Relationship between fundic endocrine cells and gastric acid secretion in hypersecretory duodenal ulcer diseases

Annibale, Bruno; Aprile, M; Ferraro, Gabriella; Marignani, Massimo; Angeletti, Stefano; D’Ambra, G.; Caruana, Pietro; Bordi, Cesare; Fave, Gianfranco Delle

doi:10.1046/j.1365-2036.1998.00365.x

Cited by 10 publications

(9 citation statements)

References 32 publications

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“…In this paper we demonstrated that H. pylori cure does not significantly affect gastric acid hypersecretion in hypersecretory duodenal ulcer patients. This finding is not in accord with those of other authors, but confirms our previous reports on smaller series 14 , . 26 27 –28 However, in this study, gastric acid hypersecretion in the absence of H. pylori infection, does not seem to be related to duodenal ulcer relapse, or to the occurrence of bleeding episodes.…”

Section: Discussionsupporting

confidence: 68%

“…Some of the patients were included in other study protocols 9 , . 14 In detail, we diagnosed seven Zollinger–Ellison Syndrome patients, 14 hypersecretory duodenal ulcer disease patients and 78 duodenal ulcer patients with acid secretion in the normal range (Table 1) As reported before, we defined patients to be affected by hypersecretory duodenal ulcer when both basal and pentagastrin‐stimulated acid output were above the normal range (10 meq/h for basal acid output, 44.5 meq/h for pentagastrin acid output), with normal gastrin values 14 . Zollinger–Ellison Syndrome diagnosis was established by demonstration of repeated basal plasma hypergastrinaemia, basal acid hypersecretion and positive secretin test, as previously described 15 …”

Section: Methodsmentioning

confidence: 99%

“…Serial 5‐μm thick sections of gastric mucosa, perpendicular to the mucosal surface, were stained with haematoxylin‐eosin for conventional histopathological examination. Giemsa staining for H. pylori evaluation was performed as previously described 14 . Assessment of gastritis was performed according to the updated Sydney system 18 …”

Section: Methodsmentioning

confidence: 99%

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Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infection

Capurso¹,

Annibale²,

Osborn³

et al. 2001

Aliment Pharmacol Ther

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BACKGROUNDHelicobacter pylori infection and gastric acid hypersecretion together with NSAID consumption, are the main factors involved in gastroduodenal injury and bleeding. 1 Peptic ulcer is the most common cause of non-variceal upper gastrointestinal bleeding, accounting for 50±60% of cases. Bleeding episodes are frequent in duodenal ulcer patients, with a prevalence of 15±20% and a mortality up to 7%. 2 Patients who have bled once are considered to be at a higher risk of re-bleeding. Of duodenal ulcer patients, 95% have H. pylori infection of the gastroduodenal mucosa and its cure signi®cantly reduces the rate of both ulcer and bleeding recurrence in those patients with previous bleeding episodes. 3±6 Acid secretion has been found to be elevated in patients with bleeding from peptic ulcer. 7 Recent reports have shown that duodenal ulcer can also recur in the absence of H. pylori infection or NSAID consumption. 8, 9 SUMMARYBackground: 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, de®ned 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

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Section: Discussionsupporting

confidence: 68%

Section: Methodsmentioning

confidence: 99%

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Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infection

Capurso¹,

Annibale²,

Osborn³

et al. 2001

Aliment Pharmacol Ther

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“…Studies also suggest the ECL mass can also have an important effect on MAO [22]. A recent study suggests that the BAO is positively correlated with the ECL-cell density in hypersecretory patients in various gastric acid hypersecretory states [78]. Since the MAO is correlated with parietal cell mass and possibly ECL cell mass and the BAO correlated with ECL-cell density, a possible explanation for the persisting hypersecretion is that contrary to what the short term studies show, after prolonged hypergastrinemia of several years duration, these ECL and/or parietal cell changes may not be completely reversible.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Acid Hypersecretion Post Curative Gastrinoma Resection

et al. 2010

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“…H. pylori has been variously reported to cause disparate changes in gastrin and acid secretion—augmentation in some studies 3 , 7 , 8 and suppression in others 11 , 12 , 24–26 , 37 —and to change the sensitivity to stimulants such as gastrin 38 or bombesin, 7 which acts via gastrin to stimulate acid secretion in humans 39 . However, in a direct study of underlying uninhibited secretion before and 1 year after H. pylori eradication, Annibale et al 13 . found no change in elevated basal or stimulated acid outputs from pre‐treatment values in non‐ZE hypersecretors.…”

Section: Discussionmentioning

confidence: 99%

Minor effects of Helicobacter pylori on gastric secretion and dose of lansoprazole during long‐term treatment in ZE and non‐ZE acid hypersecretors

Hirschowitz¹,

Simmons²,

Mohnen³

2002

Aliment Pharmacol Ther

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Background: Helicobacter pylori infection may increase or decrease acid secretion and may augment proton pump inhibitor efficacy. Pepsin effects have not been reported. In Zollinger–Ellison syndrome (ZE) specifically, H. pylori has been reported to decrease acid. Aim: To examine H. pylori effects on secretion and dose of medication in hypersecretors (basal acid output > 15 mmol/h) undergoing long‐term treatment with individually optimized lansoprazole doses. Methods: Sixty‐five patients (47 ZE and 18 non‐ZE), treated for > 3 months to 10 years, were tested every 6 months with endoscopy, gastric analysis and serum gastrin. Results: Forty‐three per cent were H. pylori‐positive. Acid, pepsin and gastrin were not different between H. pylori‐positive and H. pylori‐negative patients before or during long‐term lansoprazole treatment. Initially, H. pylori‐positive patients required less lansoprazole than H. pylori‐negative patients (68 ± 6 vs. 96 ± 8 mg/day), but after 3 years the doses converged (83 vs. 86 mg/day). The disappearance of H. pylori in 15 patients caused no significant changes in acid, pepsin, gastrin or lansoprazole dose in the following 4 years. Conclusions: H. pylori had no significant initial or long‐term physiological or potential clinical effects on acid or pepsin secretion or gastrin in these acid hypersecretors.

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Relationship between fundic endocrine cells and gastric acid secretion in hypersecretory duodenal ulcer diseases

Abstract: 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.

Cited by 10 publications

References 32 publications

Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infection

Occurrence and relapse of bleeding from duodenal ulcer: respective roles of acid secretion and Helicobacter pylori infection

Mechanism of Acid Hypersecretion Post Curative Gastrinoma Resection

Minor effects of Helicobacter pylori on gastric secretion and dose of lansoprazole during long‐term treatment in ZE and non‐ZE acid hypersecretors

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