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Background: Helicobacter pylori infection, gastric acid hypersecretion and NSAID consumption may cause peptic ulcer., Aim: To investigate the respective roles of H. pylori and acid secretion in bleeding duodenal ulcer., Patients and Methods: A total of 99 duodenal ulcer patients were referred for evaluation of acid secretion: seven with Zollinger-Ellison Syndrome; 14 with hypersecretory duodenal ulcer, defined by the coexistence of elevated basal acid output and pentagastrin acid output; and 78 duodenal ulcer patients with normal acid output. All non-Zollinger-Ellison Syndrome patients were H. pylori-positive and cured of infection. All patients were followed-up for a 36-month period, to assess the occurrence of bleeding episodes., Results: Twenty-nine patients had at least one bleeding episode in the 4 years before the study. Bleeding was more frequent in males and in patients on NSAIDs. The mean basal acid output was not higher among bleeders. In the 21 patients (14 hypersecretory duodenal ulcer, seven Zollinger-Ellison Syndrome) with basal acid output > 10 meg/h and pentagastrin acid output > 44.5 meg/h, the risk of bleeding was higher (OR 6.5; 95% CI: 2-21). In the follow-up period, three out of 83 (3.3%) non-Zollinger-Ellison Syndrome patients had a H. pylori-negative duodenal ulcer with bleeding. The risk of bleeding after H. pylori cure was not higher in hypersecretory duodenal ulcer patients (P > 0.3), nor among patients with previous bleeding episodes (P > 0.2)., Conclusions: In H. pylori-positive duodenal ulcer patients, the coexistence of elevated basal acid output and pentagastrin acid output leads to a sixfold increase in the risk of bleeding. After H. pylori cure, gastric acid hypersecretion is not a risk factor for bleeding. However, duodenal ulcer recurrence with bleeding may occasionally occur in patients cured of H. pylori, even if acid output is normal.

Background: Long-term data concerning the reappearance of Helicobacter pylori infection and duodenal ulcer (DU) recurrence after successful eradication are still few and conflicting. Inadequate histological assessment or use of indirect tests for the determination of H. pylori and bias in the selection of patients to be controlled can influence reported results. The aim of this study was to determine the rate of recurrence of H. pylori infection and ulcer relapse in a population of cured DU patients followed up for 3 years irrespective of their symptomatology., Methods: Between 1992 and 1994, 126 patients with DU disease were treated with double or triple therapy. Patients using nonsteroidal antiinflammatory drugs or aspirin or receiving maintenance antisecretory therapy were excluded. H. pylori infection was assessed by three bioptic tests from both the antrum and the body (culture, urease, histopathological examination). After 2 months from cessation of treatment, DU had healed and H. pylori infection was cured in 102 of 126 patients (81%). These patients were endoscopically followed up after 1 and 3 years, respectively, and were advised to contact us at symptom recurrence. At 1 and 3 years, we studied 95 (93.2%) and 79 (77.4%) patients, respectively, of the 102 who were cured. The other patients were untraceable or refused endoscopy because they were asymptomatic., Results: After 1 year, no patient had H. pylori recurrence, whereas three patients had a relapse of DU without evidence of infection. After 3 years, recurrence of H. pylori occurred in six patients (annual rate, 2.5%), DU relapsed in five H. pylori-positive patients (6.3%) and in two H. pylori-negative patients (annual rate, 1.9%). Fasting gastrin and acid secretion values studied in all relapsed patients were within the normal range except for one H. pylori-positive patient., Conclusions: Recurrence of H. pylori infection is very low where treatment is effective, but a DU relapse, not related to acid hypersecretion, can occur in a small percentage of cured patients.

Background: Acid hypersecretion is associated with duodenal ulcer disease in the following conditions: Zollinger-Ellison syndrome (ZES) and antral gastrin cell hyperfunction (AGCH) due to hypergastrinaemia, or hypersecretory duodenal ulcer (HDU) without hypergastrinaemia., Aim: To evaluate whether quantitative changes in fundic ECL and D cells may be involved in acid hypersecretion., Patients and Methods: Seven ZES, six AGCH and six HDU Helicobacter pylori-positive patients were compared. Basal (BAO) and pentagastrin-stimulated gastric acid secretions (PAO), and morphometry of fundic ECL and D cells were performed. The six AGCH and six HDU patients were investigated again using the same tests 1 year after H. pylori eradication., Results: Median PAO values were no different in all the hypersecretory conditions studied. The median volume density of ECL cells in ZES was significantly higher than in controls (2.75, range 1.74-5.8 vs. 0.73, 0.52-1.11: P < 0.05), whereas it was in the control range in AGCH and HDU patients (0.77, range 0.20-1.39 and 0.99, range 0.42-1.51; respectively). The count of fundic D cells was significantly lower in AGCH patients than in all other investigated groups (median 0.16, range 0.1-0.52; P < 0.05). Cure of infection in AGCH and HDU patients did not modify the ECL cell volume density, whereas a significant increase in the count of fundic D cells was observed in AGCH patients. Thus, the ECL/D cell index was significantly affected in AGCH patients (P < 0.05), being higher during H. pylori infection (median 6, range 0.7-9.25) than after the cure (median 2.12, range 1.10-3.5). BAO and PAO were not affected by H. pylori eradication in either group., Conclusions: The study provides evidence, for the first time, that quantitative alterations in the fundic endocrine cells are not involved in acid hypersecretion of patients with hypersecretory states, and that eradication of H. pylori does not restore normal acid secretion values.

Background: Antral gastrin cell hyperfunction (AGCH), is a rare cause of duodenal ulcer associated with non-tumour hypergastrinaemia and acid hypersecretion., Aim: To investigate the role of Helicobacter pylori in AGCH., Patients: Twelve AGCH patients and eight H. pyloripositive non-hypergastrinaemic duodenal ulcer patients were compared., Methods: Basal and peak acid outputs, gastrin-stimulation (meal and bombesin) tests, and immunohistochemistry for antral G and D cells were performed. One year after H. pylori eradication, six AGCH patients were again investigated with the same tests., Results: Significantly more basal, and stimulated gastrin and acid secretion, were found in AGCH compared to the H. pylori-positive duodenal ulcer patients (P < 0.01). G cell counts were significantly higher in AGCH than in duodenal ulcer patients (118.8, range 58-192.4, vs. 86.1, range 49-184; P < 0.05), and the resulting G/D cell ratio was also higher in AGCH patients (4.2, range 2.6-5.6, vs. 3.3, range 1.9-4.3; P < 0.05). H. pylori was present in the gastric mucosa of all 12 AGCH patients. Cure of infection in six AGCH individuals resulted in marked a decrease of gastrin levels associated with a significant (23.7%: P < 0.05) decrease of G cell count and an increase (12%; P < 0.05) of D cell count., Conclusions: The results indicate that AGCH may result from H. pylori overstimulation of gastrin cell function in patients with some presently undefined, familial predisposition and that an imbalance of the G/D cell ratio may have a role in the genesis of hypergastrinaemia.

We measured basal and pentagastrin-stimulated acid secretion, as well as basal and meal-stimulated plasma gastrin concentration to determine, in 67 patients affected by resistant duodenal ulcer, whether their condition could be related to gastric acid secretion and/or gastrin-related syndromes. We then compared them to 46 duodenal ulcer control patients. The outpatients were investigated consecutively. The resistant duodenal ulcer patients differed from the controls only in their higher complication rates (bleeding or perforation, P < 0.05). We identified five patients in the resistant duodenal ulcer group with Zollinger-Ellison syndrome and 12 with antral G cell hyperfunction, whereas in the control group only one patient was affected by antral G cell hyperfunction. IgG anti-Helicobacter pylori antibodies were positive for the presence of infection in 7 of the hypergastrinaemic patients. When Zollinger-Ellison syndrome or antral G cell hyperfunction were excluded, no differences could be found in gastric acid secretion, or basal and meal-stimulated plasma gastrin levels, between the resistant and control duodenal ulcer patients, except for basal acid hypersecretion (resistant duodenal ulcer 16% vs duodenal ulcer 2% P = 0.0144). In the presence of duodenal ulcer disease resistant to H2-blockers, it is mandatory to measure basal plasma gastrin concentration since it was possible to diagnose the gastrin-related syndromes, Zollinger-Ellison syndrome and antral G cell hyperfunction, in 26% of this group of patients.