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Effect of Helicobacter pylori infection on antral gastrin and somatostatin cells and on serum gastrin concentrations.open access

Authors
Park, Sill MooLee, Hyo RangKim, Jae GyuPark, Joong WonJung, GyuHan, Seong HyuckCho, Joon HyungKim, Mi Kyung
Issue Date
Jan-1999
Citation
The Korean journal of internal medicine, v.14, no.1, pp 15 - 20
Pages
6
Journal Title
The Korean journal of internal medicine
Volume
14
Number
1
Start Page
15
End Page
20
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/25575
DOI
10.3904/kjim.1999.14.1.15
ISSN
1226-3303
2005-6648
Abstract
OBJECTIVES: Helicobacter pylori infection induces selective reduction of the number of antral D-cells and results in abnormal regulation of serum gastrin secretion. The purpose of this study was to investigate the relationship between H. pylori infection and the numbers of G-cells and D-cells. METHODS: The numbers of antral G-cells and D-cells, the ratio of G-cells to D-cells and fasting serum gastrin concentrations were compared between 37 patients with (29 with duodenal ulcers and 8 with gastric ulcers) and 33 without H. pylori infection (22 with duodenal ulcers and 11 with gastric ulcers). Serum gastrin concentrations were measured using the radioimmunoassay technique. Antral mucosal biopsy specimens were examined using immunohistochemical staining with antibodies specific for gastrin and somatostatin and the numbers of G-cells and D-cells per gastric gland were counted. RESULTS: Fasting serum gastrin concentrations were significantly higher in patients with H. pylori infection compared to patients without infection (80.3 +/- 23.5 vs 47.6 +/- 14.1 pg/ml, p < 0.001). The number of G-cells per gastric gland was similar in infected and uninfected patients (7.1 +/- 3.1 vs 7.3 +/- 3.9, respectively, p > 0.5). The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3 +/- 0.4 vs 2.5 +/- 1.6, respectively, p < 0.001). The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7 +/- 2.7 vs 3.5 +/- 1.9, respectively, p < 0.001). CONCLUSIONS: These results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells. The resulting relative hypofunction of the inhibitory action of D-cells against G-cells may be responsible for increased serum gastrin secretion.
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