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.     

Comparison of clinical, serological and histological findings between non-ulcer dyspepsia patients with and without Helicobacter pylori infection

BACKGROUND AND AIMS: The role of Helicobacter pylori (H. pylori) infection in non-ulcer dyspepsia (NUD) remains controversial. This study investigates the clinical, serological and histological differences between patients with H. pylori-positive and -negative NUD. METHODS: One hundred and eighty consecutive patients with NUD were enrolled from January to December 1998. The severity of symptoms was evaluated by the Tucci's scoring system. The histological changes of gastric mucosa were assessed according to the Updated Sydney System, and a fasting blood sample was obtained to test the serum gastrin and pepsinogen I levels. RESULTS: The H. pylori-positive NUD patients were notably older than H. pylori-negative NUD patients (48.2 +/- 15.9 vs 39.8 +/- 15.7 years, P= 0.001). There were no differences in other clinical factors between the two NUD groups. The serum pepsinogen I levels were considerably higher in H. pylori-positive NUD patients than in H. pylori-negative NUD patients (78.9 +/- 42.2 vs 61.5 +/- 43.3 ng/mL, P<0.01). However, no significant differences in serum gastrin levels were discovered between the two groups. The antrum histological scores for chronic inflammation, acute inflammation, gland atrophy and lymphoid follicles were higher in H. pylori-positive NUD patients than in H. pylori-negative NUD patients (2.09 vs 1.01, P<0.001; 1.22 vs 0.36, P<0.001; 0.76 vs 0.36, P<0.01; 0.33 vs 0.13, P<0.01, respectively). CONCLUSIONS: The present study discovered marked differences in age, serum pepsinogen I levels, histological grades of acute inflammation, chronic inflammation, gland atrophy and lymphoid tissue formation between H. pylori-positive and H. pylori-negative NUD patients. Further investigation of the clinical prognosis of the two groups of patients is necessary.     

Effect of Helicobacter pylori eradication on bulbitis and duodenal gastric metaplasia

BACKGROUND/AIMS: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years. METHODOLOGY: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]. RESULTS: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07). CONCLUSIONS: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.     

Bleeding duodenal ulcer: comparison between Helicobacter pylori positive and Helicobacter pylori negative bleeders

BACKGROUND AND AIMS: To provide a direct comparison of Helicobacter pylori-positive subjects bleeding from duodenal ulcer with H. pylori-negative ones, in terms of severity of bleeding and outcome. PATIENTS AND METHODS: A case-control study was prospectively conducted in 105 H. pylori-negative duodenal ulcer bleeders and same number of sex- and age-matched H. pylori-positive ones. RESULTS: NSAID consumption was more common among H. pylori-negative subjects (81%) compared to their H. pylori-positive counterparts (58.1%, P < 0.001). H. pylori-negative bleeders were found to need more often haemostasis (55.2% versus 31.4%, P < 0.001) or surgical intervention (15.2% versus 4.8%, P = 0.011) and to have a greater proportion of rebleeding (32.4% versus 13.3%, P = 0.001), a more prolonged hospitalisation (11.6 +/- 4.1 versus 6.2 +/- 1.5 days, P < 0.001) and a higher rate of in-hospital mortality (15.2% versus 3.8%, P = 0.005). In the overall population (N = 210), H. pylori negativity, among other known risk factors, emerged as independent predictor (odds ratio: 3.2; 95% CI: 1.5, 11.2; P = 0.004) of an unfavourable outcome (surgery or death). CONCLUSIONS: Duodenal ulcer bleeding in H. pylori-negative subjects appears to be more severe, to have a higher rate of rebleeding, and to lead more often to surgery or fatality compared to the vast majority of H. pylori-positive duodenal ulcer bleeders.     

Effect of acid-suppressive therapy on Helicobacter pylori production of interleukin-8 in the gastric mucosa.

BACKGROUND: Recent studies have shown that acid-suppressive therapy increases the severity of Helicobacter pylori- associated gastritis in the corpus. PURPOSE: To evaluate interleukin (IL)-8 production in the gastric corpus mucosa before and during acid-suppressive therapy in H pylori-infected patients. PATIENTS AND METHODS: Ten patients with reflux esophagitis (five H pylori-positive and five H pylori-negative) were treated with omeprazole 20 mg. Serum gastrin concentrations, H pylori colonization density and mucosal IL-8 levels in the corpus were investigated at entry and two weeks after starting therapy. IL-8 levels were measured by ELISA. The organism density was determined, and scored according to area occupied by the bacterial colonies. The presence of H pylori was assessed by rapid urease testing and histological finding of gastric biopsy specimens. RESULTS: In H pylori-positive patients, concentrations of IL-8 during therapy significantly exceeded those before therapy (36.2+/-6. 8 versus 18.3+/-3.8 pg/mg protein; P<0.05) without altering H pylori density. In H pylori-negative patients, IL-8 levels were similar before and during therapy (6.1+/-2.7 versus 6.3+/-3.0 pg/mg protein). Concentrations of gastrin during therapy were significantly higher than those before therapy in all patients. CONCLUSIONS: The results suggest that acid suppression increases mucosal IL-8 levels in H pylori-infected patients with reflux esophagitis.     

Helicobacter pylori infection and serum gastrin, ghrelin and leptin in children of Polish shepherds

OBJECTIVE: Family unit is generally accepted as one of the contributors to Helicobacter pylori infection that is most frequently acquired in childhood, so it seems logical to diagnose and treat this infection in childhood. This study was designed to assess H. pylori prevalence in children from shepherd families having contacts with sheep. MATERIAL AND METHODS: This study involved 146 children (58 M/88 F, age 6-17 years; mean: 10.2 years) from families living in Polish Tatra Mountains with contact (group A, n=58) or without contact with sheep (group B, n=88). H. pylori status was determined by (13)C-urea breath test and was compared to 141 age- and gender-matched urban controls (group C). In both groups of mountain children, the anti-H. pylori and anti-CagA IgG were measured by ELISA and serum gastrin, ghrelin and leptin concentrations by RIA. RESULTS: The H. pylori prevalence in group A was significantly higher (58.6%) than that in group B (21.6%) and urban controls (26%). Serum gastrin concentrations were significantly higher in H. pylori-positive than in H. pylori-negative mountain children (52.2+/-5.8 pmol/L versus 22.7+/-2.1 pmol/L), while serum ghrelin and leptin concentrations were significantly lower in H. pylori-infected (741+/-112 pg/mL and 3.6+/-0.8 ng/mL) than in non-infected children (1323+/-104 pg/mL and 8.6+/-2.4 ng/mL). CONCLUSIONS: Children with sheep contact show about twice higher H. pylori prevalence and higher serum gastrin but lower ghrelin and leptin levels than those without H. pylori infection. Considering almost 100% positive 13C-urea breath test in sheep, it is reasonable to propose that H. pylori infection in shepherd children may originate from sheep and the infection might, therefore, be considered as zoonosis.     

Impact of Helicobacter pylori infection on ghrelin and various neuroendocrine hormones in plasma

AIM: Ghrelin, an endogenous ligand for growth hormone secretagogue receptor, influences appetite, energy balance, gastric motility and acid secretion. The stomach is the main source of circulating ghrelin. There are inconsistent reports on the influence of Helicobacter pylori (H pylori) infection on circulating ghrelin levels. We sought to elucidate the relationship between ghrelin and various peptides in plasma, with special reference to H pylori. METHODS: Plasma ghrelin levels were measured by radioimmunoassay in 89 subjects who were referred for upper gastrointestinal endoscopy, consisting of 42 H pylori infected and 47 uninfected ones. Plasma gastrin, somatostatin, leptin, insulin-like growth hormone 1 (IGF-1) and chromogranin A concentrations were also measured. Twelve patients were treated with anti- H pylori regimen. RESULTS: Ghrelin circulating levels were greatly decreased in H pylori-positive than negative individuals (194.2±90.2 fmol/mL and 250.4±84,1 respectively, P<0.05), but did not significantly alter following the cure of infection (176.5±79.5 vs 191.3±120.4). There was a significant negative correlation between circulating ghrelin and leptin levels, as well as body mass index, for the whole and uninfected population, but not in H pylori-infected patients. Plasma ghrelin concentrations correlated positively with IGF-1 in H pylori-negative group and negatively with chromogranin A in the infected group. There were no significant correlations among circulating levels of ghrelin, gastrin and somatostatin irrespective of H pylori status. CONCLUSION: H pylori infection influences plasma ghrelin dynamics and its interaction with diverse bioactive peptides involved in energy balance, growth and neuroendocrine function.     

Prevalence of Peptic Ulcer in Dyspeptic Patients and the Influence of Age,Sex, and <Emphasis Type="Italic">Helicobacter pylori</Emphasis> Infection

We investigated the prevalence of peptic ulcer in dyspeptic patients in China to analyze the influence of age, sex, and Helicobacter pylori (H. pylori) infection. The results showed that the prevalence of gastric and duodenal ulcer increased with age. In patients under 60 years old, the prevalence of duodenal and gastric ulcers in females was markedly lower than that in males, especially the prevalence of duodenal ulcer. The prevalence of duodenal ulcer and gastric ulcer in H. pylori-infected patients was markedly higher than in patients without H. pylori infection. In the patients under 60 years old, sex differences were still seen in both H. pylori-positive and H. pylori-negative patients. The prevalence of gastric and duodenal ulcers was markedly increased with age in both H. pylori-positive and H. pylori-negative patients. Multivariate logistic regression analysis showed that age, male sex, and H. pylori infection were three independent risk factors for gastric and duodenal ulcers.     

Response of blood endothelin-1 and nitric oxide activity in duodenal ulcer patients undergoing Helicobacter pylori eradication

AIM: To investigate the effect of Helicobacter pylori eradication on endothelin-1 (ET-1) and nitric oxide (NO) in duodenal ulcer (DU) patients. METHODS: Sixty-six Hpylori-infected active DU patients were consecutively enrolled to receive one-week triple therapy (rabeprazole, amoxicillin and metronidazole) and then one-month rabeprazole therapy. They were asked back to determine ulcer and Hpylori status using endoscopy one month later. Thirty-seven healthy controls (H pylori +/-:17/20) were enrolled for comparison. Blood samples were collected in each visit to measure plasma ET-1 and nitrate/nitrite levels using an enzyme immunoassay kit. RESULTS: Sixty DU patients finished trial per protocol. The ulcer healing and Hpylori-eradication rates were 86.7% and 83.3%, respectively. Plasma ET-1 level in DU patients was higher than that of Hpylori-negative and positive controls (3.59±0.96 vs0.89±0.54 vs0.3±0.2 pg/mL,P<0.01), while nitrate/nitrite levels among them were also significantly different (8.55±0.71 vs5.27±0.68 vs 6.39±0.92 μmol/L, P<0.05). H pylori eradication diminished ET-1 levels (3.64±0.55 vs2.64±0.55 pg/mL, P<0.01) but elevated nitrate/ nitrite level (8.16±0.84 vs11.41±1.42 umol/L,P<0.05). CONCLUSION: Both plasma ET-1 and nitrate/nitrite levels increase in active DU patients. After an effective H pylori eradication, DU healing is associated with diminished blood ET-1 level and elevated nitrate/nitrite level.     

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.     

Ablation of exaggerated meal-stimulated gastrin release in duodenal ulcer patients after clearance of Helicobacter (Campylobacter) pylori infection

An exaggerated increase in meal-stimulated gastrin is a common finding in patients with duodenal ulcer. Duodenal ulcer patients also exhibit an increase in the number of parietal cells, which results in an increase in maximum acid output. There are also data to suggest that acid hypersecretion may not predate the ulcer disease, but is acquired, possibly due to the trophic effects of the exaggerated gastrin release on parietal cells. We investigated meal-stimulated gastrin release in nine Helicobacter pylori-infected individuals; eight patients with chronic duodenal ulcer and one H. pylori-infected healthy control, both before and after therapy designed to eradicate H. pylori infection. We also simultaneously measured intragastric pH in six duodenal ulcer patients. Eradication of the H. pylori infection reversed the exaggerated meal-stimulated gastrin release (gastrin secretion fell from 141 + 16 pg/ml/h before treatment to 98 +/- 7 pg/ml/h after, p less than 0.01) without affecting intragastric pH. Whereas exaggerated meal-stimulated gastrin release may be an important pathogenetic feature of duodenal ulcer disease, we conclude that it is secondary to the H. pylori infection. This study provides further insight into the role of H. pylori in the pathogenesis of duodenal ulcer disease. We postulate that reversal of the abnormalities in gastrin secretion will be associated with a gradual return of gastric secretion to normal.     

Helicobacter pylori-negative duodenal ulcers: prevalence, clinical characteristics, and prognosis--results from a randomized trial with 2-year follow-up

OBJECTIVE: The proportion of Helicobacter pylori-negative duodenal ulcer disease appears to be increasing. Data on clinical outcome and prognosis in this subgroup are lacking. METHODS: Two hundred seventy-six duodenal ulcer patients randomized, irrespective of H. pylori status, to either eradication therapy or maintenance omeprazole (double-blind, double-dummy design) for 1 yr were studied. Patients were followed up for a total of 2 yr, with visits performed every 2 months the first year and every 6 months the following year. Endoscopies for assessment of ulcer relapse were done at 6 and 12 months or in the event of symptomatic relapse. H. pylori status was assessed by culture, immunohistochemistry, and urea breath test at entry, at 6, 12, and 24 months or at failure. The primary endpoint was discontinuation, irrespective of reason. Patients were considered H. pylori negative if all three tests were negative. Patients were considered H. pylori-positive if any of the three diagnostic tests were positive. Study staff were blinded to H. pylori results. RESULTS: Thirty-two (12%) patients were H. pylori negative at entry. There were no differences according to H. pylori status for a number of clinical and demographic characteristics. However, H. pylori-negative patients had a shorter history of ulcer symptoms and were more likely to be NSAID users (19% vs 1%, p < 0.001). Only 28% of the H. pylori-negative patients completed the study, as compared with 40% of H. pylori-positive patients (p = 0.0005). The main reasons for the poorer prognosis in H. pylori-negative patients were relapse of ulcer/ulcer not healed (35% vs 26%) and relapse of severe dyspepsia symptoms without ulcer relapse (16% vs 7%). H. pylori-negative patients randomized to eradication therapy left the study early compared with H. pylori-negative patients randomized to long-term omeprazole therapy. Outcome in omeprazole-treated patients did not differ according to H. pylori status (p = 0.3). CONCLUSIONS: Clinical characteristics in H. pylori-negative and positive duodenal ulcer patients differ little. Clinical outcome over 2 yr is significantly poorer in H. pylori-negative patients, especially if treated empirically with eradication therapy. These results suggest that H. pylori infection should be assessed in all duodenal ulcer patients before treatment is decided.     

Relationship between antral lymphocyte density and basal gastrin levels in patients with Helicobacter pylori infection

BACKGROUND: The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood. AIM: To evaluate whether antral lymphocyte density could play a role in this alteration. METHODS: A total of 12 patients with active duodenal ulcer and 10 with non-ulcer dyspepsia were enrolled upon detection of Helicobacter pylori infection at endoscopy Enrolled as controls were 7 matched dyspeptic patients without Helicobacter pylori infection. Biopsy specimens were collected for Helicobacter pylori and histological assessments, and for antral lymphocyte density assessment by a histomorphometric method. A blood sample was obtained from each patient to determine basal gastrin levels. All patients were controlled by a further endoscopy 4 weeks after the end of Helicobacter pylori treatment. RESULTS: Antral lymphocyte density (5,464 +/- 1,328 and 5,635 +/- 1,186 vs 2,267 +/- 557 lymphocytes/mm2; p<0.001 and p<0.001, respectively) and gastrin levels (66.7 +/- 14.1 and 60.4 +/- 21.7 vs 40.7 +/- 7.8 pg/dl; p=0.004 and p=0.02, respectively) were higher in duodenal ulcer and non-ulcer dyspepsia patients than in controls, while no significant differences emerged between duodenal ulcer and non-ulcer dyspepsia patients. There was a significant direct correlation between antral lymphocyte density and gastrin levels both in duodenal ulcer (r=0.77; p=0.003) and in non-ulcer dyspepsia (r=0.75; p=0.03) patients, while no correlation was found in controls [r=0.12; p=0.8). After treatment, this correlation persisted in 10 eradication failure patients (r=0.68; p=0.027), but disappeared in those successfully cured. CONCLUSIONS: These data suggest that lymphocyte density in the antral mucosa could play a role in the impaired gastrin production occurring in patients with Helicobacter pylori infection.     

Gastrin and antral G cells in course of Helicobacter pylori eradication： Six months follow up study

ABM: To assess long-term effects of Helicobacter pylori (H pylori) eradication on antral G cell morphology and function in patients with and without duodenal ulcer (DU). METHODS: Consecutive dyspeptic patients referred to the endoscopy entered the study. Out of 39 H pylori positive patients, 8 had DU (Hpylori+DU) and 31 gastritis (Hpylori +G). Control groups consisted of 11 uninfected dyspeptic patients (CG1) and 7 healthy volunteers (CG2). Basal plasma gastrin (PGL), antral tissue gastrin concentrations (ATGC), immunohistochemical and electron microscopic characteristics of G cells were determined, prior to and 6 mo after therapy. RESULTS: We demonstrated elevated PGL in infected patients compared to uninfected controls prior to therapy. Elevated PGL were registered in all H pylori+patients (H pylori +DU: 106.78±22.72 pg/mL, H pylori+G: 74.95±15.63, CG1: 68.59±17.97, CG2: 39.24±5.59 pg/mL, P<0.01). Successful eradication (e) therapy in H pylori+patients lead to significant decrease in PGL (H pylori+DU:59.93±9.40 and H pylori+Ge: 42.36±10.28 pg/mL, P<0.001). ATGC at the beginning of the study were similar in infected and uninfected patients and eradication therapy lead to significant decrease in ATGC in H pylori+gastritis, but not in DU patients. In the H pylori+DU patients, the mean number of antral G cells was significantly lower in comparison with all other groups (P<0.01), but after successful eradication was close to normal values found in controls. By contrast, G cell number and volume density were significantly decreased (P<0.01) in H pylori+Ge group after successful eradication therapy (294±32 and 0.31±0.02, respectively), in comparison to values before eradication (416±40 and 0.48±0.09). No significant change of the G cell/total endocrine cell ratio was observed during the 6 mo of follow up in any of the groups. A reversible increase in G cell secretory function was seen in all infected individuals, demonstrated by a more prominent secretory apparatus. However, differences between DU and gastritis group were identified. CONCLUSION: H pylori infection induces antral G cell hyperfunction resulting in increased gastrin synthesis and secretion. After eradication therapy complete morphological and functional recovery is observed in patients with gastritis. In the DU patients some other factors unrelated to the H pylori infection influence antral G cell morphology and function.     

Helicobacter pylori in gastric corpus of patients 20 years after partial gastric resection

AIM: To determine the long-term prevalence of Helicobacter pylori (H pylori) gastritis in patients after partial gastric resection due to peptic ulcer, and to compare the severity of H pylori-positive gastritis in the corpus mucosa between partial gastrectomy patients and matched controls. METHODS: Endoscopic biopsies were obtained from 57 patients after partial gastric resection for histological examination using hematoxylin/eosin and Warthin-Starry staining. Gastritis was graded according to the updated Sydney system. Severity of corpus gastritis was compared between H pylori-positive partial gastrectomy patients and H pylori-positive duodenal ulcer patients matched for age and gender. RESULTS: In partial gastrectomy patients, surgery was performed 20 years (median) prior to evaluation. In 25 patients (43.8%) H pylori was detected histologically in the gastric remnant. Gastric atrophy was more common in H pylori-positive compared to H pylori-negative partial gastrectomy patients (P<0.05). The severity of corpus gastritis was significantly lower in H pylori-positive partial gastrectomy patients compared to duodenal ulcer patients (P<0.01). There were no significant differences in the activity of gastritis, atrophy and intestinal metaplasia between the two groups. CONCLUSION: The long-term prevalence of H pylori gastritis in the gastric corpus of patients who underwent partial gastric resection due to peptic ulcer disease is comparable to the general population. The expression of H pylori gastritis in the gastric remnant does not resemble the gastric cancer phenotype.     

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 pyloriin gastric corpus of patients 20 years after partial gastric resection

AIM:To determine the long-term prevalence of Helicobacterpylori(H pylori)gastritis in patients after partial gastricresection due to peptic ulcer,and to compare the severityof Hpylori-positive gastritis in the corpus mucosa betweenpartial gastrectomy patients and matched controls.METHODS:Endoscopic biopsies were obtained from 57patients after partial gastric resection for histologicalexamination using hematoxylin/eosin and Warthin-Starrystaining.Gastritis was graded according to the updatedSydney system.Severity of corpus gastritis was comparedbetween Hpylori-positive partial gastrectomy patients andHpylori-positive duodenal ulcer patients matched for ageand gender.RESULTS:In partial gastrectomy patients,surgery wasperformed 20 years(median)prior to evaluation.In 25patients(43.8%)Hpyloriwas detected histologically inthe gastric remnant.Gastric atrophy was more common inH pylori-positive compared to H pylori-negative partialgastrectomy patients(P<0.05).The severity of corpusgastritis was significantly lower in Hpylori-positive partialgastrectomy patients compared to duodenal ulcer patients(P<0.01).There were no significant differences in theactivity of gastritis,atrophy and intestinal metaplasiabetween the two groups.CONCLUSION:The long-term prevalence of Hpylorigastritisin the gastric corpus of patients who underwent partialgastric resection due to peptic ulcer disease is comparableto the general population.The expression of Hpylorigastritisin the gastric remnant does not resemble the gastric cancerphenotype.     

Eradicating Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer.

Helicobacter pylori (H pylori) raises serum gastrin but it is unclear whether this stimulates increased acid secretion. Gastrin mediated acid secretion and plasma gastrin after the intravenous infusion of gastrin releasing peptide was studied in nine H pylori negative and nine H pylori positive healthy volunteers, and in 11 duodenal ulcer patients. Nine of the last group were re-examined one month after eradication of H pylori. The median acid output (mmol/h) to gastrin releasing peptide (40 pmol/kg/h) in the H pylori positive healthy volunteers was 15.1 (range 3.3-38.3), which was three times that of the H pylori negative healthy volunteers (median = 5.5, range 1.0-9.0) (p < 0.02). The median acid output in the duodenal ulcer patients with H pylori was 37 (range 8.5-57), which was > six times that of the H pylori negative healthy volunteers. Eradication of H pylori in the duodenal ulcer patients lowered their acid secretion by a median of 66% (range 30%-80%) (p < 0.01) and to values equivalent to the H pylori positive healthy volunteers. The pepsin output in response to gastrin releasing peptide followed the same pattern as the acid output. The median plasma gastrin concentrations during gastrin releasing peptide were similar in the H pylori positive duodenal ulcer patients (150 ng/l, range 95-400) and H pylori positive healthy volunteers (129 ng/l, range 23-420) and both were appreciably higher than H pylori negative healthy volunteers (60 ng/l, range 28-135) (p < 0.005 for each). Eradication of H pylori lowered the plasma gastrin in the duodenal ulcer patients to values equivalent to the H pylori negative healthy volunteers. These findings show a threefold increase in acid secretion in H pylori positive healthy volunteers that is explained by H pylori induced hypergastrinaemia and a sixfold increase in acid secretion in the duodenal ulcer patients that is explained by the combination of H pylori induced hypergastrinaemia and an exaggerated acid response to stimulation by gastrin. Eradicating H pylori lowers gastrin mediated acid secretion by 66% in duodenal ulcer patients as a result of the resolution of the hypergastrinaemia. Increased gastrin mediated acid secretion seems to be the key factor in the pathophysiology of duodenal ulceration and explains the role of H pylori infection in the disorder.     

Evidence for the role of gastric mucosa at the secretion of soluble triggering receptor expressed on myeloid cells （strem-1） in peptic ulcer disease

AIM: To investigate the role of gastric mucosa at the secretion of sTREM-1 in peptic ulcer. METHODS: Seventy two patients were enrolled; 35 with duodenal, 21 with gastric ulcer and 16 with chronic gastritis. Patients were endoscoped and gastric juice was aspirated. Patients with duodenal and gastric ulcer underwent a second endoscopy post-treatment. Biopsies were incubated in the absence/presence of endotoxins or gastric juice. Supernatants were collected and sTREM-1 and TNFα were measured by enzyme immunoabsorbent assays. Scoring of gastritis was performed before and after treatment according to updated Sydney score. RESULTS: Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis. sTREM-1 was higher in supernatants of tissue samples of H pylori-positive than of H pylori-negative patients with gastric ulcer. Median (± SE) sTREM-1 was found increased in supernatants of patients with gastric ulcer before treatment (203.21 ± 88.91 pg/1000 cells) compared to supernatants either from the same patients post-treatment (8.23 ± 5.79 pg/1000 cells) or from patients with chronic gastritis (6.21 ± 0.71 pg/1000 cells) (P < 0.001 and < 0.001, respectively). Similar differences for sTREM-1 were recorded among LPS-stimulated tissue samples of patients (P = 0.001). Similar differences were not found for TNFα. Positive correlations were found between sTREM-1 of supernatants from patients withboth duodenal and gastric ulcer before treatment and the degree of infiltration of neutrophils and monocytes. CONCLUSION: sTREM-1 secreted by the gastric mucosa is an independent mechanism connected to the pathogenesis of peptic ulcer. sTREM-1 was released at the presence of H pylori from the inflamed gastric mucosa in the field of gastric ulcer.