幽门螺杆菌感染在胆汁反流性胃炎和消化性溃疡发病中的作用。方法采用病理组织学检查和快速尿素酶试验对76例胆汁反流性胃炎及22例兼有胆汁反流性胃炎和消化性溃疡的患者行幽门螺杆菌检测,并与29例消化性溃疡患者作对照。结果胆汁反流性胃炎组幽门螺杆菌阳性率为31.6%(24/76例),兼有胆汁反流性胃炎和消化性溃疡组幽门螺杆菌阳性率为59.0%(13/22例),消化性溃疡组幽门螺杆菌阳性率为72.4%(21/29例),前二组比较,差异有显著意义(P<0.05),后二组比较,差异无显著意义(P>0.05)。结论胆汁反流在胆汁反流性胃炎的发病中起主要作用,幽门螺杆菌感染在消化性溃疡的发病中起主要作用。胆汁反流和幽门螺杆菌感染在胆汁反流性胃炎和消化性溃疡的共同发病中互不明显影响,幽门螺杆菌感染所起的作用可能更大一些。