Correlation between Helicobacter pylori-associated gastric diseases and colorectal neoplasia

AIM: To explore the correlation between Helicobacter pylori(H. pylori)-associated gastric diseases and colorectal neoplasia.METHODS: Patients included in this study underwent a colonoscopy and esophago-gastro-duodenoscopy(EGD) along with histopathological measurement between March 2012 and March 2015 at Qi-Lu Hospital of Shandong University, who also had results of H. pylori detection. A total of 233 cases were selected. Demographic data, H. pylori infection status(including results of rapid urease tests and gastric mucosa pathological examinations) and histopathological examination results of gastric and colorectal mucosa were gathered and analyzed. The statistical analysis focused on the prevalence of colorectal neoplasms among patients with various histopathological categories of the stomach. ORs and their 95%CI were calculated to describe the strengths of the associations.RESULTS: The incidence rates of colorectal adenoma without high-grade intraepithelial neoplasia(HGIEN)(OR = 2.400, 95%CI: 0.969-5.941), adenoma with HGIEN(5.333, 1.025-27.758) and adenocarcinoma(1.455, 0.382-5.543) were all higher for patients with H. pylori-associated gastritis than for those in the control group. The incidence rate of colorectal adenoma with HGIEN(3.218, 0.767-13.509) was higher in patients with intestinal metaplasia than in the control group, while the incidence rates of adenoma without HGIEN(0.874, 0.414-1.845) and adenocarcinoma(0.376, 0.096-1.470) were lower in the intestinal metaplasia group than in the control group. The incidence rate of colorectal adenoma without HGIEN(3.111, 1.248-7.753) was significantly higher in the gastric intraepithelial neoplasia group than in the control group, while the rates of adenoma with HGIEN(1.481, 0.138-15.941) and adenocarcinoma(2.020, 0.561-7.272) were higher in the gastric intraepithelial neoplasia group. Incidence rates of colorectal adenoma without HGIEN(1.067, 0.264-4.314), adenoma with HGIEN(2.667, 0.231-30.800) and adenocarcinoma(2.182, 0.450-10.585) were all higher in the gastric adenocarcinoma group than in the control group.CONCLUSION: H. pylori infection as well as H. pylori-associated gastric diseases are risk factors for colorectal neoplasia.

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

INTRODUCTIONChronic gastritis(CG)and peptic ulcer(PU)arefrequently-occurring diseases.It is now well recognizedthat Helicobacter pylori(Hp)is a major factor that leadsto CG and PU.In order to study the relationshipamong T lymphocyte subsets,NO,Hexosamine and

Global whole family based-Helicobacter pylori eradication strategy to prevent its related diseases and gastric cancer

Helicobacter pylori (H.pylori) infects approximately 50% of the world population.The multiple gastrointestinal and extra-gastrointestinal diseases caused by H.pylori infection pose a major healthcare threat to families and societies;it is also a heavy economic and healthcare burden for countries that having high infection rates.Eradication of H.pylori is recommended for all infected individuals.Traditionally,"test and treat"and"screen and treat"strategies are available for various infected populations.However,clinical practice has noticed that these strategies have some shortfalls and may need refinement,mostly due to the fact that they are not easily manageable,and are affected by patient compliance,selection of treatment population and cost-benefit estimations.Furthermore,it is difficult to control infections from the source,therefore,development of additional,compensative strategies are encouraged to solve the above problems and facilitate bacteria eradication.H.pylori infection is a family-based disease,but few studies have been performed in a whole family-based approach to curb its intra-familial transmission and the development of related diseases.In this work,a third,novel whole family-based H.pylori eradication strategy is introduced.This approach screens,identifies,treats and follows up on all H.pylori-infected individuals in entire families to control H.pylori infection among family members,and reduce its long-term complications.This strategy is high-risk population-oriented,and able to reduce H.pylori spread among family members.It also has good patient-family compliance and,importantly,is practical for both high and low H.pylori-infected communities.Future efforts in these areas will be critical to initiate and establish healthcare policies and management strategies to reduce H.pylori-induced disease burden for society.

Reciprocal impact of host factors and Helicobacter pylori genotypes on gastric diseases

AIM: To assess the impact of Helicobacter pylori(H. pylori) genotypes and patient age and sex on the development of gastric diseases.METHODS: H. pylori-infected patients(n = 233) referred to the endoscopy unit at Tehran University of Medical Sciences(Tehran,Iran) were diagnosed with chronic gastritis(CG),gastric ulcer(GU),or duodenal ulcer(DU). Brucella blood agar was used for biopsy cultures and H. pylori isolation under microaerobic conditions. H. pylori isolates were confirmed with biochemical tests and through amplification of the 16 S r RNA gene. DNA was extracted from fresh cultures of the H. pylori isolates and used for amplification of vac A alleles and the cag A gene. Statistical analysis was performed to determine the association between H. pylori genotypes,age(< 40 years vs > 40 years) and sex of the patient,and gastric diseases.RESULTS: CG was the most prevalent gastric disease(113/233; 48.5%),compared to GU(64/233; 27.5%)and DU(56/233; 24%). More patients were male,and gastric diseases were more frequent in patients > 40 years(P < 0.05). The percentage of CG and GU patients that were male and female did not show a significant difference; however DU was more common in males(P < 0.05). Interestingly,a diagnosis of CG in patients > 40 years was more common in females(18.5%) than males(11.6%)(P = 0.05),whereas a diagnosis of GU or DU in patients > 40 years was more frequent in males(14.6% vs 10.7% and 12.4% vs 4.3%,respectively). Overall,genotyping of the H. pylori isolates revealed that the vac A s1(82%),vac A m2(70%),and cag A+(72.5%) alleles were more frequent than vac A s2(18%),vac A m1(29.2%),and cag A-(all P < 0.05). The vac A s1m2 cag A+ genotype was the most prevalent within the three disease groups. vac A s1m2 frequency was 56.2% with a similar occurrence in all diagnoses,while vac A s1m1 appeared more often in DU patients(33.9%). A genotype of vac A s2m2 occurred in 15% of isolates and was more common in CG patients(21.2%); vac A s2m1 was the least common genotype(3%). The vac A s1 allele was found to be a risk factor for DU,vac A s2 for CG,and vac A s1 and vac A s2 for GU(all P < 0.05). The vac A s2m2 genotype was associated with the development of CG and GU compared to DU(P < 0.05). No correlation was found between vac A m or cag A and gastric diseases.CONCLUSION: The outcome of H. pylori infection is the result of interaction between bacterial genotypes and the age and sex of infected individuals.

Curative resection with endoscopic submucosal dissection of early gastric cancer in Helicobacter pylori-negative Ménétrier’s disease:A case report

BACKGROUND Adult-onset Ménétrier’s disease is strongly associated with Helicobacter pylori(H.pylori)infection and an elevated risk of carcinogenesis.Cases of early-stage gastric cancer developed in H.pylori-negative Ménétrier’s disease are extremely rare.We report a case of early gastric cancer in H.pylori-negative Ménétrier’s disease that was curatively resected with endoscopic submucosal dissection(ESD).CASE SUMMARY A 60-year-old woman was referred to our hospital after her medical examination detected anemia.Contrast-enhanced upper gastrointestinal(UGI)radiography revealed translucency of the nodule-aggregating surface with giant rugae.Blood tests showed hypoproteinemia and were negative for serum H.pylori immunoglobulin G antibodies.The 99mTc-DTPA-human serum albumin scintigraphy showed protein loss from the stomach.UGI endoscopy showed a 40-mm protruding erythematous lesion on giant rugae of the greater curvature of lower gastric body,suggesting early-stage gastric cancer due to Ménétrier’s disease.En bloc resection with ESD was performed for diagnosis and treatment.Histology of ESD showed well-differentiated tubular adenocarcinoma.The cancer was confined to the mucosa,and complete curative resection was achieved.Foveolar hyperplasia and atrophy of the gastric glands were observed in non-tumor areas,histologically corresponding to Ménétrier’s disease.Three years after ESD,gastric cancer had not recurred,and Ménétrier’s disease remained in remission with spontaneous regression of giant gastric rugae.CONCLUSION Complete curative resection was achieved through ESD in a patient with earlystage gastric cancer and H.pylori-negative Ménétrier’s disease.

Effect of cagE gene on Helicobacter pylori-associated gastritis and levels of interleukin-8

Objective: To investigate the status of cagE gene of Helicobacter pylori(H. pylori) isolated from patients with various gastrointestinal diseases and its relationship with the pathological inflammation grade and levels of IL 8 in the gastric mucosa and IL 8 secretion in gastric epithelial cells stimulated by H. pylori . Methods: cagE was amplified by polymerase chain reaction (PCR) in 145 clinical isolates. The inflammation grade of gastric mucosa was evaluated pathologically. IL 8 levels of gastric mucosa and IL 8 concentration of the supernatant of the cocultured SGC 7 901 cells and H. pylori was assayed by enzyme linked immunosorbent assay (ELISA). Results: cagE was positive in 79.3% of all the H. pylori strains. The mean score of the cagE positive gastritis in the antrum and corpus was (1.865±0.335) and (1.759±0.310). Meanwhile, the cagE negative grade was (1.689±0.294), (1.608±0.284). There was no significant difference ( P >0 05). The mean levels of IL 8 in cagE positive group in antrum and corpus were (390.6±101.4) pg/mg and (368.6±91.2) pg/mg; and cagE negative group were (328.6±102.8) pg/mg and (332.6±96.7) pg/mg. IL 8 in SGC7901 cells induced by cagE positive and negative group averaged (789.5±146.7) pg/ml and (757.6±136.4) pg/ml. There was still no significant difference( P >0.05). Conclusion: Positive rate of cagE is very high in Chinese patients regardless of the clinical outcome. And there was no direct relationship between cagE gene and the inflammation grade and IL 8 levels of H. pylori infected gastric mucosa and IL 8 secretion in gastric epithelial cells stimulated by H. pylori .

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.

Type Ⅰ and type Ⅱ Helicobacter pylori infection status and their impact on gastrin and pepsinogen level in a gastric cancer prevalent area

BACKGROUND Type I Helicobacter pylori(H.pylori)infection causes severe gastric inflammation and is a predisposing factor for gastric carcinogenesis.However,its infection status in stepwise gastric disease progression in this gastric cancer prevalent area has not been evaluated;it is also not known its impact on commonly used epidemiological gastric cancer risk markers such as gastrin-17(G-17)and pepsinogens(PGs)during clinical practice.AIM To explore the prevalence of type I and type II H.pylori infection status and their impact on G-17 and PG levels in clinical practice.METHODS Thirty-five hundred and seventy-two hospital admitted patients with upper gastrointestinal symptoms were examined,and 523 patients were enrolled in this study.H.pylori infection was confirmed by both 13C-urea breath test and serological assay.Patients were divided into non-atrophic gastritis(NAG),nonatrophic gastritis with erosion(NAGE),chronic atrophic gastritis(CAG),peptic ulcers(PU)and gastric cancer(GC)groups.Their serological G-17,PG I and PG II values and PG I/PG II ratio were also measured.RESULTS A total H.pylori infection rate of 3572 examined patients was 75.9%,the infection rate of 523 enrolled patients was 76.9%,among which type I H.pylori infection accounted for 72.4%(291/402)and type II was 27.6%;88.4%of GC patients were H.pylori positive,and 84.2%of them were type I infection,only 11.6%of GC patients were H.pylori negative.Infection rates of type I H.pylori in NAG,NAGE,CAG,PU and GC groups were 67.9%,62.7%,79.7%,77.6%and 84.2%,respectively.H.pylori infection resulted in significantly higher G-17 and PG II values and decreased PG I/PG II ratio.Both types of H.pylori induced higher G-17 level,but type I strain infection resulted in an increased PG II level and decreased PG I/PG II ratio in NAG,NAGE and CAG groups over uninfected controls.Overall PG I levels showed no difference among all disease groups and in the presence or absence of H.pylori;in stratified analysis,its level was increased in GC and PU patients in H.pylori and type I H.pylori-positive groups.CONCLUSION Type I H.pylori infection is the major form of infection in this geographic region,and a very low percentage(11.6%)of GC patients are not infected by H.pylori.Both types of H.pylori induce an increase in G-17 level,while type I H.pylori is the major strain that affects PG I and PG IIs level and PG I/PG II ratio in stepwise chronic gastric disease.The data provide insights into H.pylori infection status and indicate the necessity and urgency for bacteria eradication and disease prevention in clinical practice.

Helicobacter pylori and gastric cancer: Indian enigma

Helicobacter pylori(H. pylori) is a gram negative microaerophilic bacterium which resides in the mucous linings of the stomach. It has been implicated in the causation of various gastric disorders including gastric cancer. The geographical distribution and etiology of gastric cancer differ widely in different geographical regions and H. pylori, despite being labeled as a grade Ⅰ carcinogen, has not been found to be associated with gastric cancer in many areas. Studies in Asian countries such as Thailand, India, Bangladesh, Pakistan, Iran, Saudi Arabian countries, Israel and Malaysia, have reported a high frequency of H. pylori infection co-existing with a low incidence of gastric cancer. In India, a difference in the prevalence of H. pylori infection and gastric cancer has been noted even in different regions of the country leading to a puzzle when attempting to find the causes of these variations. This puzzle of H. pylori distribution and gastric cancer epidemiology is known as the Indian enigma. In this review we have attempted to explain the Indian enigma using evidence from various Indian studies and from around the globe. This review covers aspects of epidemiology, the various biological strains present in different parts of the country and within individuals, the status of different H. pylori-related diseases and the molecular pathogenesis of the bacterium.

Helicobacter pylori:Does it add to risk of coronary artery disease

Helicobacter pylori(H. pylori) is a known pathogen implicated in genesis of gastritis, peptic ulcer disease, gastric carcinoma and gastric lymphoma. Beyond the stomach, the organism has also been implicated in the causation of immune thrombocytopenia and iron deficiency anemia. Although an area of active clinical research, the role of this gram negative organism in causation of atherosclerosis and coronary artery disease(CAD) remains enigmatic. CAD is a multifactorial disease which results from the atherosclerosis involving coronaryarteries. The major risk factors include age, diabetes mellitus, smoking, hypertension and dyslipidemia. The risk of coronary artery disease is believed to increase with chronic inflammation. Various organisms like Chlamydia and Helicobacter have been suspected to have a role in genesis of atherosclerosis via causation of chronic inflammation. This paper focuses on available evidence to ascertain if the role of H. pylori in CAD causation has been proven beyond doubt and if eradication may reduce the risk of CAD or improve outcomes in these patients.

Genetic predisposition to Helicobacter pylori-induced gastric precancerous conditions

Gastric cancer is the most common malignancy of the gastrointestinal tract in East Asian populations and the second most frequent cause of cancer-related mortality in the world. While previous studies have investigated the genetic factors involved in gastric carcinogenesis, there still exist relatively few studies that have investigated the genetic traits associated with the risk of gastric precancerous conditions. In this paper we will review the biology and genetic polymorphisms involved in the genesis of gastric precancerous conditions reported to date and discuss the future prospects of this field of study. The associations of gastric precancerous conditions with polymorphisms in the cytotoxin-associated gene A-related genes (e.g. PTPN11 G/A at intron 3, rs2301756), those in the genes involved in host immunity against Helico-bacter pylori (H. pylori) infection (e.g.TLR4 +3725G/C, rs11536889) or polymorphisms of the genes essential for the development/ differentiation of the gastric epithelial cells (e.g. RUNX3 T/A polymorphism at intron 3, rs760805) have been reported to date. Genetic epide-miological studies of the associations between H. pylori-induced gastric precancerous conditions and other gene polymorphisms in these pathways as well as polymor-phisms of the genes involved in other pathways like oxidative DNA damage repair pathways would provide useful evidence for the individualized prevention of these H. pylori-induced gastric precancerous conditions.

Helicobacter pylori and its reservoirs:A correlation with the gastric infection

Helicobacter pylori(H. pylori) has long been found to cause gastric diseases such as gastritis, gastric ulcers and gastric cancer. The transmission medium of this bacterium has yet to be determined, though several studies have speculated that the oral cavity is a reservoir for H. pylori. Others have also reported that the oral cavity may be a source of both transmission and gastric reinfection; however, such results are controversial. We reviewed the literature and selected studies that report an association among H. pylori detections in the oral cavity(dental plaque, saliva, tongue, tonsil tissue, root canals, oral mucosa) in humans and in animals, as well as in the human stomach. The oral cavity may be considered the main reservoir for H. pylori. There are a correlations between H. pylori infection in the oral cavity and periodontal disease, oral tissue inflammation, H. pylori transmission, and gastric reinfection. We believe that the mouth is a reservoir and that it plays a crucial role in both H. pylori transmission and gastric infection.

Effect of Helicobacter pylori on gastric epithelial cells

The gastrointestinal epithelium has cells with features that make them a powerful line of defense in innate mucosal immunity. Features that allow gastrointestinal epithelial cells to contribute in innate defense include cell barrier integrity, cell turnover, autophagy, and innate immune responses. Helicobacter pylori(H. pylori) is a spiral shape gram negative bacterium that selectively colonizes the gastric epithelium of more than half of the world's population. The infection invariably becomes persistent due to highly specialized mechanisms that facilitate H. pylori 's avoidance of this initial line of host defense as well as adaptive immune mechanisms. The host response is thus unsuccessful in clearing the infection and as a result becomes established as a persistent infection promoting chronic inflammation. In some individuals the associated inflammation contributes to ulcerogenesis or neoplasia. H. pylori has an array of different strategies to interact intimately with epithelial cells and manipulate their cellular processes and functions. Among the multiple aspects that H. pylori affects in gastric epithelial cells are their distribution of epithelial junctions, DNA damage, apoptosis, proliferation, stimulation of cytokine production, and cell transformation. Some of these processes are initiated as a result of the activation of signaling mechanisms activated on binding of H. pylori to cell surface receptors or via soluble virulence factors that gain access to the epithelium. The multiple responses by the epithelium to the infection contribute to pathogenesis associated with H. pylori.

Molecular cross-talk between Helicobacter pylori and human gastric mucosa

Helicobacter pylori (H.pylori) has co-evolved with humans to be transmitted from person to person and to colonize the stomach persistently.A well-choreographed equilibrium between the bacterial effectors and host responses permits microbial persistence and health of the host,but confers a risk for serious diseases including gastric cancer.During its long coexistence with humans,H.pylori has developed complex strategies to limit the degree and extent of gastric mucosal damage and in? ammation,as well as immune effector activity.The present editorial thus aims to introduce and comment on major advances in the rapidly developing area of H.pylori/human gastric mucosa interaction (and its pathological sequelae),which is the result of millennia of co-evolution of,and thus of reciprocal knowledge between,the pathogen and its human host.

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.

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.

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.

Helicobacter pylori infection:How does age influence the inflammatory pattern?

The inflammatory pattern during Helicobacter pylori(H.pylori)infection is changeable and complex.During childhood,it is possible to observe a predominantly regulatory response,evidenced by high concentrations of key cytokines for the maintenance of Treg responses such as TGF-β1 and IL-10,in addition to high expression of the transcription factor FOXP3.On the other hand,there is a predominance of cytokines associated with the Th1 and Th17 responses among H.pylori-positive adults.In the last few years,the participation of the Th17 response in the gastric inflammation against H.pylori infection has been highlighted due to the high levels of TGF-β1 and IL-17 found in this infectious scenario,and growing evidence has supported a close relationship between this immune response profile and unfavorable outcomes related to the infection.Moreover,this cytokine profile might play a pivotal role in the effectiveness of anti-H.pylori vaccines.It is evident that age is one of the main factors influencing the gastric inflammatory pattern during the infection with H.pylori,and understanding the immune response against the bacterium can assist in the development of alternative prophylactic and therapeutic strategies against the infection as well as in the comprehension of the pathogenesis of the outcomes related to that microorganism.

Polymorphism of -765G > C COX-2 is a risk factor for gastric adenocarcinoma and peptic ulcer disease in addition to H pylori infection:A study from northern India

AIM: To investigate -765G > C COX-2 polymorphism and H pylori infection in patients with gastric adenocarcinoma, peptic ulcer disease (PUD) and non- ulcer dyspepsia (NUD). METHODS: We enrolled 348 adult patients (62 gastric adenocarcinoma, 45 PUD and 241 NUD) undergoing upper gastrointestinal endoscopy at two referral centers between September, 2002 and May, 2007. H pylori infection was diagnosed when any of the four tests (RUT, culture, histopathology and PCR) were positive. Genotyping for -765G > C polymorphism of COX-2 was performed by PCR-RFLP analysis. RESULTS: Frequency of C carrier had significantassociation with gastric adenocarcinoma as compared to NUD [77.4% vs 29%, P < 0.001, odds ratio (OR) 8.20; 95% confidence interval (95% CI), 4.08-16.47] and PUD (77.4% vs 31.1%, P < 0.001; OR 8.04; 95% CI, 3.25-19.90). Risk of gastric adenocarcinoma was significantly higher in patients having C carrier with (OR 7.83; 95% CI 3.09-19.85) and without H pylori infection (OR 7.06; 95% CI, 2.61-19.09). Patients with C carrier and H pylori infection had significant risk for the development of PUD (P < 0.001; OR 5.65; 95% CI, 2.07-15.34). CONCLUSION: -765G > C COX-2 polymorphism with or without H pylori could be a marker for genetic susceptibility to gastric adenocarcinoma. COX-2 polymorphism in presence of H pylori infection might be useful in predicting the risk of PUD.

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.