Serological markers for gastric atrophy in asymptomatic patients infected with Helicobacter pylori

OBJECTIVE: Atrophic gastritis is a precancerous condition that is commonly caused by chronic Helicobacter pylori (H. pylori) infection. This blinded, controlled study was designed to determine if serum gastrin and pepsinogens were reliable markers of atrophy in asymptomatic patients. METHODS: One hundred and forty-seven asymptomatic patients underwent endoscopy with multiple gastric biopsies obtained for histology, culture, and rapid urease test. Fasting serum gastrin (total and G-17) and serum pepsinogens (I-II) were determined by standard immunoassays. Gastric atrophy was histologically assessed in accordance with internationally accepted criteria; three main patterns of gastritis were distinguished: (a) nonatrophic gastritis, (b) atrophic antrum-restricted and antrum-predominant gastritis, and (c) corpus-restricted gastritis. Receiving operating characteristic (ROC) analysis was used to determine the best cut-off for each serum test in nonatrophic gastritis versus antrum-restricted/antrum-predominant atrophic gastritis. RESULTS: No significant differences in serum gastrin and pepsinogens I-II were detected in nonatrophic gastritis versus patients with antrum-restricted/antrum-predominant atrophic gastritis. The positive likelihood ratios for an abnormal serum test to detect antrum-restricted/antrum-predominant atrophy in the gastric body were total serum gastrin 2.13 (95% CI 0.99, 4.6), gastrin-17: 1.55 (95% CI 0.75, 36.17), pepsinogen I: 2.74 (1.4, 5.4), pepsinogen II: 1.74 (1.27, 2.39), and the ratio of pepsinogen I and II: 1.8 (1.2-2.8). Negative likelihood ratios ranged from 0.20 to 0.65. CONCLUSION: In an asymptomatic population, serum gastrin (total and G-17) and pepsinogens I-II (and their ratio) do not discriminate nonatrophic versus antrum-restricted/predominant atrophic gastritis.     

Helicobacter pylori and hypergastrinaemia during proton pump inhibitor therapy.

The rise in serum gastrin and pepsinogen I after 5 days' treatment with the proton pump inhibitor pantoprazole (40 mg/day) was examined in eight duodenal ulcer patients with Helicobacter pylori infection and compared with eight in whom it had been eradicated. Before treatment, the post-prandial serum gastrin concentrations were higher in the H. pylori-positive than -eradicated patients (p less than 0.05). The median rise in pre-prandial serum gastrin concentrations on treatment was similar in the H. pylori-positive (41%) and -eradicated patients (45%). The rise in post-prandial serum gastrin was also similar in the H. pylori-positive (81%) and -eradicated patients (69%), resulting in significantly higher gastrin concentrations during treatment in the former. The median rise in serum pepsinogen I on treatment was greater in the H. pylori-positive (114%) than in the -eradicated patients (8%), resulting in significantly higher concentrations during treatment in the former. These observations indicate that eradication of H. pylori may be a means of moderating the hypergastrinaemia caused by acid-inhibitory therapy. They also indicate that H. pylori-related hypergastrinaemia is not due to an increase of the antral surface pH by the bacterium's urease activity.     

Effect of Helicobacter pylori eradication on development of dyspeptic and reflux disease in healthy asymptomatic subjects

BACKGROUND AND AIM: There are few data on the course of Helicobacter pylori infection in asymptomatic subjects. The aim of this study was to assess the effect of eradication therapy on the development of dyspeptic and gastro-oesophageal reflux disease in a cohort of asymptomatic individuals observed over a prolonged period. METHODS: A total of 169 blood donors infected with H pylori who had volunteered for studies on eradication in 1990 formed the cohort. To be included in this cohort subjects had to have no symptoms, as determined by a validated symptom questionnaire at the baseline visit. Eighty eight subjects were infected with H pylori while 81 had successfully undergone eradication therapy. Subjects were followed up (annually) using the same symptom questionnaire and in 2000 they underwent repeat endoscopy. RESULTS: Thirteen subjects developed symptoms during follow up. The incidence of symptoms in H pylori positive subjects was 1.893/100 person-years of follow up and in H pylori negative individuals 0.163/100 person-years of follow up. H pylori infected subjects were significantly more likely to develop symptoms (log rank test, p=0.003) as well as those infected with CagA positive strains (log rank test, p=0.017). The development of symptomatic gastro-oesophageal reflux disease was no different in individuals with and without eradication (odds ratio 0.57 (95% confidence interval 0.26-1.24); p=0.163). CONCLUSIONS: H pylori eradication prevents the development of dyspeptic symptoms and peptic ulcer disease in healthy asymptomatic blood donors and is not associated with an increase in the incidence of symptomatic gastro-oesophageal reflux disease.     

Serum paraoxonase-1 activity in Helicobacter pylori infected subjects

Previous studies have suggested that Helicobacter pylori (H. pylori) infection may play an important role in the process of atherosclerosis. The objective of this study was to investigate serum paraoxonase and arylesterase activities, and lipid hydroperoxide (LOOH) and total thiol (SH) levels along with lipid parameters in H. pylori infected subjects. Fifty-six H. pylori positive subjects and 43 H. pylori negative subjects were enrolled. Serum paraoxonase and arylesterase activities were measured spectrophotometrically. LOOH levels were measured by FOX-2 assay. Serum SH levels, paraoxonase and arylesterase activities were significantly lower in H. pylori positive group than H. pylori negative group (all p<0.05), while LOOH levels were significantly higher (p<0.05). In H. pylori positive subjects, serum LOOH levels were correlated with SH levels (r=-0.247, p<0.05), serum paraoxonase (r=-0.432, p<0.05) and arylesterase activities (r=-0.404, p<0.001), and triglyceride (r=0.305, p<0.05), total cholesterol (r=0.568, p<0.05), high-density lipoprotein-cholesterol (HDL-C) (r=-0.300, p<0.05) and low-density lipoprotein-cholesterol (LDL-C) (r=0.577, p<0.05) levels. Serum paraoxonase and arylesterase activities were also correlated with HDL-C levels (r=0.221, p<0.05 and r=0.291, p<0.05, respectively), while no correlation was observed with triglyceride, total cholesterol and LDL-C levels (both p>0.05). In conclusion, paraoxonase and arylesterase activities decrease significantly in H. pylori infected subjects. Lower serum paraoxonase-1 (PON1) activity seems to be related to decrease in HDL-C and, in part, to increased oxidative stress and inflammatory condition induced by H. pylori infection. Measurement of serum PON1 activity may help in the early identification of H. pylori infected subjects with increased risk of atherosclerotic disease.     

Helicobacter pylori anti-CagA antibodies: prevalence in symptomatic and asymptomatic subjects in Turkey.

BACKGROUND: Several reports have shown the prevalence of anti-CagA antibodies to be associated with the development of peptic ulcer diseases, while others have indicated that there is no such association. AIM: To examine the prevalence of antibodies to CagA and other Helicobacter pylori antigens in symptomatic and asymptomatic subjects in Turkey. subjects and Methods: Sixty-six symptomatic subjects, 16 to 74 years of age, were examined for H pylori by biopsy-based tests and ELISA. One hundred nineteen asymptomatic subjects, 20 to 65 years of age, were also tested serologically for the presence of H pylori. Samples from both groups that were found to be positive for H pylori by ELISA were then tested by immunoblotting. RESULTS: Fifty-four (82%) symptomatic subjects and 76 (64%) asymptomatic subjects were found to be H pylori-positive by ELISA. Samples from 30 symptomatic subjects who were found to be H pylori-positive by ELISA were analyzed by immunoblotting. Antibodies to CagA (116 kDa) antigen were detected in immunoblots of 11 of 14 (79%) with chronic gastritis, 12 of 13 (92%) with duodenal ulcer and three of three (100%) with gastric cancer. Antigens of the following molecular weights were also detected in these 30 subjects: 89 kDa (VacA) in 21 (70%), 37 kDa in 21 (70%), 35 kDa in 19 (63%), 30 kDa in 27 (90%) and 19.5 kDa in 19 (63%). Immunoblots of 40 ELISA-positive asymptomatic subjects showed that 33 (83%) had antibodies to CagA antigen, 26 (65%) to VacA antigen, 30 (75%) to a 37 kDa antigen, 30 (75%) to a 35 kDa antigen, 39 (98%) to a 30 kDa antigen and 36 (90%) to a 19.5 kDa antigen. CONCLUSIONS: Antibodies to CagA antigen were prevalent in both groups, regardless of the presence of gastroduodenal disease.     

Age dependent hypergastrinaemia in children with Helicobacter pylori gastritis--evidence of early acquisition of infection.

Acute Helicobacter pylori associated gastritis causes achlorhydria, a powerful stimulus to gastrin secretion. If H pylori infection is acquired primarily in early childhood, then the degree of hypergastrinaemia in seropositive children should be age dependent. Anti-Helicobacter antibodies and fasting gastrin concentrations were measured in 439 children aged 4 to 13 years attending hospital for routine day case surgery not connected with any gastrointestinal disorder. Thirty per cent were seropositive for H pylori. There was an inverse relationship between the fasting gastrin concentration and age; the mean fasting gastrin in children aged 4-5 years, 155 ng/l, was significantly higher than that seen in children aged 12-13 years, 90 ng/l. The more noticeable hypergastrinaemia seen in young children with H pylori associated gastritis may reflect achlorhydria associated with acute H pylori infection and suggests that this is primarily acquired in early childhood.     

Sero-prevalence of Helicobacter pylori infection among asymptomatic healthy Omani blood donors

Objective

To investigate the prevalence of Helicobacter pylori (H. pylori) infection, a cross-sectional epidemiological study, based on the age and gender-specific seroprevalence of H. pylori antibodies in asymptomatic healthy Omani blood donors attending the SQUH blood bank.

Methods

Analysis of the sera from 133 apparently healthy subjects, based on the serological determination of the IgM, IgG and IgA antibodies against H. pylori, was carried out using a commercially available kit ELISA (NovaLisa, NovaTec, Germany). While the presence of H. pylori-specific IgG antibodies is the marker for a “chronic” infection with this pathogen. Therefore, there was no indicator of the time of acquisition of the infection. However, the H. pylori-specific IgM antibody was a more specific marker for a recently acquired infection with H. pylori.

Results

Of the 133 subjects, there were 100 (74%) males and 33 (26%) females. The age range was 15 to 50 years with a mean of 25.75±3.75 years. The overall prevalence of H. pylori infection in our study was 69.5%. The overall seroprevalence was found to be increased 69%-86% with age. Subjects between 15–20 years of age showed 71% seroprevalence, while those between 21–40 years showed gradual increase (63%–70%) with age and reached up to 87% in subjects between 41–50 years of age. A significant inverse association was found between sex and age groups. This is when each age group was examined individually; a higher positive percentage of H. pylori antibodies increasing with age was seen in males between 21–40 years of age group in comparison to the females of the same age group. Male subjects with age group between 21 to 40 years were found to have a significant seropositivity compared to the female subjects within the same group. This may reflect how frequent were the male subjects being exposed to the outer environment and their conduct than the females in this society like Oman.

Conclusions

The seropositivity of H. pylori is moderately higher between ages of 21 to 30 more than any other age group.     

Frequency of Helicobacter pylori and gastritis in healthy subjects without gastrointestinal symptoms.

To investigate the frequency of Helicobacter pylori and gastritis in asymptomatic adults, 30 healthy volunteers underwent upper endoscopy. Biopsy specimens were obtained from the corporeal and antral mucosa of the stomach. The specimens were examined by light microscopy for gastritis and the occurrence of H. pylori. In 12 subjects signs of gastritis were noted at endoscopy, but only in 7 of them was this diagnosis confirmed histologically. No other abnormalities were observed by the endoscopist. Histologic examination was normal in 17 subjects, but in 13 subjects (43%) inflammation was found in the gastric specimens. Ten had inflammation both in the corpus and in the prepyloric specimens, and in six of these subjects H. pylori was discovered. H. pylori was only found in subjects with inflammation in both the corpus and the antrum. Subjects with gastritis were slightly older than subjects with normal gastric mucosa (median age, 47 versus 37 years; not significant). In the group of subjects with gastritis, persons with H. pylori were older than those without (median age, 53.5 versus 36 years; p = 0.05). The results of our study indicate that gastritis is present before colonization with H. pylori occurs. This could imply that H. pylori is not the cause of gastritis but that the presence of gastritis is a prerequisite for colonization of the bacterium in the stomach.     

Eradicating Helicobacter pylori reduces hypergastrinaemia during long term omeprazole treatment

Background—Both proton pump inhibitor drugtreatment and Helicobacter pylori infection causehypergastrinaemia in man.
Aims—To determine whether eradicating Hpylori is a means of reducing hypergastrinaemia duringsubsequent proton pump inhibitor treatment.
Methods—Patients with H pylori wererandomised to treatment with either anti-H pylori orsymptomatic treatment. One month later, all received four weekstreatment with omeprazole 40 mg/day for one month followed by 20 mg/dayfor six months. Serum gastrin concentrations were measured before andfollowing each treatment.
Results—In the patients randomised toanti-H pylori treatment, eradication of the infectionlowered median fasting gastrin by 48% and meal stimulated gastrin by46%. When gastrin concentrations one month following anti-Hpylori/symptomatic treatment were used as baseline,omeprazole treatment produced a similar percentage increase in serumgastrin in the H pylori infected and H pylori eradicated patients. Consequently, in the patients in which H pylori was not eradicated, median fasting gastrin concentration was 38 ng/l (range 26-86) at initial presentation and increased to 64 ng/l (range 29-271) after seven months omeprazole, representing amedian increase of 68% (p<0.005). In contrast, in the patients randomised to H pylori eradication, median fasting gastrinat initial presentation was 54 ng/l (range 17-226) and was unchanged after seven months omeprazole at 38 ng/l (range 17-95).
Conclusion—Eradicating H pylori is ameans of reducing the rise in gastrin during subsequent long termomeprazole treatment. In view of the potential deleterious effects ofhypergastrinaemia it may be appropriate to render patients Hpylori negative prior to commencing long term proton pumpinhibitor treatment.

Keywords:hypergastrinaemia; Helicobacter pylori; omeprazole

     

Helicobacter pylori seropositivity in subjects with acute myocardial infarction.

OBJECTIVE: To determine whether Helicobacter pylori infection increases the risk of myocardial infarction. DESIGN: Case-control study. SETTING: University teaching hospital. METHODS: Serological evidence of H pylori infection was determined in 342 consecutive patients with acute myocardial infarction admitted into the coronary care unit and in 236 population-based controls recruited from visitors to patients on medical and surgical wards. RESULTS: 206/342 (60.2%) of cases were H pylori positive compared with 132/236 (55.9%) of controls (P = 0.30). Age and sex stratified odds ratio for myocardial infarction associated with H pylori seropositivity was 1.05 (95% CI 0.7 to 1.53, P = 0.87) and this remained non-significant (P = 0.46) when other risk factors for ischaemic heart disease were taken into account using logistic regression analysis. H pylori seropositivity was not associated with several coronary risk factors in either cases or controls. CONCLUSION: No increase was found in H pylori seropositivity in subjects with acute myocardial infarction. This suggests that previous H pylori infection is not a major risk factor for acute myocardial infarction.     

Helicobacter pylori related hypergastrinaemia is the result of a selective increase in gastrin 17.

Helicobacter pylori infection increases the serum concentration of gastrin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylori. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that > 90% of the circulating gastrin consisted of gastrin (G) 17 and G34 both before and after eradicating the infection. The basal median total immunoreactive gastrin concentration fell from 26 pmol/l (range 11-43) to 19 pmol/l (8-39) (p < 0.05), entirely because of a fall in G17 from 6 pmol/l (< 2.4-25) to < 2.4 pmol/l (< 2.4-23) (p < 0.001). The median (range) basal G34 values were similar before (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The median total immunoreactive gastrin concentration determined 20 minutes postprandially fell from 59 pmol/l (38-114) to 33 pmol/l (19-88) (p < 0.005), and again this was entirely the result of a fall in G17 from 43 pmol/l (9-95) to 17 pmol/l (< 2.4-52) (p < 0.001). The median postprandial G34 values were similar before (13 pmol/l, range 6-42) and after (15 pmol/l, range 6-30) eradication. Eating stimulated a noticeable rise in G17 but little change in G34, both in the presence and absence of H pylori. The finding that H pylori infection selectively increases G17 explains why the infection causes mainly postprandial hypergastrinaemia. G17 is increased selectively because H pylori predominantly affects the antral mucosa which is the main source of G17 whereas G34 is mainly duodenal in origin. This study also indicates that the increased concentration of gastrin in H pylori infection is the result of an increase in one of the main biologically active forms of the hormone.     

Association of Helicobacter pylori infection with systemic inflammation and endothelial dysfunction in healthy male subjects

OBJECTIVES: The goal of the present study was to determine whether seropositivity to Helicobacter pylori (HP), Chlamydia pneumoniae (CP), and cytomegalovirus (CMV) is associated with systemic inflammation and endothelial dysfunction in healthy male subjects. BACKGROUND: Chronic infection with certain bacteria and viruses may play an important role in inflammation as the pathogenesis of atherosclerosis. METHODS: The serum levels of immunoglobulin G antibodies to HP, CP, CMV, high-sensitivity C-reactive protein, soluble intercellular adhesion molecule-1, and soluble vascular cell adhesion molecule-1 were determined in 81 healthy Japanese men (40 +/- 10 years of age). High-frequency ultrasonographic imaging of the brachial artery was used to study endothelium-dependent (flow-mediated vasodilation) and endothelium-independent (nitroglycerin-induced) vasodilation. RESULTS: Prevalences of seropositive antibodies to HP, CP, and CMV were 67.9%, 61.7%, and 56.8%, respectively. Infection with HP, CP, or CMV had no relationship with age, blood pressure, or level of serum glucose, lipid, or soluble vascular cell adhesion molecule-1. The levels of C-reactive protein and soluble intercellular adhesion molecule-1 were significantly higher, and flow-mediated vasodilation was significantly lower in subjects with seropositive antibodies to HP than in subjects with seronegative antibodies to HP. Endothelium-independent vasodilation was similar in both groups. CONCLUSIONS: Chronic infection with HP may be involved in the development of the atherosclerosis via endothelial dysfunction and systemic and vascular inflammation.     

Helicobacter pylori infection in Chinese subjects with type 2 diabetes.

The relationship between diabetes and Helicobacter pylori (HP) infection is controversial. In this study, we examined the possible relationship between HP infection and type 2 diabetes in Chinese subjects. Sixty-three Chinese type 2 diabetic patients (mean age +/- SD: 49.9 +/- 12.0 years; range: 17-76 years) were recruited irrespective of the duration of diabetes or type of therapy. Twenty-nine (46%) of them had upper gastrointestinal symptoms and the other 34 (54%) did not. Another 55 age- and sex-matched non-diabetic subjects (mean age +/- SD: 45.6 +/- 15.6 years, p=0.098; range 18-79 years) with dyspepsia indicated for upper endoscopy were recruited as a comparison group. Upper endoscopy was performed with antral mucosal biopsy specimens taken for rapid urease test (CLO test). HP infection was considered to be present if the rapid urease test was positive. The rates of HP infection of the diabetic and non-diabetic individuals were 50.8% and 56.4% respectively (p: NS). The rate of HP infection was similar between the 2 groups of diabetic patients with or without gastrointestinal symptoms (42.9% vs. 56.3%, p: NS). Using logistic regression analysis (forward stepwise) with age, sex, glycaemic control, duration of diabetes and upper gastrointestinal symptoms as independent variables to predict the risk of HP infection in diabetic patients, none of the parameters enter into the model. In conclusion, the rate of HP infection in Hong Kong Chinese subjects with type 2 diabetes is around 50%, which is similar to control subjects. No association was found between HP infection, glycaemic status, and duration of diabetes and upper gastrointestinal symptoms in these diabetic subjects.     

Serum pepsinogen II levels are doubled with Helicobacter pylori infection in an asymptomatic population of 40,383 Chinese subjects

Pepsinogen (PG) I and II are crucial in the gastric digestive processes. This study is to examine the relationship of serum PGI, PGII, and PGI/PGII ratio with Helicobacter pylori (Hp) infection, age, sex, and body mass index (BMI) in subjects in Beijing, China.A total of 40,383 asymptomatic subjects, who underwent medical examination in Beijing Rehabilitation Hospital, were included in this study. Serum PG levels were measured using chemoluminescence techniques. The age, sex, and BMI data were collected, and Hp infection was identified with ¹³C-urea breath test. Statistical analysis was conducted with Python, Pandas and Seaborn software.Asymptomatic subjects with Hp infection (Hp+) had a significantly higher level of PGI in the serum (111 ng/mL [median]) than those without Hp infection (Hp−) (94 ng/mL, P < .001). The asymptomatic Hp+ subjects had 2-fold higher PGII levels (7.2 ng/mL) than Hp− subjects (3.2 ng/mL, P < .001). These changes produced significantly lower PGI/II ratio in Hp+ patients than in Hp− subjects (16:30, P < .001). The serum PGI and PGII levels were higher in males than in females (PGI: 104 ng/mL vs 95 ng/mL, PGII: 4.3 ng/mL vs 3.7 ng/mL, both P < .001), PGI/II ratio of males is at 95% of that in females (P < .001). PGI and PGII levels gradually increased in older people (P < .001), whereas the PGI/II ratio decreased significantly with age (P < .001). The levels of the two serum PGs were decreased and the ratio increased when BMI were higher than 28 kg/cm² (P < .05).The levels of serum PGI, especial PGII, were increased by Hp infection, and also influenced by age, sex, and BMI. Therefore, these influencing factors should be considered during clinical practice.     

Dental caries is common in Finnish children infected with Helicobacter pylori.

Childhood factors such as low socioeconomic status are risk factors for Helicobacter pylori infection and Streptococcus mutans-related dental caries. We examined whether H. pylori infection and dental caries are present today in the same group of children examined previously. We reviewed the public dental health service files of 21 H. pylori-positive children (upper gastrointestinal endoscopy at a median age of 13.5 y) and 27 H. pylori-negative children (endoscopy at a median age of 12.5 y) examined during 1995-98 at the Helsinki University Central Hospital, Finland. All H. pylori-positive children had experienced dental caries in their primary or permanent teeth or in both whereas among H. pylori-negative children the respective proportion was 70% (p < 0.01). At the age of 7 y, 18% (3/17) of the H. pylori-positive children had experienced caries in permanent teeth as compared to 0% among H. pylori-negative children (0/24; p < 0.05). At the age of 12 y, H. pylori-positive children had more decayed, missing or filled permanent teeth than H. pylori-negative children (80% vs. 38%; p < 0.05). Although a causal relationship between H. pylori and dental caries is unlikely, it is possible that H. pylori-infected children have an increased risk of other health problems, such as dental caries, for which proper treatment is needed.     

Indistinguishable cellular changes in gastric mucosa between Helicobacter pylori infected asymptomatic tribal and duodenal ulcer patients

AIM： To investigate the changing pattern of different histological parameters occurring in the stomach tissue of Helicobacter pylori （H pylori） infected tribal populations and duodenal ulcer patients among ethnic Bengalis and correlation of the genotypes of H pylori with different histological parameters. METHODS： One hundred and twelve adult individuals were enrolled into this study between 2002 and 2004. Among them, 72 had clinical features of duodenal ulcer （DU） from ethnic Bengali population and 40 were asymptomatic ethnic tribals. Endoscopic gastric biopsy samples were processed for histology, genotyping and rapid urease test. Histologically, haematoxylin and eosin staining was applied to assess the pathomorphological changes and a modified Giemsa staining was used for better detection of Hpylori. For intestinal metaplasia, special stainings, i.e. Alcian blue periodic acid-Schiff and high iron diamine-Alcian blue staining, were performed. PCR was performed on bacterial DNA to characterize the presence or absence of virulence-associated genes, like cagA, and distribution of different alleles of vacA and iceA. RESULTS： Intraglandular neutrophil infiltration, a hallmark of activity of gastritis, was present in 34 （94%） of tribals （TRs） and 42 （84%） of DU individuals infected with H pylori. Lymphoid follicles and aggregates, which are important landmarks in H pylori infection, were positive amongst 15 （41%） of TRs and 20 （40%） of DU subjects. Atrophic changes were observed in 60% and 27.7%, respectively, among DU cases and tribals （P 〉 0.003）. Metaplastic changes were detected in low numbers in both groups. Moderate to severe density distribution of Hpylori in the gastric mucosa was 63% among TRs, whereas it was 62% in DU subjects. There were no significant differences in the distribution of virulence-associated genes like cagA, vacA and iceA of H pylori strains carried by these two populations. CONCLUSION： Our study showed almost similar distribution of inflammatory cells among asymptomatic tribals and DU Bengali patients. Interestingly, the tribal population are free from any clinical symptoms despite evidence of active histologic gastritis and infection with Hpylori strains carrying similar virulence markers as of strains isolated from patients with DU. There was an increased cellular response, especially in terms of neutrophil infiltration, but much lower risk of developing atrophy and metaplastic changes among the tribal population.