Antral gastrin cell hyperfunction and Helicobacter pylori infection

被引:9
作者
Annibale, B
Rindi, G
DAmbra, G
Marignani, M
Solcia, E
Bordi, C
DelleFave, G
机构
[1] UNIV ROMA LA SAPIENZA,GASTROENTEROL UNIT,ROME,ITALY
[2] UNIV PAVIA,DEPT HUMAN MED,I-27100 PAVIA,ITALY
[3] UNIV PARMA,DEPT PATHOL,I-43100 PARMA,ITALY
关键词
D O I
10.1046/j.1365-2036.1996.31173000.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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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页码:607 / 615
页数:9
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