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.     

Helicobacter pylori vacA genotypes, cagA status and ureA-B polymorphism in isolates recovered from an Argentine population.

Several reports have evidenced geographic differences in the prevalence of vacA (vacuolating cytotoxin gene) alleles and cagA (cytotoxin-associated gene) status among Helicobacter pylori isolates. We investigated the occurrence of these virulence-associated genes status among our isolates, and their relationship with ulcer disease outcome. Besides, ureA-B polymorphism was studied. One hundred isolates, comprising 32 from patients with ulcer disease (UD) and 68 from patients with non-ulcer dyspepsia (NUD), were analyzed. Eighty-four percent of isolates were cagA-positive without statistically significant difference in prevalence between patients with UD or NUD. Genotype vacA-s1m1 was predominant, although unlike other South American regions, subtype s1am1 occurrence was higher than s1b. The multivariate model used to estimate the predictive value of cagA and vacA status for UD development disclosed infection with vacA-s1am1 isolates as the only variable that increased the risk of UD onset. ureAB fingerprinting showed considerable genetic divergence among isolates, however, confirmed that certain DNA banding profiles are conserved worldwide.     

Direct detection and analysis of vacA genotypes and cagA gene of Helicobacter pylori from gastric biopsies by a novel multiplex polymerase chain reaction assay

Several tests/methods for the infection, detection, and genotyping of Helicobacter pylori have been developed in the past; all these differ in specificity and sensitivity and thereby could not be routinely used in clinical study especially in resource-poor developing countries. In the present study, a novel method based on multiplex polymerase chain reaction (PCR) assay was developed to detect H. pylori in patients suffering from gastrointestinal diseases. This method does not require steps of sonication, boiling, or centrifugation for obtaining DNA from biopsy samples, which are otherwise prerequisite in detecting H. pylori by PCR assay. Two hundred seventy-six patients were examined, of which 182 cases (excluding 36 patients having multiple H. pylori strain infection and 8 showing amplification of 16S rDNA only) were H. pylori positive. The dominant vacA genotype was s1 and m1 being present in 168 (92.3%) and 106 (58.2%) patients, respectively, followed by m2 (41.7%), and the lowest being s2 (7.7%). Detection of H. pylori by this method seems rapid, simpler, and suitable for both types 1 and 2 bacteria. Furthermore, genotyping of vacA and cagA genes could also be routinely performed in a large number of patients for diagnostic purposes.     

Helicobacter pylori oipA genetic diversity and its associations with both disease and cagA, vacA s, m, and i alleles among Bulgarian patients

Prevalence of outer inflammatory protein (oipA) gene functional status in Helicobacter pylori strains from Southeastern Europe is still unclear. H. pylori strains from 70 symptomatic patients were polymerase chain reaction (PCR) assessed for cagA and vacA types, and oipA gene functional status was evaluated by PCR and sequencing. Our results demonstrated a high prevalence of strains with oipA status “on” genes (81%) and strong association between them and peptic ulcers, cagA, and vacA s1 and s1/m1 genotypes, regardless of the patient gender, place of residence, and age. Importantly, most vacA i1 strains (93%) harbored oipA status “on” versus only 57% of those with vacA i2 type. The vacA i1 genotype was less frequent (66%) than both cagA and vacA s1 types. The virulent strains with cagA⁺ and vacA s1, m1, and i1 were detected in 35% as a predominant genotype and almost all (96%) of these strains harbored oipA status “on”. In conclusion, the high prevalence of in-frame oipA gene strains (81%), associated with peptic ulcers and cagA⁺, vacA s1, m1, m2, and, importantly, i1 genotypes, indicates a strong synergistic activity of H. pylori virulence factors.     

Association of cagA+ Helicobacter pylori with adenotonsillar hypertrophy

Cytotoxin-associated gene A (cagA) of Helicobacter pylori (H. pylori) encodes a highly immunogenic and virulence-associated protein. The presence of cagA(+) H. pylori strains in tonsil and adenoid tissues may affect clinical outcome. The aim of the present study was to determine the presence of H. pylori cagA gene in tonsil and adenoid tissues and to establish the potential association of cagA(+) H. pylori in recurrent adenotonsillitis (RAT) and adenotonsillar hypertrophy (ATH). For this aim, a total of 118 tissue samples (71 tonsil and 47 adenoid tissues) were collected from a total of 71 children: 28 cases with RAT and 43 cases with ATH. The samples were analyzed for glmM gene to detect the infection with H. pylori by polymerase chain reaction (PCR). H. pylori-positive samples were further analyzed for the presence of the cagA gene. The PCR analysis showed that 29 samples (24.6%) were positive for H. pylori. Seventeen out of these 29 samples (58.6%) were found positive for cagA; the cagA gene was detected in 12 samples of ATH and 5 samples of RAT. The presence rate of cagA gene was significantly higher (p < 0.05) in ATH patients than that found in RAT patients. These results suggest that presence of cagA(+) H. pylori may be associated with development of ATH.     

Phospholipase C activity of Helicobacter pylori is not associated with the presence of the cagA gene

BACKGROUND: Knowledge about the possible role of phospholipase C (PLC) activity of microbial pathogens in the development of disease is increasing. Recently attention has focused on investigating PLC activity elaborated by Helicobacter pylori, but the role of this enzyme in H. pylori pathogenesis is still unknown. The aim of this study was to correlate PLC-activity of H. pylori on the basis of the cagA status with the clinical diagnosis of the patients. MATERIALS AND METHODS: Helicobacter pylori was isolated from patients with gastritis (G; n = 38), duodenal ulcer (DU; n = 15), gastric ulcer (GU; n = 11) and gastric cancer (GC; n = 12). Polymerase chain reaction primers DZ3/R009 which amplified a 1350-bp fragment were used to detect the cagA gene. PLC activity was determined using p-nitrophenylphosphorylcholine as substrate. RESULTS: Of the strains, 60% were cagA(+) and 40% were cagA(-). All strains showed PLC activity (2.20 +/- 0.91 U mg(-1) protein). PLC activity showed no association with the cagA status: cagA(+) (2.21 +/- 1.03 U mg(-1) protein), cagA(-) (2.18 +/- 0.79 U mg(-1) protein). Patients with GU had the highest PLC activity (2.77 +/- 1.26 U mg(-1) protein) and patients with GC had the lowest activity (1.8 +/- 0.57 U mg(-1) protein). CONCLUSIONS: Although PLC activity was present in all strains tested, it may only have pathological importance in patients with GU. However, the extent of PLC activity was independent of the presence of the cagA gene.     

Helicobacter pylori eradication and associated changes in the gastric mucosa

Persistent Helicobacter pylori infection contributes towards the development of chronic gastritis. To clarify the changes in chronic gastritis as a precursor of gastric cancer secondary to H. pylori eradication is an important issue, as it has significant implications for reducing the risk of gastric cancer. Studies published to date, however, are far from consistent with regard to the morphologic changes reported following H. pylori eradication. Of these, some papers reported improvement in gastric atrophy or intestinal metaplasia, versus others reporting no improvement, with the majority of papers published after 2000 reporting improvement in these end points. The inconsistent results concerning the impact of H. pylori eradication on gastric atrophy could be due to the inconsistency of the diagnostic criteria employed for evaluation of the morphology, confounded by the difficulties involved in evaluating atrophic changes in the gastric mucosa. While adherence to the Updated Sydney System available for evaluation of gastritis is primarily required worldwide to ensure consistency in evaluating gastritis, long-term research into the morphologic changes associated with H. pylori eradication is also required to explore strategies for the prevention of gastric cancer with H. pylori eradication.     

Helicobacter pylori eradication and associated changes in the gastric mucosa

Persistent Helicobacter pylori infection contributes towards the development of chronic gastritis. To clarify the changes in chronic gastritis as a precursor of gastric cancer secondary to H. pylori eradication is an important issue, as it has significant implications for reducing the risk of gastric cancer. Studies published to date, however, are far from consistent with regard to the morphologic changes reported following H. pylori eradication. Of these, some papers reported improvement in gastric atrophy or intestinal metaplasia, versus others reporting no improvement, with the majority of papers published after 2000 reporting improvement in these end points. The inconsistent results concerning the impact of H. pylori eradication on gastric atrophy could be due to the inconsistency of the diagnostic criteria employed for evaluation of the morphology, confounded by the difficulties involved in evaluating atrophic changes in the gastric mucosa. While adherence to the Updated Sydney System available for evaluation of gastritis is primarily required worldwide to ensure consistency in evaluating gastritis, long-term research into the morphologic changes associated with H. pylori eradication is also required to explore strategies for the prevention of gastric cancer with H. pylori eradication.     

Helicobacter pylori antibiotic resistance patterns and genotypes in adult dyspeptic patients from a regional population in North Wales

OBJECTIVE: Surveillance data on Helicobacter pylori antibiotic susceptibilities in Wales are limited, despite resistance being a key factor in treatment failure. A single-centre survey was undertaken over 3 years to determine local antibiotic resistance rates on isolates from dyspeptic patients in Bangor, Gwynedd (North Wales). METHODS: Susceptibilities were determined for 363 isolates by disc diffusion and the Etest. Isolates were also genotyped (cagA presence and vacA allelic types). RESULTS: Overall in vitro resistance rates were 24% for metronidazole and 7% for clarithromycin, with 4% resistant to both antibiotics. Resistant strains typically had high MICs of >256 mg/L. Tetracycline resistance was identified in only one isolate whereas no isolates showed resistance to amoxicillin. There was a two-fold increase in resistance over the study period. No gender and age associations with resistance were detected. Resistant and susceptible isolates were genotypically diverse with respect to cagA/vacA type but the vacA s1m2 form was a feature of all clarithromycin-resistant isolates compared with 56% of the susceptible isolates. CONCLUSION: Although the overall antibiotic resistance rates of H. pylori from North Wales were low compared with many other regions in Europe, continued surveillance, particularly of high-level resistance (MIC >256 mg/L), is recommended to monitor the effects of the 'test and treat' strategy for H. pylori eradication.     

Relationship between bacterial load, morbidity and cagA gene in patients infected by Helicobacter pylori

One hundred and seventy-six biopsies of the gastric corpus and antrum from 97 patients were processed using classical and molecular methods in order to study the relationship between the factor cagA of Helicobacter pylori, bacterial load and morbidity. Bacterial load in patients with cagA was greater than in patients without it, both in the antrum and corpus (p<0.01). There was a statistically significant association between cagA and consumption of proton pump inhibitors (adjusted odds ratio 3.11). Haemorrhage of the upper digestive tract was more associated with bacterial load than with the cagA gene (adjusted odds ratio 2.34 and 1.12, respectively), but none of these associations yielded statistical significance.     

Helicobacter pylori and non-Helicobacter pylori bacterial flora in gastric mucosal and tumour specimens of patients with primary gastric lymphoma

There is an association between Helicobacter pylori (H. pylori) and gastric mucosa-associated lymphoid tissue (MALT) and MALT lymphoma. Histologically, mainly non-specific stains are used to detect H. pylori, such as haematoxylin–eosin (HE) or modified Giemsa (MG). In this study, both a MG and a specific immunohistochemical stain (IMM) for H. pylori (Dako B471) were performed on sequential slides of resected material containing tumour and non-tumorous gastric mucosa from patients with primary gastric lymphoma (n = 52). Special attention was paid to the presence of non-H. pylori bacterial flora diagnosed by a positive MG (according to form and localization) and a subsequently negative IMM. On all slides, bacterial density was scored semiquantitatively (grades 0, 1, 2, 3). In total, 32 (61.5%) patients were H. pylori positive using IMM and 34 (65.4%) were non-H. pylori positive using MG. In 24 out of the 34 patients, the non-H. pylori flora consisted mainly of cocci in combination with rods in 15 patients, mostly in minor quantities; in another 10 patients, high numbers of both cocci and different types of rods were present. Most non-H. pylori bacteria were localized superficially, although in 22 patients minor quantities of non-H. pylori were also seen in the glandular lumina. After all of the patients had been analysed, no differences in the density of H. pylori and of non-H. pylori flora were found. Only when comparing patients who had a small-cell lymphoma with those who had a large-cell lymphoma was a significantly higher density of H. pylori found in the corpus mucosa of large-cell lymphomas and a higher prevalence of non-H. pylori was found in tumours, in antrum or corpus, of patients with large-cell lymphomas. In conclusion, with joint evaluation using MG and a H. pylori-specific immunohistochemical stains, the proportion of H. pylori-positive gastric lymphoma patients was lower than in most previous studies but other bacteria were found in a relatively high proportion. The role of the non-H. pylori intragastric bacterial flora identified in this study has to be further elucidated in the aetiopathogenesis of primary gastric lymphoma.     

幽门螺杆菌毒力基因分型与消化性溃疡患者早期肾损伤相关性研究

目的探讨幽门螺杆菌(Hp)不同毒力基因分型与消化性溃疡患者早期肾损伤的相关性。方法选取504例消化性溃疡患者,根据是否出现Hp感染分为Hp(-)组和Hp(+)组;另选取100名健康体检者作为健康对照组。分析不同组别肾功能指标变化情况,探讨Hp毒力基因、炎症因子、免疫应答因子与早期肾脏病变的关系。采用Logistic回归分析评估消化性溃疡患者早期肾损伤的影响因素。采用受试者工作特征(ROC)曲线评价各项指标诊断消化性溃疡患者早期肾损伤的效能。结果 Hp(+)组尿视黄醇结合蛋白(RBP)、尿β₂-微球蛋白(β₂-MG)、尿α₁-微球蛋白(α₁-MG)、尿转铁蛋白(TF)、胱抑素C(CysC)、高敏C反应蛋白(hs-CRP)、免疫球蛋白(Ig)A1、蚕豆凝集素(VVL)-IgA1结合力与Hp(-)组、健康对照组比较,差异均有统计学意义(P<0.05)。Hp(+)组早期肾损伤患者cagA+vacA检出率高于无肾损伤患者(P<0.05)。Logistic回归分析结果显示,病程、α₁     

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.     

胃肠道相关疾病患者幽门螺杆菌CagA抗体阳性率分析

目的探讨胃肠道相关疾病患者幽门螺杆菌（HP）感染、CagA抗体检测阳性与所患疾病类型间的关系。方法纳入研究的对象包括本院消化内科住院的320例胃肠道相关疾病患者和同期于本院进行体检的健康体检者200例,共520例。采用蛋白质印迹（WB）法和”C-尿素呼气试验对520例上述人群进行HP感染的检测,采用WB检测CagA抗体,并对检测结果进行比较分析。结果320例患者和200例健康体检者”c-尿素呼气试验阳性率分别为60．9％（195／320）和55％（110／200）,WB检测HP抗体的阳性率分别为68．4％（219／320）和61．0％（122／320）。2种方法检测HP感染的阳性率差异无统计学意义（P〉O．05）;患者和健康体检者HP感染的阳性率差异无统计学意义（P〉0．05）。慢性胃炎、胃及十二指肠溃疡、食管炎、胃癌患者及健康体检者CagA抗体的阳性率分别为43．1％、66．7％、51．3％、70．0％、21．5％;不同胃相关疾病患者CagA抗体阳性率的差异无统计学意义（P〉O．05）;不同胃肠道相关疾病患者CagA抗体阳性率均高于健康体检者（P〈O．05）。结论CagA是HP分泌的重要毒力因子之一,感染的HP大多数为CagA阳性菌株,抗体阳性较阴性者更易放生严重的组织炎症和损伤,同胃肠道相关疾病的发生密切相关。     

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.     

Oxidative stress expression status associated to Helicobacter pylori virulence in gastric diseases

OBJECTIVES: To analyze the status of expression of inflammation markers, antioxidant and oxidant enzymes in biopsies from patients diagnosed with gastritis, gastric ulcer (GU) and gastric cancer (GC) and the Helicobacter pylori virulence from these isolated biopsies in order to evaluate a possible association among these factors. METHODS: H. pylori genotype from isolated biopsies was performed by PCR. The pattern of expression of inflammation (TNF-alpha, IL-1beta, IL-8, IL-10 and IL-12), oxidant (iNOS and Nox1) and antioxidant markers (MnSOD, GPX and CAT) of biopsies from gastritis, GU, GC and control groups was performed by RT-PCR. RESULTS: Different from other gastric diseases studied here, gastritis is characterized by an oxidative stress with significant expression of TNF-alpha, IL-8, IL-12, iNOS and Nox and significant absence of MnSOD and GPX expression. Gastritis was the only condition where there was an association between TNF-alpha or IL-8 expression and H. pylori cagA+/vacAs1 genotype. In this case, TNF-alpha expression was about 3 times higher when compared to control subjects. CONCLUSION: In this study, only gastritis was found to be associated with significant oxidative stress marker expression of TNF-alpha and IL-8 that was also related to H. pylori virulence, suggesting that they are the main oxidant stress markers responsible to trigger an increase in ROS level that contributes to decrease the expression of the MnSOD and GPX.     

胃增生性息肉和胃底腺息肉患者血清胃功能指标及幽门螺杆菌感染情况的分析

目的分析比较胃增生性息肉和胃底腺息肉患者血清胃功能指标及幽门螺杆菌(Helicobacter pylori,Hp)感染情况.方法选取2017年12月至2018年12月于徐州医科大学附属医院行胃镜检查发现胃息肉且病理证实为胃增生性息肉和胃底腺息肉患者135例,其中增生性息肉组68例,胃底腺息肉组67例.采用免疫印迹法对两组患者血清Hp抗体[尿素酶A(urease A,UreA)、尿素酶B(urease B,Ure B)、细胞毒素相关蛋白(cytotoxin associated gene A, CagA)、空泡细胞毒素(vacuolating cytotoxin,VacA)]进行定性检测.选取慢性浅表性胃炎80例为对照组.酶联免疫吸附(enzymelinkedimmunosorbent assey,ELISA)法检测3组血清胃功能指标[胃蛋白酶原(pepsinogen,PG)Ⅰ、PG-Ⅱ、胃泌素-17(gastrin,G-17)],并计算PGⅠ、PGⅡ比值(PGⅠ and PGⅡ ratio,PGR).结果胃增生性息肉组血清PGⅡ(13.13(8.15,20.30)μg /L)、G17(8.44(3.72,27.17)pmol/L)水平高于对照组(9.16(5.56,15.14)μg /L与1.83(0.87,5.95)pmol/L)(P均<0.05),PGR水平低于对照组(P<0.05);胃底腺息肉组血清PGⅠ(120.12(86.72,174.70)μg /L)、PGⅡ(11.92(7.27,22.26)μg/L)、G17(5.68(1.79,14.65)pmol/L)水平高于对照组(101.32(79.17,131.33)μg /L、9.16(5.56,15.14)μg /L、1.83(0.87,5.95)pmol/L)(P 均<0.05);胃增生性息肉组血清 G17 (8.44 (3.72, 27.17)pmol/L)水平高于胃底腺息肉组(5.68(1.79,14.65)pmol/L)(P<0.05);胃增生性息肉组Hp感染率61.76%(42/68)高于胃底腺息肉组40.30%(27/67)(P<0.05),且以Ⅰ型Hp为主(P<0.05);胃增生性息肉组Hp阳性者血清PGⅡ、G17水平均高于Hp阴性者(P均<0.05);胃底腺息肉组Hp阳性与阴性者血清PGⅠ、PGⅡ、G17、PGR水平比较差异无统计学意义;胃增生性息肉组Hp Ⅰ型者血清PGⅠ、PGR水平高于Hp Ⅱ型者(P<0.05),胃底腺息肉组Hp Ⅰ型血清PGⅠ、PGⅡ、G17、PGR水平与Ⅱ型比较差异无统计学意义.结论胃增生性息肉、胃底腺息肉患者血清PG、G17水平高于慢性浅表性胃炎患者,胃增生性息肉患者较胃底腺息肉患者Hp感染率高且胃功能指标存在异常.     

耐甲硝唑幽门螺杆菌cagA基因检测与rdxA基因突变研究

目的研究cagA基因、rdxA基因变异与幽门螺杆菌(Hp)甲硝唑耐药的关系。方法收集临床分离Hp 180株,用E-test法检测对甲硝唑的最低抑菌浓度(MIC),PCR扩增cagA、rdxA基因,并对rdxA基因进行测序。结果幽门螺杆菌对甲硝唑的耐药率为43.3%,其中甲硝唑高水平耐药菌54株,占69.2%;rdxA基因突变率为56.7%;cagA阳性菌中高耐药菌所占的比例和rdxA基因的突变率均明显高于cagA阴性菌。结论本地区幽门螺杆菌感染以高毒力菌株为主,rdxA基因突变在cagA基因阳性菌对甲硝唑产生高水平耐药可能起一定作用。     

上海崇明地区幽门螺杆菌cagA基因多态性与感染临床结局的关系

目的探讨上海崇明地区幽门螺杆菌（Helicobacter pylori,Hp）的cagA基因的多态性与感染临床结局的关系。方法采用PCR法检测100株临床分离株cagA基因亚型,获得东亚型和西方型2种基因型。分析cagA基因亚型与消化道疾病间的关系。结果100株Hp中72株检出cagA基因,其中81．9％为cagA基因东亚型,15．3％为西方型,2．8％为同时存在着2种基因型。胃癌与慢性萎缩性胃炎患者中cagA基因东亚型菌株均显著高于胃溃疡、十二指肠溃疡患者,而十二指肠溃疡cagA基因西方型菌株的比率显著高于其余4种疾病类型。结论本地区感染Hp以cagA基因东亚型为主,cagA基因东亚型菌株与胃癌、慢性萎缩性胃炎密切相关,而cagA基因西方型菌株与十二指肠溃疡密切相关。推测cagA基因多态性对由Hp引起的感染性疾病的发病机制可能起一定的作用。