History of Helicobacter pylori,duodenal ulcer,gastric ulcer and gastric cancer

Helicobacter pylori (H. pylori) infection underlies gastric ulcer disease, gastric cancer and duodenal ulcer disease. The disease expression reflects the pattern and extent of gastritis/gastric atrophy (i.e., duodenal ulcer with non-atrophic and gastric ulcer and gastric cancer with atrophic gastritis). Gastric and duodenal ulcers and gastric cancer have been known for thousands of years. Ulcers are generally non-fatal and until the 20th century were difficult to diagnose. However, the presence and pattern of gastritis in past civilizations can be deduced based on the diseases present. It has been suggested that gastric ulcer and duodenal ulcer both arose or became more frequent in Europe in the 19th century. Here, we show that gastric cancer and gastric ulcer were present throughout the 17th to 19th centuries consistent with atrophic gastritis being the predominant pattern, as it proved to be when it could be examined directly in the late 19th century. The environment before the 20th century favored acquisition of H. pylori infection and atrophic gastritis (e.g., poor sanitation and standards of living, seasonal diets poor in fresh fruits and vegetables, especially in winter, vitamin deficiencies, and frequent febrile infections in childhood). The latter part of the 19th century saw improvements in standards of living, sanitation, and diets with a corresponding decrease in rate of development of atrophic gastritis allowing duodenal ulcers to become more prominent. In the early 20th century physician’s believed they could diagnose ulcers clinically and that the diagnosis required hospitalization for “surgical disease” or for “Sippy” diets. We show that while H. pylori remained common and virulent in Europe and the United States, environmental changes resulted in changes of the pattern of gastritis producing a change in the manifestations of H. pylori infections and subsequently to a rapid decline in transmission and a rapid decline in all H. pylori-related diseases.

Does Helicobacter pylori eradication therapy for peptic ulcer prevent gastric cancer?

AIM:To investigate the effects of Helicobacter pylori (H pylori)eradication therapy for treatment of peptic ulcer on the incidence of gastric cancer. METHODS:A multicenter prospective cohort study was conducted between November 2000 and December 2007 in Yamagata Prefecture,Japan.The study included patients with H pylori-positive peptic ulcer who decided themselves whether to receive H pylori eradication(eradication group)or conventional antacid therapy(non-eradication group).Incidence of gastric cancer in the two groups was determined based on the results of annual endoscopy and questionnaire surveys,as well as Yamagata Prefectural Cancer Registry data,and was compared between the two groups and by results of H pylori therapy.RESULTS:A total of 4133 patients aged between 13 and 91 years(mean 52.9 years)were registered,and 56 cases of gastric cancer were identified over a mean follow-up of 5.6 years.The sex-and age-adjusted incidence ratio of gastric cancer in the eradication group, as compared with the non-eradication group,was 0.58 (95%CI:0.28-1.19)and ratios by follow-up period(<1 year,1-3 years,>3 years)were 1.16(0.27-5.00),0.50 (0.17-1.49),and 0.34(0.09-1.28),respectively.Longer follow-up tended to be associated with better prevention of gastric cancer,although not to a significant extent.No significant difference in incidence of gastric cancer was observed between patients with successful eradication therapy(32/2451 patients,1.31%)and those with treatment failure(11/639 patients,1.72%).Among patients with duodenal ulcer,which is known to be more prevalent in younger individuals,the incidence of gastric cancer was significantly less in those with successful eradication therapy(2/845 patients,0.24%)than in those with treatment failure(3/216 patients,1.39%). CONCLUSION:H pylori eradication therapy for peptic ulcer patients with a mean age of 52.9 years at registration did not significantly decrease the incidence of gastric cancer.

Characteristics of gastric cancer in peptic ulcer patients with Helicobacter pylori infection

AIM:To evaluate the incidence and clinical characteristics of gastric cancer(GC) in peptic ulcer patients with Helicobacter pylori(H.pylori) infection.METHODS:Between January 2003 and December 2013, the medical records of patients diagnosed with GC were retrospectively reviewed.Those with previous gastric ulcer(GU) and H.pylori infection were assigned to the Hp GU-GC group(n = 86) and those with previous duodenal ulcer(DU) disease and H.pylori infection were assigned to the Hp DUGC group(n = 35).The incidence rates of GC in the Hp GU-GC and Hp DU-GC groups were analyzed.Data on demographics(age, gender, peptic ulcer complications and cancer treatment), GC clinical characteristics [location, pathological diagnosis, differentiation, T stage, Lauren's classification, atrophy of surrounding mucosa and intestinal metaplasia(IM)], outcome of eradication therapy for H.pylori infection, esophagogastroduodenoscopy number and the duration until GC onset were reviewed.Univariate and multivariate analyses were performed to identify factors influencing GC development.The relative risk of GC was evaluated using a Cox proportional hazards model.RESULTS:The incidence rates of GC were 3.60%(86/2387) in the Hp GU-GC group and 1.66%(35/2098) in the Hp DU-GC group.The annual incidence was 0.41% in the Hp GU-GC group and 0.11% in the Hp DUGC group.The rates of moderate-to-severe atrophy of the surrounding mucosa and IM were higher in the Hp GU-GC group than in the Hp DU-GC group(86% vs 34.3%, respectively, and 61.6% vs 14.3%, respectively, P < 0.05).In the univariate analysis, atrophy of surrounding mucosa, IM and eradication therapy for H.pylori infection were significantly associated with the development of GC(P < 0.05).There was no significant difference in the prognosis of GC patients between the Hp GU-GC and Hp DU-GC groups(P = 0.347).The relative risk of GC development in the Hp GUGC group compared to that of the Hp DU-GC group,after correction for age and gender,was 1.71(95%CI:1.09-2.70;P=0.02).CONCLUSION:GU patients with H.pylori infection had higher GC incidence rates and relative risks.Atrophy of surrounding mucosa,IM and eradication therapy were associated with GC.

Association of Helicobacter pylori babA2 with peptic ulcer disease and gastric cancer

AIM: To investigate the association between babA2 gene and peptic ulcer disease (PUD) and gastric cancer (GC) in Helicobacter pylori -infected populations. METHODS: We evaluated the relationship between babA2 and clinical outcomes (PUD and GC) using a meta-analysis. A literature search was performed using the PubMed and Web of Science databases for relevant case-control studies that met the defined inclusion criteria. The ORs and 95%CIs were calculated to estimate the association between babA2 genotype and clinical outcomes. A fixed-effect or random-effect model was performed depending on the absence or presence of significant heterogeneity. RESULTS: A total of 25 articles with 38 studies met the inclusion criteria and were finally included in this metaanalysis. The results showed that the babA2 genotype was significantly associated with an increased risk of PUD (OR = 2.069, 95%CI: 1.530-2.794, P < 0.001) and especially in the subgroup of duodenal ulcer (OR = 1.588, 95%CI: 1.141-2.209, P = 0.006). Moreover, a significant association between babA2 gene and PUD and duodenal ulcer (OR = 2.739, 95%CI: 1.860-4.032, P < 0.001; OR = 2.239, 95%CI: 1.468-3.415, P < 0.001, respectively) was observed in western countries but not in Asian countries. CONCLUSION: We demonstrated that the presence of babA2 may be associated with increased risks for PUD, especially duodenal ulcer, in western countries.

Lewis blood genotypes of peptic ulcer and gastric cancer patients in Taiwan

AIM： The Lewis b （Le^b） antigen has been implicated as a possible binding site for attachment of Helicobacter pylori （H pylon） to gastric mucosa. However, studies both supporting and denying this association have been reported in the literature. Differences in secretor （Se） genotype have been suggested as a possible reason for previous discrepancies. Therefore, we investigated the relationship between Le and Se genotypes and Hpylori infection rates in people with peptic ulcer or gastric cancer. METHODS： Peripheral blood samples were obtained from 347 patients with endoscopic evidence of peptic ulcer disease （235 cases of duodenal ulcer, 62 of gastric ulcer, and 50 of combined duodenal ulcer/gastric ulcer） and 51 patients with gastric cancer on endoscopy. Peripheral blood specimens from 101 unrelated normal volunteers were used as controls. Lewis phenotype was determined using an antibody method, whereas Le and Se genotypes were determined by DNA amplification and restriction enzyme analysis. Gastric or duodenal biopsies taken from patients with endoscopic evidence of peptic ulcer or gastric cancer were cultured for Hpylotri Isolates were identified as Hpylori by morphology and production of urease and catalase. The Hpyloriinfection status was also evaluated by rapid urease test （CLO test）, and urea breath test （13^C-UBT）. Results of studies were analyzed by chi-square test （taken as significant）. RESULTS： Hpyloriwas isolated from 83.7% （303/347） of patients with peptic ulcer disease. Statistical analysis did not show any significant difference in Lewis phenotype or genotype between patients with and without Hpylori infection. No significant association was found between Lewis genotype and peptic ulcer or gastric cancer.CONCLUSION： Lewis blood genotype or phenotype may not play a role in the pathogenesis of Hpyloriinfection. However, bacterial strain differences and the presence of more than one attachment mechanism may limit the value of epidemiological studies in elucidating this matter.

Rare case of Helicobacter pylori -related gastric ulcer: Malignancy or pseudomorphism?

Helicobacter pylori (H. pylori ) is a pathogen and the most frequent cause of gastric ulcers. There is also a close correlation between the prevalence of H. pylori infection and the incidence of gastric cancer. We present the case of a 38-year-old woman referred by her primary care physician for screening positron emission tomography-computed tomography (PET-CT), which showed a nodular strong accumulation point with standardized uptake value 5.6 in the gastric fundus. Gastroscopy was then performed, and a single arched ulcer, 12 mm in size, was found in the gastric fundus. Histopathological examination of the lesion revealed chronic mucosal inflammation with acute inflammation and H. pylori infection. There was an obvious mitotic phase with widespread lymphoma. Formal anti-H. pylori treatment was carried out. One month later, a gastroscopy showed a single arched ulcer, measuring 10 mm in size in the gastric fundus. Histopathological examination revealed chronic mucosal inflammation with acute inflammation and a very small amount of H. pylori infection. The mitotic phase was 4/10 high power field, with some heterotypes and an obvious nucleolus. Follow-up gastroscopy 2 mo later showed the gastric ulcer in stage S2. The mucosal swelling had markedly improved. The patient remained asymptomatic, and a follow-up PET-CT was performed 6 mo later. The nodular strong accumulation point had disappeared. Follow-up gastroscopy showed no evidence of malignant cancer. H. pylori-associated severe inflammation can lead to neoplastic changes in histiocytes. This underscores the importance of eradicating H. pylori , especially in those with mucosal lesions, and ensuring proper follow-up to prevent or even reverse early gastric cancer.

Isolation of lymphocytes from the human gastric mucosa

Flow cytometry is widely used for lymphocyte immunophenotyping in clinical settings.However,few studies have applied it for analyzing lymphocytes of the gastric mucosa.This review offers an overview of methodologies for isolating lymphocytes from the human stomach.Previously reported articles were reviewed,focusing on procedures for isolating human gastric mucosal lymphocytes.Helicobacter pylori-associated peptic diseases and gastric cancer are two major subjects of research in this field.Enzymatic dissociation,mechanical dissociation,or a combination of the two have been used to isolate lymphocytes from the stomach.Intra-epithelial and lamina propria lymphocytes were separately isolated in several studies.We also summarize the history and present trends in analyzing lymphocytes in patients with gastric disease.

GC/MS-based differential metabolic profiling of human peptic ulcer disease to study Helicobacter pylori-induced metabolic perturbations

Helicobacter pylori infection has been significantly linked to Peptic Ulcer Disease and Gastric Cancer.Metabolomic fingerprinting may offer a principal way of early diagnosis and to understand the molecular mechanism of H.pylori-induced pathogenicity.The rationale of the study is to explore the underlying distinct metabolic mechanisms of H.pylori-induced PUD and to identify potential biomarkers for disease diagnosis and associated risks using Gas chromatography/mass spectrometry.GC/MS-based analytical method was used to compare metabolic profiles of healthy controls(N=20)and peptic ulcer patients(N=45).Acquired metabolomic data were analyzed by constructing a diagnostic model using principal component analysis and a non-parametric two-tailed paired Wilcoxon analysis to identify disease-specific metabolic biomarkers.A total of 75 low-molecular-weight endogenous metabolites were detected during comparative metabolomic analysis of PUD vs.healthy gut tissues,among which 16 metabolites are being proposed to be diagnostic markers of Human PUD.Perturbations related to amino acids,carbohydrates,fatty acids,organic acids,and sterol metabolism were significantly revealed during this differential metabolomic profiling.Results convincingly suggest that metabolic profiles can contribute immensely in early diagnosis of the disease and understanding molecular mechanisms of disease progression for predicting novel drug targets for prophylactic and anaphylactic measures.

Clinical proteomics identifies potential biomarkers in Helicobacter pylori for gastrointestinal diseases

The development of gastrointestinal diseases has been found to be associated with Helicobacter pylori (H. pylori) infection and various biochemical stresses in stomach and intestine. These stresses, such as oxidative, osmotic and acid stresses, may bring about bi-directional effects on both hosts and H. pylori, leading to changes of protein expression in their proteomes. Therefore, proteins differentially expressed in H. pylori under various stresses not only reflect gastrointestinal environment but also provide useful biomarkers for disease diagnosis and prognosis. In this regard, proteomic technology is an ideal tool to identify potential biomarkers as it can systematically monitor proteins and protein variation on a large scale of cell&#x02019;s translational landscape, permitting in-depth analyses of host and pathogen interactions. By performing two-dimensional polyacrylamide gel electrophoresis (2-DE) followed by liquid chromatography-nanoESI-mass spectrometry (nanoLC-MS/MS), we have successfully pinpointed alkylhydroperoxide reductase (AhpC), neutrophil-activating protein and non-heme iron-binding ferritin as three prospective biomarkers showing up-regulation in H. pylori under oxidative, osmotic and acid stresses, respectively. Further biochemical characterization reveals that various environmental stresses can induce protein structure change and functional conversion in the identified biomarkers. Especially salient is the antioxidant enzyme AhpC, an abundant antioxidant protein present in H. pylori. It switches from a peroxide reductase of low-molecular-weight (LMW) oligomers to a molecular chaperone of high-molecular-weight (HMW) complexes under oxidative stress. Different seropositivy responses against LMW or HMW AhpC in H. pylori-infected patients faithfully match the disease progression from disease-free healthy persons to patients with gastric ulcer and cancer. These results has established AhpC of H. pylori as a promising diagnostic marker for gastrointestinal maladies, and highlight the utility of clinical proteomics for identifying disease biomarkers that can be uniquely applied to disease-oriented translational medicine.

Curcumin as a potential therapeutic candidate for Helicobacter pylori associated diseases

Curcumin, a yellow pigment and principal polyphenolic Curcuminoid obtained from the turmeric rhizome Curcuma longa, is commonly used as a food-coloring agent. Studies suggest that curcumin has a wide range of beneficial properties e.g., anti-inflammatory, antioxidant, anti-cancer, anti-proliferative, anti-fungal and anti-microbial. These pleiotropic activities prompted several research groups to elucidate the role of curcumin in Helicobacter pylori(H. pylori) infection. This is the first review with this heading where we discussed regarding the role of curcumin as an anti-H. pylori agent along with its potential in other gastrointestinal diseases. Based on several in vitro, early cell culture, animal research and few pre-clinical trials, curcumin projected as a potential therapeutic candidate against H. pylori mediated gastric pathogenesis. This review sheds light on the anti-H. pylori effects of curcumin in different models with meticulous emphasis on its anti-oxidant, anti-inflammatory and anti-carcinogenic effects as well as some critical signaling and effecter molecules. Remarkably, non-toxic molecule curcumin fulfills the characteristics for an ideal chemopreventive agent against H. pylori mediated gastric carcinogenesis but the foremost challenge is to obtain the optimum therapeutic levels of curcumin, due to its low solubility and poor bioavailability. Further, we have discussed about the possibilities for improving its efficacy and bioavailability. Lastly, we concluded with the anticipation that in near future curcumin may be used to develop a therapeutic drug against H. pylori mediated gastric ailments through improved formulation or delivery systems, facilitating its enhanced absorption and cellular uptake.

Helicobacter pylori:Commensal,symbiont or pathogen?

This review considers the data on Helicobacter pylori(H.pylori),which have been accumulated over 40 years since its description as an etiological factor in gastrointestinal diseases.The majority of modern publications are devoted to the study of the pathogenic properties of the microorganism in the development of chronic gastritis,peptic ulcer disease,and gastric cancer,as well as methods for its eradication.However,in recent years,there have been more and more studies which have suggested that H.pylori has a beneficial,or potentially positive,effect on the human body.The authors have attempted to objectively analyze the information accumulated in the literature on H.pylori.Some studies consider it as one of the recently identified human bacterial pathogens,and special attention is paid to the evidence suggesting that it is probably part of the composition of the human microbiome as a commensal(commensal from French to English is a table companion)or even a symbiont.The presented data discussing the presence or absence of the effect of H.pylori on human health suggest that there is an apparent ambiguity of the problem.The re-assessment of the data available on H.pylori infection is important in order to answer the question of whether it is necessary to create a program of mass H.pylori eradication or to apply a more personalized approach to treating patients with H.pylori-associated gastrointestinal diseases and to perform eradication therapy.

Immune responses to Helicobacter pylori infection

Helicobacter pylori (H. pylori) infection is one of the most common infections in human beings worldwide. H. pylori express lipopolysaccharides and flagellin that do not activate efficiently Toll-like receptors and express dedicated effectors, such as &#x003b3;-glutamyl transpeptidase, vacuolating cytotoxin (vacA), arginase, that actively induce tolerogenic signals. In this perspective, H. pylori can be considered as a commensal bacteria belonging to the stomach microbiota. However, when present in the stomach, H. pylori reduce the overall diversity of the gastric microbiota and promote gastric inflammation by inducing Nod1-dependent pro-inflammatory program and by activating neutrophils through the production of a neutrophil activating protein. The maintenance of a chronic inflammation in the gastric mucosa and the direct action of virulence factors (vacA and cytotoxin-associated gene A) confer pro-carcinogenic activities to H. pylori. Hence, H. pylori cannot be considered as symbiotic bacteria but rather as part of the pathobiont. The development of a H. pylori vaccine will bring health benefits for individuals infected with antibiotic resistant H. pylori strains and population of underdeveloped countries.

Novel virulence factor dupA of Helicobacter pylori as an important risk determinant for disease manifestation:An overview

Helicobacter pylori(H.pylori)is a microaerophilic,Gram-negative,human gastric pathogen found usually in the mucous lining of stomach.It infects more than 50%of the world’s population and leads to gastroduodenal diseases.The outcome of disease depends on mainly three factors:Host genetics,environment and bacterial factors.Among these,bacterial virulence factors such as cagA,vacA are well known for their role in disease outcomes.However,based on the global epidemiological results,none of the bacterial virulence(gene)factors was found to be associated with particular diseases like duodenal ulcer(DU)in all populations.Hence,substantial importance has been provided for research in strain-specific genes outside the cag pathogenicity island,especially genes located within the plasticity regions.dupA found within the plasticity regions was first demonstrated in 2005 and was proposed for duodenal ulcer development and reduced risk of gastric cancer in certain geographical regions.Due to the discrepancies in report from different parts of the world in DU development related to H.pylori virulence factor,dupA became an interesting area of research in elucidating the role of this gene in the disease progression.In this review,we shed light on the detailed information available on the polymorphisms in dupA and their clinical relevance.We have critically appraised several pertinent studies on dupA and discussed their merits and shortcomings.This review also highlights dupA gene as an important biomarker for DU in certain populations.

Helicobacter pylori neutrophil activating protein as target for new drugs against H.pylori inflammation

Helicobacter pylori(H.pylori) infection is among the most common human infections and the major risk factor for peptic ulcer disease and gastric cancer.With-in this work we present the implication of C-terminal region of H.pylori neutrophil activating protein in the stimulation of neutrophil activation as well as the evi-dence that the C-terminal region of H.pylori activating protein is indispensable for neutrophil adhesion to endothelial cells,a step necessary to H.pylori inflammation.In addition we show that arabino galactan proteins derived from chios mastic gum,the natural resin of the plant Pistacia lentiscus var.Chia inhibit neutrophil activation in vitro.

Helicobacter pylori and upper gastrointestinal diseases: A review

Since its first isolation by Marshall and Warren, Helicobacter pylori (H. pylori) has been recognized to have a causal role in the upper gastrointestinal diseases development, especially in chronic gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue (MALT lymphoma) and gastric adenocarcinoma. H. pylori is a spiral-shaped gram-negative flagellate bacterium that has a high genetic diversity, which is an important factor in its adaptation to the host stomach and also for the clinical outcome of the infection, an aspect that remains unclear. However, it is thought to involve a interplay among the virulence of the infecting strain, host genetics and environmental factors. This review chapter brings the principal characteristics of the diseases associated with H. pylori infection and summarizes some important characteristics concerning the virulence of bacterium strain, host genetics and external environment.

To be or not to be:The host genetic factor and beyond in Helicobacter pylori mediated gastro-duodenal diseases

Helicobacter pylori(H.pylori)have long been associated with a spectrum of disease outcomes in the gastroduodenal system.Heterogeneity in bacterial virulence factors or strains is not enough to explain the divergent disease phenotypes manifested by the infection.This review focuses on host genetic factors that are involved during infection and eventually are thought to influence the disease phenotype.We have summarizedthe different host genes that have been investigated for association studies in H.pylori mediated duodenal ulcer or gastric cancer.We discuss that as the bacteria co-evolved with the host;these host gene also show much variation across different ethnic population.We illustrate the allelic distribution of interleukin-1B,across different population which is one of the most popular candidate gene studied with respect to H.pylori infections.Further,we highlight that several polymorphisms in the pathway gene can by itself or collectively affect the acid secretion pathway axis(gastrin:somatostatin)thereby resulting in a spectrum of disease

Study on relationship between acute gastrointestinal disease and Helicobacter pylori infections

Objective: To assess the relation between acute gastrointestinal disease and Helicobacter pylori (H. pylori) infections. Methods: Over the 18-month period, a total of 323 patients referred to three hospitals in Babol (north of Iran) were enrolled in this cross-sectional study. H. pylori status (rapid urease test), endoscopic findings in the patients, personal habits (smoking or alcohol intake) and administration of drugs, such as non-steroidal anti-inflammatory drugs (NSAIDs) were analyzed using standard Chi-square test and multinomial logistic regression analysis. Results: Results showed that acute gastric ulcer patients had a significant association with alcohol (P=0.001, OR=6.183), opium (P=0.022, OR=2.823), smoking (P=0.016, OR=2.579) and NSAIDs (P=0.046, OR=2.071). However, patients with in acute duodenal ulcer have a significant association with opium (P=0.023, OR=2.326) and alcohol (P=0.003, OR=3.888). As well as, gastric cancer had significant association with alcohol (P<0.05, OR=6.937), smoking (P=0.012, OR=2.738), family history (P=0.005, OR=4.380) and gender (P≤0.05, OR=5.103). Conclusions: Current investigation shows that H. pylori infection, alcoholism, male gender, age and family history have an additive impact on the incidence of gastric cancer. In addition, alcoholism, opium usage, NSAIDs and family history have more impact on the incidence of acute gastric ulcer and acute duodenal ulcer in patients.

Topic highlight on texture and color enhancement imaging in gastrointestinal diseases

Olympus Corporation developed texture and color enhancement imaging(TXI)as a novel image-enhancing endoscopic technique.This topic highlights a series of hot-topic articles that investigated the efficacy of TXI for gastrointestinal disease identification in the clinical setting.A randomized controlled trial demonstrated improvements in the colorectal adenoma detection rate(ADR)and the mean number of adenomas per procedure(MAP)of TXI compared with those of white-light imaging(WLI)observation(58.7%vs 42.7%,adjusted relative risk 1.35,95%CI:1.17-1.56;1.36 vs 0.89,adjusted incident risk ratio 1.48,95%CI:1.22-1.80,respectively).A cross-over study also showed that the colorectal MAP and ADR in TXI were higher than those in WLI(1.5 vs 1.0,adjusted odds ratio 1.4,95%CI:1.2-1.6;58.2%vs 46.8%,1.5,1.0-2.3,respectively).A randomized controlled trial demonstrated non-inferiority of TXI to narrow-band imaging in the colorectal mean number of adenomas and sessile serrated lesions per procedure(0.29 vs 0.30,difference for non-inferiority-0.01,95%CI:-0.10 to 0.08).A cohort study found that scoring for ulcerative colitis severity using TXI could predict relapse of ulcerative colitis.A cross-sectional study found that TXI improved the gastric cancer detection rate compared to WLI(0.71%vs 0.29%).A cross-sectional study revealed that the sensitivity and accuracy for active Helicobacter pylori gastritis in TXI were higher than those of WLI(69.2%vs 52.5%and 85.3%vs 78.7%,res-pectively).In conclusion,TXI can improve gastrointestinal lesion detection and qualitative diagnosis.Therefore,further studies on the efficacy of TXI in clinical practice are required.

幽门螺杆菌毒力基因分型和宿主遗传多态性与胃病关系研究进展

幽门螺杆菌(Helicobacter pylori)感染能导致慢性胃炎、消化性溃疡、胃粘膜相关的淋巴样组织(Mu-cosa-associated lymphoid tissue,MALT)淋巴瘤和胃腺癌等疾病的发生。1994年世界卫生组织国际癌症研究中心(IARC)将H.pylori列为胃癌第一级因子。H.pylori感染引起的不同临床结局主要与H.pylori致病因子和宿主遗传易感性有关,大部分重大疾病发生在特定的细菌毒力因子(如cagA,vacA)与易感宿主遗传背景共同存在时。文章综述了H.pylori菌株的毒力基因的分型和宿主的遗传多态性对胃病发生的影响。

IL-17在幽门螺旋杆菌感染相关消化道疾病中的作用

幽门螺旋杆菌感染是诸如胃炎、胃溃疡、胃癌等各种消化道疾病的重要诱因且在感染过程中会产生许多细胞因子。近年来的研究证明,白介素-17在感染的病理生理学以及免疫介导的消化系统疾病中扮演着重要较色。幽门螺旋杆菌感染使患者胃黏膜中IL-17增加,从而通过MAPK/ERK1/2信号通路的激活导致IL-8的分泌表达。IL-8可趋化中性粒细胞而促进炎症反应,调节性T细胞可抑制该炎症反应。目前,幽门螺旋杆菌诱发的炎症反应的机制尚未被完全清楚,宿主和病原菌均可促进炎症反应,如细胞毒力相关基因A、空泡毒素A。白细胞介素-1β(IL-1β)、IL-6、肿瘤坏死因子-α(TNF-α)、转化生长因子-β1、IL-17、IL-18、IL-21以及IL-22均与幽门螺旋杆菌诱发的胃黏膜炎症反应有关,但具体细节与炎症反的不同模式仍然不清楚。大量的研究表明IL-17在急性及慢性炎症进展过程中具有重要功能,本文就IL-17在胃炎、胃溃疡及胃癌相关消化系统疾病中的作用进行了回顾。