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Antral gastrin cell hyperfunction and Helicobacter pylori infection |
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| Authors: | B. ANNIBALE,G. RINDI,G. D'AMBRA,M. MARIGNANI,E. SOLCIA,C. BORDI,& G. DELLE FAVE |
| Affiliation: | Gastroenterology Unit; Semeiotica Chirurgica IV, University 'La Sapienza' Rome, Italy; Department of Human Pathology, University of Pavia, Pavia, Italy; Department of Pathology, University of Parma, Italy |
| Abstract: | 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. pylori -positive 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. |
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