Helicobacter pylori Infection Reduces Intraluminal Nitric Oxide

Background: Nitric oxide (NO) plays an important role in gastrointestinal mucosal protection. We have previously shown that Helicobacter pylori infection is associated with a lower concentration of NO in the human stomach. The aim of this study is to explore the pathogenesis of this finding using an animal model. Methods: Mongolian gerbils were divided into four groups: H. pylori-negative and -positive, each with and without the intraperitoneal addition of superoxide dismutase (SOD). Intraluminal NO and serum nitrate were measured by using a chemiluminescence system. Inducible nitric oxide synthase (iNOS) levels in gastric mucosa were measured by using the NOSdetect Assay Kit. Results: iNOS levels in H. pylori-positive gerbils were significantly greater than in those without infection. Intraluminal NO levels in H. pylori-positive gerbils were significantly lower than those in H. pylori-negative ones and increased after SOD administration. Serum nitrate levels in H. pylori-positive gerbils were significantly greater than those in H. pylori negative ones and decreased after SOD administration. Conclusions: The low level of NO in the gastric lumen in H. pylori infection is likely a result of superoxide production related to H. pylori-induced inflammation.     

Intragastric nitric oxide/nitrite in Helicobacter pylori-infected subjects

BACKGROUND: Nitrite (NO2-) in swallowed saliva is reduced to nitric oxide (NO) and other nitrogen oxides by the intragastric acidity. This mechanism is probably important for the intragastric clearance of ingested micro-organisms and nitrosating compounds. The study examines the balance between intragastric NO and NO2- in relation to endogenous acid production and infection with Helicobacter pylori. METHODS: Six healthy H. pylori-negative and six H. pylori-positive volunteers with no known gastroduodenal pathology were examined after an overnight fast. Gastric NO was measured using a chemiluminescence technique and pH as well as NO2- were analysed in gastric aspirates. RESULTS: Gastric NO was slightly lower in H. pylori-positive subjects (1560 +/- 211 ppb) than in uninfected controls (2112 +/- 430 ppb; P > 0.05) during basal conditions, whereas both pH and NO2- concentration were similar in the two groups. During inhibition of acid secretion (omeprazole 20 mg b.i.d. over 5 days) median pH and mean NO2- concentration in gastric aspirates were significantly higher in H. pylori positives than in the controls. Furthermore, during omeprazole treatment the intragastric NO levels were almost absent in H. pylori positives, whereas approximately 50% remained in H. pylori-negative individuals. CONCLUSION: Proton-pump inhibition in H. pylori-infected individuals abolishes the intragastric chemical reduction of swallowed NO2- in the fasting stomach.     

H. pylori decreases gastric mucin synthesis via inhibition of galactosyltransferase

BACKGROUND/AIMS: Alterations of gastric mucin have been postulated as important pathogenic properties of Helicobacter pylori. In this study, we investigated gastric mucin synthesis in H. pylori-infected gastric mucosa by measuring UDP-galactosyltransferase activity, a key enzyme for the synthesis of mucin, and the amount of intracellular mucin in the gastric mucosa. METHODOLOGY: Gastric biopsy specimens were obtained from thirty-seven patients (20 H. pylori-positive and 17 H. pylori-negative). UDP-galactosyltransferase activity of the biopsy specimens was measured by an assay system we had developed, using a peanut agglutinin lectin. The amount of intracellular mucin in the gastric epithelial cells was analyzed by measuring the cells' periodic acid-Schiff-alcian blue staining-positive substances. RESULTS: UDP-galactosyltransferase activities in the antral mucosa, but not in the body mucosa, of H. pylori-positive patients were significantly lower than those of H. pylori-negative patients (p < 0.05). The amount of intracellular mucin in antral epithelial cells of H. pylori-positive patients was significantly lower than that of H. pylori-negative patients (p < 0.01). CONCLUSIONS: These findings suggest that H. pylori infection decreases gastric mucin synthesis via inhibition of UDP-galactosyltransferase. This effect may impair the gastric mucosal barrier and contribute to the mucosal injury induced by H. pylori infection.     

Helicobacter pylori infection influences tumor growth of human gastric carcinomas

BACKGROUND: Helicobacter pylori infection is considered a risk factor for gastric carcinoma. However, the effect of eradication therapy in gastric carcinoma patients is not well known. The aim of this study was to investigate the relationship between H. pylori infection and tumor growth of gastric carcinoma. METHODS: Fifty-one patients with gastric carcinoma participated in the study. Thirty-three were H. pylori-positive, 6 were H. pylori-negative, and 12 were diagnosed with gastric carcinoma after eradication of H. pylori. To investigate tumor growth of gastric carcinoma, cell proliferation and angiogenesis of the tumors were evaluated by immunohistochemical techniques using Ki-67 and CD34. RESULTS: The Ki-67 labeling index was 47.9 +/- 2.6 (mean +/- s) in the H. pylori-positive group, 38.1 +/- 3.6 in the H. pylori-eradicated group, and 22.2 +/- 5.5 in the H. pylori-negative group. It was significantly lower in the H. pylori-eradicated and H. pylori-negative groups than in the H. pylori-positive one, and a significant difference was also found between the H. pylori-positive and H. pylori-eradicated groups. The microvessel counts were 62.5 +/- 3.0, 50.2 +/- 4.0, and 66.0 +/- 9.8 in the positive, eradicated, and negative groups, respectively. A significant difference was found between the H. pylori-positive and H. pylori-eradicated groups. CONCLUSION: Our results suggest that H. pylori infection is associated with cell proliferation, and its eradication may influence tumor vascularity of gastric carcinoma. Therefore, H. pylori eradication therapy may contribute to the suppression of tumor growth.     

Gastric acid secretion of normal Japanese subjects in relation to Helicobacter pylori infection, aging, and gender

BACKGROUND: In Japan, where the incidence of gastric cancer is high, Helicobacter pylori infection could affect gastric acid secretion differently from that in Western countries. The aim of this study was to investigate the relationship between H. pylori infection, acid secretion, aging, and gender in normal Japanese subjects. METHODS: The study comprised 193 Japanese subjects who had undergone routine endoscopy. Gastrin-stimulated acid output was performed during the routine endoscopic examination using the endoscopic method of gastric acid secretory testing (EGT: endoscopic gastrin test), which has been reported previously. H. pylori status was determined by histology, rapid urease test, and serology. RESULTS: Mean EGT values were 3.9 +/- 1.5 mEq/10 min in H. pylori-negative men, 1.6 +/- 2.5 in H. pylori-positive men, 2.2 +/- 0.9 in H. pylori-negative women, and 1.5 +/- 1.2 in H. pylori-positive women. Although acid secretion was lower in H. pylori-positive subjects compared with H. pylori-negative subjects in both men and women, the decrease was more marked in men with H. pylori infection. Multiple linear regression analysis showed that aging is positively associated with gastric acid secretion in the H. pylori-negative subjects, whereas a negative association was found between them in the H. pylori-positive subjects. CONCLUSIONS: In Japanese subjects, aging affects gastric acid secretion differently depending on the status of H. pylori infection. H. pylori infection showed a stronger inhibitory effect on the acid secretion in men than in women. This gender-related difference in the susceptibility of acid secretion to H. pylori infection may explain the higher rates of gastric cancer in men in Japan.     

Clinical usefulness of serum pepsinogen II in the management of Helicobacter pylori infection

BACKGROUND: Serum pepsinogen II (sPGII) levels are known to increase during Helicobacter pylori infection. AIM: To assess H. pylori infection and success of H. pylori therapy by means of sPGII levels. METHODS: sPGII levels were determined in 156 H. pylori-positive and 157 H. pylori-negative consecutive patients with dyspeptic symptoms. Additionally, sPGII determination was performed in 70 H. pylori-positive patients 2 months after H. pylori eradication therapy. In 29 of these 70 patients, gastroscopy was performed to evaluate the effect of H. pylori therapy on gastric activity. RESULTS: H. pylori-positive subjects demonstrated a significantly higher mean of sPGII levels than H. pylori-negative subjects (16.8 +/- 7.4 vs. 8.6 +/- 3.7 microg/l; p < 0.001). The best sPGII cut-off for predicting H. pylori infection was 9.93 microg/l (sensitivity 83%, specificity 73%). The best cut-off values to evaluate success of therapy were: sPGII of 9.47 microg/l, a sPGII variation level (difference between baseline and after therapy) of 4.54 microg/l, and a sPGII Deltavalue (sPGII variation divided by sPGII before therapy) of 25% (sensitivity 93%, specificity 91%). CONCLUSIONS: sPGII levels may be used as a reliable marker of H. pylori infection in the initial diagnosis as well as to evaluate H. pylori eradication and subsequent changes in gastric inflammation.     

The influence of Helicobacter pylori infection on gastrin and somatostatin values present in serum

BACKGROUND/AIMS: Recent studies on the role of Helicobacter pylori in pathogenesis of duodenal ulcers have focused on the mechanism by which H. pylori infections causes exaggerated gastrin release. METHODOLOGY: We compared the gastrin and somatostatin serum values between two groups of patients; 37 H. pylori-positive ones and 29 H. pylori-negative ones. We applied radioimmunoassay technique to determine the gastrin and somatostatin values in serum. H. pylori was confirmed by urease test and by histopathological color according to Giemsa. RESULTS: The level of gastrin in the serum of Helicobacter pylori-positive patients with chronic gastritis were significantly higher in relation to H. pylori-negative patients. The somatostatin concentration in the sera of H. pylori-positive patients with duodenal ulcer (16.27 +/- 9.49 pg/mL) were less in comparison with those without duodenal ulcer (23.25 +/- 13.59 pg/mL). CONCLUSIONS: The results suggest that H. pylori infection suppresses the somatostatin secretion.     

Gastric electrical activity and gastrointestinal hormones in dyspeptic patients

AIMS: To explore the patterns of gastric electrical activity, gastric emptying and gastrointestinal hormones in dyspeptic patients and relate them to Helicobacter pylori status. METHODS: Twenty-two patients with functional dyspepsia and 29 healthy volunteers underwent cutaneous electrogastrography and dynamic ultrasound before and after a test meal. All dyspeptic patients underwent endoscopy and biopsy; all subjects were examined for the presence of antibodies to H. pylori, and the plasma levels of gastrin, neurotensin, cholecystokinin, and pancreatic polypeptide were measured. RESULTS: The area under the curve (AUC) of the normal slow wave percentage was lower in dyspeptic patients than controls (Kruskal-Wallis p = 0.016; Dunn's test: H. pylori-positive patients: 21,235.5 [19,101.0-22,688.8] vs. H. pylori-negative controls: 22,532.0 [20,133.0-23,755.0], p < 0.05). The AUC of the tachygastria percentage was higher in dyspeptic patients than controls (p = 0.0001; H. pylori-positive patients: 2,173.5 [325.8-3,055.3] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05; H. pylori-negative patients: 1,843.0 [1,107.0-4,277.0] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05). The AUC of gastrin was higher in H. pylori-positive than H. pylori-negative subjects (p = 0.0002; H. pylori-positive patients: 16,146.5 [11,368.8-33,141.7] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05; H. pylori-positive controls: 20,250.0 [12,070.0-64,430.0] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05). In the total group of dyspeptic patients and in the H. pylori-positive patients, a negative correlation was found between the AUC of neurotensin and the total score for postprandial fullness (dyspeptic patients r = -0.51, p = 0.01; H. pylori-positive patients r = -0.66, p = 0.02). CONCLUSIONS: In dyspeptic patients, alterations in gastric electrical activity were not related to H. pylori infection. Nevertheless, H. pylori infection induces higher gastrin levels in both patients and asymptomatic subjects.     

Helicobacter pylori infection upregulates endothelial nitric oxide synthase expression and induces angiogenesis in gastric mucosa of dyspeptic patients

BACKGROUND: Helicobacter pylori (H. pylori) infection induces nitric acid (NO) overproduction through inducible NO synthase (NOS) expression, subsequent DNA damage and enhanced antiapoptosis signal transduction sequence in the human gastric mucosa, whereas its possible effect on endothelial nitric oxide synthase (eNOS) expression has not as yet been investigated. The aim of this study was to evaluate the effect of H. pylori infection in the expression of eNOS in gastric mucosa. PATIENTS AND METHODS: We prospectively studied 30 nonsmoking dyspeptic patients (12 men, 18 women, mean age 54.26+/-12.89 years). The diagnosis of H. pylori infection was based mainly on histology. The histological grading of H. pylori infection was evaluated according to the modified Sydney classification. Histological grading of eNOS expression and microvessel density as estimated by CD34 expression were determined by immunohistochemistry (degree 0-3) and correlated with H. pylori infection and histological degree of gastritis. RESULTS: Twelve patients were H. pylori-positive and 18 patients were H. pylori-negative. The two groups were matched for age (P=0.139), sex (P=0.342) and similar degree of gastritis. Intensity of eNOS and CD34 expression in the corpus and antrum were significantly correlated (P<0.001). eNOS expression was correlated with H. pylori infection in the mucosa of the body and antrum (P=0.013 and 0.037, respectively) but not with gastric inflammation and activity (P=0.848 and 0.871, respectively, for the corpus and P=0.565 and 0.793, respectively, for the antrum). H. pylori-positive patients showed higher expression of CD34-positive blood vessels in the mucosa of the antrum (P=0.048). CD34 expression was correlated with gastric inflammation and activity (P=0.03 and 0.044, respectively) in the mucosa of the antrum of H. pylori-positive patients. CONCLUSION: H. pylori infection upregulates eNOS, and induces angiogenesis, contributing to H. pylori-associated pathophysiology in gastric mucosa.     

Prevalence of Helicobacter pylori infection, endoscopic gastric findings and dyspeptic symptoms among a young Japanese population born in the 1970s

BACKGROUND: With the prevalence of Helicobacter pylori (H. pylori) infection rapidly decreasing in Japan, endoscopic findings and dyspeptic symptoms need to be re-evaluated. METHODS: In a health check-up program, endoscopy was performed on 530 young Japanese subjects (371 men and 159 women) born in the 1970s. Helicobacter pylori infection was evaluated using serology and a rapid urease test. Endoscopic gastritis was classified according to the Sydney classification system, in addition to nodular gastritis. Dyspeptic symptoms were also recorded before endoscopy. RESULTS: Of the 530 subjects, 87 (16.4%) were H. pylori positive. Of the 443 H. pylori-negative subjects, 349 (78.8%) were considered to have endoscopically normal gastric mucosa. However, of the 87 H. pylori-positive subjects, only 19 (21.8%) tested normal (P < 0.001). The prevalence of several types of gastritis was significantly higher in H. pylori-positive subjects compared with H. pylori-negative subjects: atrophic gastritis (37.9% vs 1.1%, P < 0.001), flat erosive gastritis (29.9% vs 7.2%, P < 0.001), rugal hyperplastic gastritis (12.6% vs 0.0%, P < 0.001), and nodular gastritis (13.8% vs 0.0%, P < 0.001). Other types of gastritis were not related to H. pylori status. The prevalence of subjects with dyspeptic symptoms was significantly higher in H. pylori-positive subjects compared with H. pylori-negative ones (28.7% vs 6.5%, P < 0.001). CONCLUSION: It is suggested that in consideration of its recent low prevalence and the slow increase in its infection, the prevalence of H. pylori-related gastritis will gradually decrease in Japan. Further studies will be required to ascertain if there is a need for H. pylori eradication in this young population.     

Effects of Helicobacter pylori Infection on gastric mucin expression

AIMS: This study was performed to determine the gastric distributions of MUC5AC and MUC6 depending on Helicobacter pylori (H. pylori) infection, and to evaluate whether the expressions of MUC5 and MUC6 change in H. pylori-associated gastroduodenal diseases. In addition, MUC5AC and MUC6 expressional changes were investigated before and after H. pylori eradication. METHODS: In the 224 individuals (136 H. pylori-positive and 88 H. pylori-negative) who came from control (N=48), duodenal ulcer (N=35), benign gastric ulcer (N=61), dysplasia plus stomach cancer (N=80) groups, MUC5AC and MUC6 expressions were determined by immunohistochemical staining in the antrum and body, respectively. This staining for MUC5AC and MUC6 were reperformed in 113 of the 136 H. pylori-positive patients after successful H. pylori eradication by proton pump inhibitor-based triple therapy. RESULTS: (1) No difference was found between the H. pylori-positive and negative groups in terms of MUC5AC expression. In contrast, MUC6 expression was significantly lower in the H. pylori-positive group than in the H. pylori-negative group in the gastric body. Moreover, reduced MUC6 expression increased to the H. pylori-negative level after eradication. (2) Expressions of MUC5AC and MUC6 were significantly lower in the dysplasia plus cancer group than those of control in case of H. pylori positive. Similarly, MUC5AC and MUC6 expressions were significantly lower in the presence of atrophic gastritis with intestinal metaplasia in case of H. pylori positive. (3) Aberrant expressions of MUC6 in foveolar cells were observed in both antrum (11.3%) and body (5.3%) only in the H. pylori-positive group, but this reverted to normal after H. pylori eradication. CONCLUSION: These results suggest that H. pylori infection causes alterations of mucin expression, closely related with the development of gastric atrophy with intestinal metaplasia, probably contributing to carcinogenesis.     

Apoptosis, proliferation and p53 gene expression of H. pylori associated gastric epithelial lesions

AIM:To study the relationship between Helicobacter pylori(H.pylori)and gaatric carcinoma and its possiblepathogenesis by H.pylori.METHODS:DNEL technique and immunohistochemicaltechnique were used to study the state of apoptosis,proliferation and p53 gone expression.A total of 100 gastricmucosal biopsy specimens,including 20 normal mucosa,30H.pylori-negative and 30 H.pylori-positive gastricprecancerous lesions along with 20 gastric carcinomas werestudied.RESULTS:There were several apoptotic cells in thesuperficial epithelium and a few proliferative cells within theneck of gestric glands,and no p53 protein expression innormal mucosa.In gestric carcinoma,there ware fewapoptotic cells,while there were a large number ofproliferative cells,and expression of p53 proteinsignificantly was increased.In the phase of metaplasia,theapoptotic index(Al,4.36%±1.95%),proliferative index(Pl,19.11%±6.79%)and positivity of p53 expression(46.7%)in H.pylori-positive group ware higher than thosein normal mucosa(P<0.01).Al in H.pylori-positive groupwas higher than that in H.pylori-negative group(3.81%±1.76%),Pl in H.pylori-positive group was higher than thatin H.pylori-negative group(12.23%±5.63%,P<0.01).Inthe phase of dysplasia,Al(2.31%±1.10%) in H.pylori-positive group was lower(3.05%±1.29%)than that in H.pylori-negative group,but Pl(33.89%±11.65%)wassignificantly higher(22.09±8018%,P<0.01).In phases ofmetaplasia,dysplasia and gastric cancer in the H.pylori-positive group,Als had an evidently greduall decreasingtrend(P<0.01),while Pls had an evidently gradualincreasing trend(P<0.05 or P<0.01),and there was alsoa trend of gradual increase in the expression of p53 gone.CONCLUSION:In the course of the formation of gastriccarcinoma,proliferation of gastric mucosa can be greatlyIncreased by H.pylori,and H.pylori can induce apoptosisin the phase of metaplasia,but in the phase of dysplesia H.pylorl can inhibit cellular apptosis.And H.pylori infectioncan strengthen the expression of mutated p53 gene.     

Direct measurement of gastric H^＋／K^＋-ATPase activities in patients with or without Helicobacterpylori-associated chronic gastritis

AIM: The role of Helicobacter pylori (H pylori) infection in gastric acid secretion of patients with chronic gastritis remains controversial. This study was designed to elucidate the effect of H pylori on H+/K+-ATPase activities in gastric biopsy specimens. METHODS: Eighty-two patients with chronic gastritis who had undergone upper endoscopy were included in this study. H pylori infection was confirmed by rapid urease test and histology. Gastric H+/K+-ATPase activities and serum gastrin concentrations were measured by an enzymatic method and radioimmunoassay, respectively. For those patients who received triple therapy for eradicating H pylori, changes in the activity of gastric H+/K+-ATPase and serum gastrin levels were also measured. RESULTS: The mean gastric H+/K+-ATPase activity in Hpylori-positive group (42 patients) was slightly higher than that in Hpylori-negative group (29 patients) (169.65±52.9 and 161.38±43.85nmol P/(mg·h),respectively, P=0.301). After eradication of H pylori, the gastric H+/K+-ATPase activities slightly decreased compared to prior therapy (165.03±59.50 and 158.42±38.93 nmol P/(mg·h), respectively, P=0.805). The mean basal gastrin concentration was slightly higher in H pylori-positive patients than in H pylori-negative patients (87.92±39.65 pg/mL vs75.04±42.57 pg/mL, P= 0.228). The gastrin levels fell significantly after the eradication of H pylori. (Before treatment 87.00±30.78 pg/mL, after treatment 64.73±18.96 pg/mL, P=0.015). CONCLUSION: Gastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronic gastritis.     

Helicobacter pylori infection in patients with autoimmune thrombocytopenic purpura

AIM: To compare the prevalence of Helicobacter pylori(Hpylori) infection in autoimmune thrombocytopenic purpura (AITP) patients with that of nonthrombocytopenic controls,and to evaluate the efficacy of the treatment in Hpylori(+)and Hpylori(-) AITP patients.METHODS: The prevalence of gastric Hpyloriinfection in 38 adult AITP patients (29 female and 9 male; median age 27 years; range 18-39 years) who consecutively admitted to our clinic was investagated.RESULTS: Hpyloriinfection was found in 26 of 38 AITP patients (68.5%). Hpyloriinfection was found in 15 of 23 control subjects (65.2%). The difference in Hpyloriinfection between the 2 groups was not significant. Thrombocyte count of Hpylori-positive AITP patients was significantly lower than that of Hpylori-negative AITP patients (P＜0.05).Thrombocyte recovery of Hpylori-positive group was less than that of Hpylori-negative group (P＜0.05).CONCLUSION: Hpyloriinfection should be considerecd in the treatment of AITP patients with Hpyloriinfection.     

Transfer of metronidazole to gastric juice: impact of Helicobacter pylori infection and omeprazole

BACKGROUND: The effects of Helicobacter pylori infection associated with inhibition of gastric acid secretion on the distribution of medications used for H. pylori eradication are poorly understood. The aim of this study was to investigate the effects of a 7-day administration of 20 mg omeprazole on the transfer of metronidazole from plasma to the gastric juice of individuals with and without H. pylori infection. METHODS: Fourteen H. pylori-positive and 14 H. pylori-negative male volunteers were enrolled in a study with an open, randomized, two-period crossover design with a 21-day washout period between phases. Plasma, salivary, and gastric juice concentrations of metronidazole in subjects with and without omeprazole treatment were measured with reversed-phase high-performance liquid chromatography/liquid chromatography. RESULTS: Metronidazole peak concentration (Cmax) was similar in plasma and saliva and was approximately threefold higher in gastric juice in all groups. Omeprazole treatment increased gastric pH and did not affect metronidazole Cmax or the time required for this to be reached (tmax) in plasma, saliva, or gastric juice. However, omeprazole significantly reduced metronidazole transfer from plasma to gastric juice in H. pylori-positive but not H. pylori-negative subjects, as shown by statistical analysis of AUC(0-2 h). CONCLUSION: Short-term treatment with omeprazole in H. pylori- positive volunteers reduces the amount of metronidazole transferred from plasma to gastric juice. This seems to occur in a pH-independent form.     

Effect of age and Helicobacter pylori infection on gastric acid secretion

BACKGROUND: Whether gastric acid secretion decreases with age is still controversial. With the discovery of Helicobacter pylori, the association of this bacterium with gastric acid secretion has also been discussed. The aim of this study was to investigate the relationship between gastric acid secretion, age and H. pylori infection. METHODS: The presence of H. pylori infection, the grade of fundic atrophic gastritis (FAG), and gastric acid secretion were investigated in 280 subjects without localized lesions in the upper gastrointestinal tract. Helicobacter pylori infection was confirmed by Giemsa and immunohistochemical staining, and FAG of biopsy specimens was graded on a scale of 0-4. RESULTS: Both basal and maximal acid output decreased with age in H. pylori-positive subjects, while they did not change with age in H. pylori-negative subjects. Gastric acid secretion decreased with the progression of FAG. An age-correlated decrease in gastric acid secretion in H. pylori-positive subjects depended on an increasing prevalence of FAG with age. CONCLUSIONS: In the population studied, advancing age had no influence on gastric acid secretion in H. pylori-negative subjects. Gastric acid secretion decreases with age in H. pylori-positive subjects because of the increasing prevalence of FAG with age.     

Helicobacter pylori infection and increased nitrite synthesis in the stomach: Inflammation and atrophy connections

BACKGROUND: We have previously shown that the nitrite content in the gastric juice of Helicobacter pylori-positive patients is significantly higher than that of H. pylori-negative patients and it decreases after eradication of H. pylori. AIM: To examine the relationship between the nitric oxide synthesis in the gastric lumen and histological findings. METHODS: Eighty-five middle aged Japanese patients were studied. Four specimens, each obtained from the greater and lesser curvature of antrum and gastric body were processed for the determination of histopathological scores using the updated Sydney System. Gastric juice was collected endoscopically to determine the concentration of nitrite using a modified Griess reaction. RESULTS: There was a significant positive correlation between the nitrite and the pH levels (r = 0.81, P < 0.001) and between the pH levels and the histopathological scores in the corpus. The gastric juice pH and concentration of the nitrite increased in patients with histological diagnosis of normal, antral-predominant gastritis, pangastritis and corpus-predominant gastritis in due order. CONCLUSIONS: H. pylori infection effects nitric oxide synthesis in the gastric lumen which is mainly connected with hypoacidity. The gastric juice pH is one of the useful markers for corpus dominant gastritis and probably for high-risk group of gastric cancer.