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.     

Clinical characteristics of Helicobacter pylori-negative drug-negative peptic ulcer bleeding

AIM: To investigate the clinical characteristics and outcomes of idiopathic Helicobacter pylori (H. pylori)-negative and drug-negative] peptic ulcer bleeding (PUB).METHODS: A consecutive series of patients who experienced PUB between 2006 and 2012 was retrospectively analyzed. A total of 232 patients were enrolled in this study. The patients were divided into four groups according to the etiologies of PUB: idiopathic, H. pylori-associated, drug-induced and combined (H. pylori-associated and drug-induced) types. We compared the clinical characteristics and outcomes between the groups. When the silver stain or rapid urease tests were H. pylori-negative, we obtained an additional biopsy specimen by endoscopic re-examination and performed an H. pylori antibody test 6-8 wk after the initial endoscopic examination. For a diagnosis of idiopathic PUB, a negative result of an H. pylori antibody test was confirmed. In all cases, re-bleeding was confirmed by endoscopic examination. For the risk assessment, the Blatchford and the Rockall scores were calculated for all patients.RESULTS: For PUB, the frequency of H. pylori infection was 59.5% (138/232), whereas the frequency of idiopathic cases was 8.6% (20/232). When idiopathic PUB was compared to H. pylori-associated PUB, the idiopathic PUB group showed a higher rate of re-bleeding after initial hemostasis during the hospital stay (30% vs 7.4%, P = 0.02). When idiopathic PUB was compared to drug-induced PUB, the patients in the idiopathic PUB group showed a higher rate of re-bleeding after initial hemostasis upon admission (30% vs 2.7%, P < 0.01). When drug-induced PUB was compared to H. pylori-associated PUB, the patients in the drug-induced PUB were older (68.49 ± 14.76 years vs 47.83 ± 15.15 years, P < 0.01) and showed a higher proportion of gastric ulcer (77% vs 49%, P < 0.01). However, the Blatchford and the Rockall scores were not significantly different between the two groups. Among the patients who experienced drug-induced PUB, no significant differences were found with respect to clinical characteristics, irrespective of H. pylori infection.CONCLUSION: Idiopathic PUB has unique clinical characteristics such as re-bleeding after initial hemostasis upon admission. Therefore, these patients need to undergo close surveillance upon admission.     

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.     

Different risk factors influence peptic ulcer disease development in a Brazilian population

AIM: To investigate age, sex, histopathology and Helicobacter pylori (H. pylori) status, as risk factors for gastroduodenal disease outcome in Brazilian dyspeptic patients.tients submitted to upper gastroscopy at Hospital das Clinicas of Marilia, antral biopsy specimens were obtained and subjected to histopathology and H. pylori diagnosis. All patients presenting chronic gastritis (CG) and peptic ulcer (PU) disease localized in the stomach, gastric ulcer (GU) and/or duodenal ulcer (DU) were included in the study. Gastric biopsies (n = 668) positive for H. pylori by rapid urease test were investigated for vacuolating cytotoxin A (vacA ) medium (m) region mosaicism by polymerase chain reaction. Logistic regression analysis was performed to verify the association of age, sex, histopathologic alterations, H. pylori diagnosis and vacA m region mosaicism with the incidence of DU, GU and CG in patients. RESULTS: Of 1466 patients submitted to endoscopy, 1060 (72.3%) presented CG [male/female = 506/554; mean age (year) ± SD = 51.2 ± 17.81], 88 (6.0%) presented DU [male/female = 54/34; mean age (year) ± SD = 51.4 ± 17.14], and 75 (5.1%) presented GU [male/female = 54/21; mean age (year) ± SD = 51.3 ± 17.12] and were included in the comparative analysis. Sex and age showed no detectable effect on CG incidence (overall c 2 = 2.1, P = 0.3423). Sex [Odds ratios (OR) = 1.8631, P = 0.0058] but not age (OR = 0.9929, P = 0.2699) was associated with DU and both parameters had a highly significant effect on GU (overall c 2 = 30.5, P 0.0001). The histopathological results showed a significant contribution of ageing for both atrophy (OR = 1.0297, P 0.0001) and intestinal metaplasia (OR = 1.0520, P 0.0001). Presence of H. pylori was significantly associated with decreasing age (OR = 0.9827, P 0.0001) and with the incidence of DU (OR = 3.6077, P 0.0001). The prevalence of m1 in DU was statistically significant (OR = 2.3563, P = 0.0018) but not in CG (OR = 2.678, P = 0.0863) and GU (OR = 1.520, P = 0.2863). CONCLUSION: In our population, male gender was a risk factor for PU; ageing for GU, atrophy and metapla-sia; and H. pylori of vacA m1 genotype for DU.     

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.     

Helicobacter pylori-negative,non-steroidal anti-inflammatory drug:Negative idiopathic ulcers in Asia

Since the discovery of Helicobacter pylori(H.pylori)infection in the stomach,the bacteria infection and non-steroidal anti-inflammatory drugs(NSAIDs)use had been considered to be the 2 main causes of peptic ulcers.However,there have been recent reports of an increase in the proportion of peptic ulcers without these known risk factors;these are termed idiopathic peptic ulcers.Such trend was firstly indicated in 1990s from some reports in North America.In Asia,numerous studies reported that idiopathic ulcers accounted for a small percentage of all ulcers in the 1990s,but in the2000s,multiple studies reported that the proportion of idiopathic ulcers had reached 10%-30%,indicating that the incidence of idiopathic ulcers in Asia has also been rising in recent years.While a decline in H.pylori infection rates of general population in Asia is seen as the main reason for the increased incidence of idiopathic ulcers,it is also possible that the absolute number of idiopathic ulcer cases has increased.Advanced age,serious systemic complication,and psychological stress are considered to be the potential risk factors for idiopathic ulcers.Management of idiopathic ulcers is challenging,at present,because there is no effective preventative measure against recurrence in contrast with cases of H.pylori-positive ulcers and NSAIDs-induced ulcers.As it is expected that H.pylori infection rates in Asia will decline further in the future,measures to treat idiopathic ulcers will also likely become more important.     

Association of the myeloperoxidase-468G→A polymorphism with gastric inflammation and duodenal ulcer risk

AIM: To eluddate the relations between the myeloperoxidase-468G→A polymorphism and the development of duodenal ulcer (DU), and to investigate the impacts of this host genetic polymorphism on the histopathological features of Helicobacter pylori ( H pylori)-related gastritis.METHODS: In a case-control study of 115 consecutive DU patients and 182 controls, the myeloperoxidase-468G→A polymorphism was genotyped, Additionally, gastric mucosal changes were examined according to the updated Sydney System,RESULTS: The two study groups differed in the distributions of myeloperoxidasegenotypes (P= 0.008). All six individuals carrying myeloperoxidase A/A genotypes were in the DU group. The carriage of myeloperoxidaseallele A and Hpylori infection were associated with an increased risk of DU with odds ratios (OR) of 2.3 and 5.8, respectively. The combined risk of the carriage of myeloperoxidase allele A and Hpyloriinfection for DU was 8.7 (95% CI, 3.5-21.8).In the H pylori-infected individuals, allele A carriers displayed higher bacterial density scores (P = 0.04) in the antrum than did non-carriers.CONCLUSION: This work verifies for the first time the association of myeloperoxidase -468G→A polymorphism with antral H pylori density and DU disease. The mechanisms underlying this genetic polymorphism in developing DU disease merit further investigations,     

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output >10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence ofHelicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis).Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P<0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found amongHelicobacter pylori-positive compared toHelicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr wereHelicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence ofHelicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.     

Serum pepsinogen Ⅱ is a better diagnostic marker in gastric cancer

AIM:To investigate screening makers for gastric cancer,we assessed the association between gastric cancer and serum pepsinogens(PGs).METHODS:The subjects comprised 450 patients with gastric cancer,111 individuals with gastric atrophy,and 961 healthy controls.Serum anti-Helicobacter pylori(H.pylori) immunoglobulin G(IgG),PGⅠand PG Ⅱ were detected by enzyme-linked immunosorbent assay.Gastric atrophy and gastric cancer were diagnosed by endoscopy and histopathological examinations.Odds ratios and 95%CIs were calculated using multivariate logistic regression.RESULTS:Rates of H.pylori infection remained high in Northeastern China.Rates of H.pylori IgG positivity were greater in the gastric cancer and gastric atrophy groups compared to the control group(69.1% and 75.7% vs 49.7%,P 0.001).Higher levels of PG Ⅱ(15.9 μg/L and 13.9 μg/L vs 11.5 μg/L,P 0.001) and lower PGⅠ/PG Ⅱ ratio(5.4 and 4.6 vs 8.4,P 0.001) were found in patients with gastric cancer or gastric atrophy compared to healthy controls,whereas no correlation was found between the plasma PGⅠconcentration and risk of gastric cancer(P = 0.537).In addition,multivariate logistic analysis indicated that H.pylori infection and atrophic gastritis were independent risk factors for gastric cancer.Lower plasma PGⅠ/PG Ⅱ ratio was associated with higher risks of atrophy and gastric cancer.Furthermore,plasma PG Ⅱ?level?significantly?correlated?with?H.pyloriinfected gastric cancer.CONCLUSION:Serum PG Ⅱ concentration and PG Ⅰ/PG Ⅱ ratio are potential biomarkers for H.pyloriinfected gastric disease.PG Ⅱ is independently associated with risk of gastric cancer.     

Associations between the Plasticity Region Genes of Helicobacter pylori and Gastroduodenal Diseases in a High-Prevalence Area

Background/Aims

Genes associated with the Helicobacter pylori (H. pylori) plasticity region may play a role in the pathogenesis of H. pylori. We compared the genes jhp0940, jhp0947, and jhp0986 in H. pylori isolates from patients with different gastroduodenal diseases and in different age groups.

Methods

The H. pylori hyperplasticity region genes jhp0940, jhp0947, and jhp0986 were studied by PCR. We also evaluated whether these genes were related to the cytotoxin-associated gene (cagA) and histology findings.

Results

Of the patient cohort, 71 (62%) were positive for jhp0940, 67 (59%) for jhp0947, 12 (10%) for jhp0986, and 69 (60%) for cagA. jhp0940 (n=18, 67%) and jhp0947 (n=23, 85%) were found more frequently in duodenal ulcer (DU) patients than in gastritis patients (n=14, 39%; p=0.029 and p<0.001, respectively). Gastric ulcer (GU) was more frequently associated with jhp0940 (17 patients, 77%; p=0.003) than with gastritis (14 patients, 39%). Gastric carcinoma (GC) was more strongly associated with both jhp0940 (22 patients, 76%; p=0.003) and jhp0947 (22 patients, 76%; p=0.003) than was gastritis (14 patients, 39%). jhp0947 was more frequently associated with chronic active inflammation (58 patients, 87%; p=0.009) than with chronic inflammation (9 patients, 13%). Multivariate analysis demonstrated that jhp0947 was associated with DU (odds ratio, 6.1; 95% confidence interval, 1.87-20).

Conclusions

The genes jhp0947 and jhp0940 were identified in H. pylori isolates from patients with GC and DU, while jhp0940 was also isolated from patients with GU. jhp0947 was independently associated with DU.     

Cost-effectiveness study on treatment of duodenal ulcer

AIM: To compare the efficiency of therapy with a 2-week regimen of amoxicillin plus metronidazole and six weeks of Tagamet (AMT group) vs the efficacy of therapy with 6 wk of omeprazole plus 2 wk of amoxicillin (OA group) for ulcer healing, Helicobacter pylori (Hp) eradication, and decreasing the recurrence of duodenal ulcers.METHODS: This cost-effectiveness analysis was based on results shown in a randomized controlled trial conducted in 1995 in patients with a duodenal ulcer (OA group, 46 patients; AMT group, 43 patients) and treated at class grade III A hospitals in Shanghai, China.RESULTS: The costs of treatment in the AMT group were less than those in the OA group for ulcer healing (￥546.25 vs ￥1296.76 per case, P < 0.01), Hp eradication (￥702.32 vs ￥1742.53 per case, P < 0.01), and decreasing ulcer recurrence (￥640.39 vs 1424.54 per case, P < 0.01). Direct costs comprised the major cost involved in treatment of duodenal ulcers. The difference in the cost of treating ulcers in the two groups was primarily due to the costs of the different drugs. There was no significant difference between the two groups regarding their direct non-medical costs and indirect costs.CONCLUSION: When based on therapeutic effectiveness and financial costs, AMT therapy was more cost-efficient than OA therapy. AMT therapy is recommended for its low cost, acceptable ulcer healing rates, ability to cure of an Hp infection, and especially when treating patients with an ulcer < 1 cm in diameter.     

Low prevalence of idiopathic peptic ulcer disease: An Italian endoscopic survey

Background

Peptic ulcer disease (PUD) represents a common condition, although its incidence is decreasing. Previous studies reported a high rate of idiopathic PUD prevalence.

Aim

To investigate prevalence, relative distribution of etiologic factors and prevalence of complication of PUD in an Italian endoscopic series.

Materials and methods

All gastroscopies performed in adult patients during 3 years were considered. Patients with PUD, with antral and corporal histology, were included in the study. Helicobacter pylori infection was assessed by histology. Idiopathic PUD was defined as an ulcer without evidence H. pylori infection or prior exposure to NSAIDs.

Results

300 patients with PUD out of 11,148 gastroscopies were included in our study accounting for a prevalence of 2.7%. H. pylori-associated PUD was diagnosed in 62.3%, NSAID/aspirin-associated PUD in 22%, H. pylori/NSAID/aspirin-associated PUD in 11.6%, and idiopathic PUD in the remaining 4% of cases. Regarding ulcer complications the logistic regression analysis identified the following significant risk factors for GI bleeding: NSAIDs and/or aspirin use, age >65 years and coexistent gastric and duodenal ulcers.

Conclusion

Our data found a low endoscopic prevalence of peptic ulcer. Both H. pylori infection and NSAIDs and/or aspirin use remain the main determinants and idiopathic ulcer prevalence is very low.     

Helicobacter pylori and oral pathology:Relationship with the gastric infection

Helicobacter pylori(H.pylori)has been found in the oral cavity and stomach,and its infection is one of the most frequent worldwide.We reviewed the literature and conducted a Topic Highlight,which identified studies reporting an association between H.pylori-infection in the oral cavity and H.pylori-positive stomach bacterium.This work was designed to determine whether H.pylori is the etiologic agent in periodontal disease,recurrent aphthous stomatitis(RAS),squamous cell carcinoma,burning and halitosis.Record selection focused on the highest quality studies and meta-analyses.We selected 48 articles reporting on the association between saliva and plaque and H.pylori-infection.In order to assess periodontal disease data,we included 12 clinical trials and 1 meta-analysis.We evaluated 13 published articles that addressed the potential association with RAS,and 6 with squamous cell carcinoma.Fourteen publications focused on our questions on burning and halitosis.There is a close relation between H.pylori infection in the oral cavity and the stomach.The mouth is the first extra-gastric reservoir.Regarding the role of H.pylori in the etiology of squamous cell carcinoma,no evidence is still available.     

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease

Background. It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid.Aims. To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions.Methods. Duodenal (anterior, superior, inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and ¹³C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment.Results. Duodenal gastric metaplasia regression was observed in all ( ) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0.001).Conclusions. The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.     

vacA genotypes of Helicobacter pylori in the oral cavity and stomach of patients with chronic gastritis and gastric ulcer

Introduction

Helicobacter pylori adheres to various components of the human saliva. Therefore, the objective of this research was to simultaneously detect H. pylori in saliva and in gastric biopsy, and to determine the agreement between the vacA genotypes in both saliva and gastric biopsy.

Materials and methods

A total of 162 patients with chronic gastritis and 34 with gastric ulcer were studied, and saliva and biopsy samples were collected from each patient. H. pylori DNA was detected by conventional PCR and nested PCR was used for vacA genotyping.

Results

In 24% of the patients (47/196) H. pylori DNA was found in saliva and in biopsy; 52.5% (103/196) were saliva^negative/biopsy^positive and 6.6% (13/196) were saliva^positive/biopsy^negative. In either or both H. pylori vacAs1m1 or s1m2 genotypes were detected in saliva in 41.5% of the patients with chronic gastritis. Forty-seven percent had >1 genotype, and the s1m1/s1m2 combination was found in 36% of them. H. pylori vacAs1m1 and s1m2 were also found in the saliva and biopsy of patients with gastric ulcer. The genotypes found in saliva and biopsy of the same patient had 51.1% agreement. In 27.6% of the 47 patients saliva^positive/biopsy^positive two genotypes were found in saliva, and one or both in the stomach.

Conclusions

The s1m1/s1m2 genotypes, alone or together, are found simultaneously in saliva and gastric biopsy of the same patient. These results suggest that H. pylori reaches the oral cavity by various ways, and that saliva can be the transmitting and re-infecting vector.     

Helicobacter pylori infection following partial gastrectomy for gastric cancer

Gastric remnants are an inevitable consequence of partial gastrectomy following resection for gastric cancer.The presence of gastric stumps is itself a risk factor for redevelopment of gastric cancer.Helicobacter pylori(H.pylori)infection is also a well-known characteristic of gastric carcinogenesis.H.pylori colonization in the remnant stomach therefore draws special interest from clinicians in terms of stomach cancer development and pathogenesis;however,the H.pylori-infected gastric remnant is quite different from the intact organ in several aspects and researchers have expressed conflicting opinions with respect to its role in pathogenesis.For instance,H.pylori infection of the gastric stump produced controversial results in several recent studies.The prevalence of H.pylori infection in the gastric stump has varied among recent reports.Gastritis developing in the remnant stomach presents with a unique pattern of inflammation that is different from the pattern seen in ordinary gastritis of the intact organ.Bilerefluxate also has a significant influence on the colonization of the stomach stump,with several studies reporting mixed results as well.In contrast,the elimination of H.pylori from the gastric stump has shown a dramatic impact on eradication rate.H.pylori elimination is recognized to be important for cancer prevention and considerable agreement of opinion is seen among researchers.To overcome the current discrepancies in the literature regarding the role of H.pylori in the gastric stump,further research is required.