Relationship of CagA to Serum Gastrin Concentrations and Antral G, D Cell Densities in Helicobacter pylori Infection

Jung Hwan Kim, HyoJin Park, Jun Sik Cho, Kwi Soon Lee, Sang In Lee, In Suh Park, Chang Keun Kim

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Abstract

The purpose of this study was to investigate whether the densities of antral gastrin and somatostatin-immunoreactive cells in Helicobacter pylori (H. pylori) infection were related to the bacterial expression of cytotoxin-associated gene A (CagA). 32 patients who had underwent diagnostic esophagogastroduodenoscopy were studied. On the histologic examination all patients had antral gastritis. We divided the subjects into three groups. Group I consisted of 6 patients who had chronic superficial gastritis, group II, 9 patients who had H. pylori-associated gastritis but with no expression of CagA, and group III, 17 patients who had H. pylori-associated gastritis with the expression of CagA. In group I and II, serum gastrin levels, and antral G cell and D-cell were measured. In group III, serum gastrin levels, and antral G cell and D-cell were measured, before and after the eradication of H. pylori. The results were as follows. Firstly, serum gastrin concentrations were significantly higher in the patients with H. pylori infection than in the negative controls. Nextly, there was no correlation between the changes in antral G or D-cell density and H. pylori infection. Thirdly, group III had a significant increase in serum gastrin concentrations and a significant decrease in antral D-cell density than group I. Forthly, eradication of H. pylori in group III showed a significantly increased antral D-cell density. Our results suggest that hypergastrinemia in H. pylori-associated gastritis is relevant to the presence of CagA, and the possible mechanism of hypergastrinemia may be related to antral D-cell deficiency, which is caused by H. pylori infection with the expression of CagA.

Original languageEnglish
Pages (from-to)301-306
Number of pages6
JournalYonsei medical journal
Volume40
Issue number4
DOIs
Publication statusPublished - 1999 Jan 1

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Gastrin-Secreting Cells
Somatostatin-Secreting Cells
Gastrins
Cytotoxins
Helicobacter Infections
Helicobacter pylori
Cell Count
Gastritis
Serum
Genes
Digestive System Endoscopy
Antral

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Kim, Jung Hwan ; Park, HyoJin ; Cho, Jun Sik ; Lee, Kwi Soon ; Lee, Sang In ; Park, In Suh ; Kim, Chang Keun. / Relationship of CagA to Serum Gastrin Concentrations and Antral G, D Cell Densities in Helicobacter pylori Infection. In: Yonsei medical journal. 1999 ; Vol. 40, No. 4. pp. 301-306.
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title = "Relationship of CagA to Serum Gastrin Concentrations and Antral G, D Cell Densities in Helicobacter pylori Infection",
abstract = "The purpose of this study was to investigate whether the densities of antral gastrin and somatostatin-immunoreactive cells in Helicobacter pylori (H. pylori) infection were related to the bacterial expression of cytotoxin-associated gene A (CagA). 32 patients who had underwent diagnostic esophagogastroduodenoscopy were studied. On the histologic examination all patients had antral gastritis. We divided the subjects into three groups. Group I consisted of 6 patients who had chronic superficial gastritis, group II, 9 patients who had H. pylori-associated gastritis but with no expression of CagA, and group III, 17 patients who had H. pylori-associated gastritis with the expression of CagA. In group I and II, serum gastrin levels, and antral G cell and D-cell were measured. In group III, serum gastrin levels, and antral G cell and D-cell were measured, before and after the eradication of H. pylori. The results were as follows. Firstly, serum gastrin concentrations were significantly higher in the patients with H. pylori infection than in the negative controls. Nextly, there was no correlation between the changes in antral G or D-cell density and H. pylori infection. Thirdly, group III had a significant increase in serum gastrin concentrations and a significant decrease in antral D-cell density than group I. Forthly, eradication of H. pylori in group III showed a significantly increased antral D-cell density. Our results suggest that hypergastrinemia in H. pylori-associated gastritis is relevant to the presence of CagA, and the possible mechanism of hypergastrinemia may be related to antral D-cell deficiency, which is caused by H. pylori infection with the expression of CagA.",
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Relationship of CagA to Serum Gastrin Concentrations and Antral G, D Cell Densities in Helicobacter pylori Infection. / Kim, Jung Hwan; Park, HyoJin; Cho, Jun Sik; Lee, Kwi Soon; Lee, Sang In; Park, In Suh; Kim, Chang Keun.

In: Yonsei medical journal, Vol. 40, No. 4, 01.01.1999, p. 301-306.

Research output: Contribution to journalArticle

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AB - The purpose of this study was to investigate whether the densities of antral gastrin and somatostatin-immunoreactive cells in Helicobacter pylori (H. pylori) infection were related to the bacterial expression of cytotoxin-associated gene A (CagA). 32 patients who had underwent diagnostic esophagogastroduodenoscopy were studied. On the histologic examination all patients had antral gastritis. We divided the subjects into three groups. Group I consisted of 6 patients who had chronic superficial gastritis, group II, 9 patients who had H. pylori-associated gastritis but with no expression of CagA, and group III, 17 patients who had H. pylori-associated gastritis with the expression of CagA. In group I and II, serum gastrin levels, and antral G cell and D-cell were measured. In group III, serum gastrin levels, and antral G cell and D-cell were measured, before and after the eradication of H. pylori. The results were as follows. Firstly, serum gastrin concentrations were significantly higher in the patients with H. pylori infection than in the negative controls. Nextly, there was no correlation between the changes in antral G or D-cell density and H. pylori infection. Thirdly, group III had a significant increase in serum gastrin concentrations and a significant decrease in antral D-cell density than group I. Forthly, eradication of H. pylori in group III showed a significantly increased antral D-cell density. Our results suggest that hypergastrinemia in H. pylori-associated gastritis is relevant to the presence of CagA, and the possible mechanism of hypergastrinemia may be related to antral D-cell deficiency, which is caused by H. pylori infection with the expression of CagA.

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