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Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis
  1. Y Liu1,
  2. G D C Vosmaer2,
  3. G N J Tytgat3,
  4. S-d Xiao4,
  5. F J W Ten Kate1
  1. 1Department of Pathology, Academic Medical Centre, University of Amsterdam, 1100 DD Amsterdam, The Netherlands
  2. 2Department of Gastroenterology, Inwendige Geneeskunde Scheperziekenhuis, 7822 HL Emmen, The Netherlands
  3. 3Department of Gastroenterology, Academic Medical Centre, University of Amsterdam
  4. 4Shanghai Institute of Digestive Disease, Shanghai Second Medical University, 200001 Shanghai, The People’s Republic of China
  1. Correspondence to:
 Dr Y Liu
 Department of Pathology, Academic Medical Centre, University of Amsterdam, 1100 DD Amsterdam, The Netherlands; y.liuamc.uva.nl

Abstract

Background: Gastrin G cells and somatostatin D cells are important regulators of gastric acid secretion and alterations in their relative numbers may play a key role in gastroduodenal disease.

Aim: To investigate the effect of Helicobacter pylori infection on the density of immunoreactive G and D cells in gastric antral and corpus biopsies from patients with dyspeptic complaints.

Methods: One hundred and twenty two patients with dyspeptic complaints had two antrum and two corpus biopsies taken during upper endoscopy. The severity of inflammation and the density of H pylori were evaluated semiquantitatively. In addition, the density and distribution of neuroendocrine cells, especially G and D cells, were examined using immunohistochemistry. Patients were divided into three groups, those with H pylori positive gastritis, H pylori negative gastritis, and histologically normal gastric mucosa.

Results: The number of immunoreactive G cells was significantly higher and the number of immunoreactive D cells lower in patients with H pylori positive gastritis compared with H pylori negative gastritis or histological normal gastric mucosa. The percentage of G cells as a percentage of mucosal endocrine cells was also raised and that of D cells was decreased.

Conclusions:Helicobacter pylori infection produces alterations in the number of endocrine cells responsible for regulating acid secretion in relation to intragastric pH and feeding. The alterations correlate best with the severity of inflammation and not with H pylori density.

  • ABC, avidin–biotin complex
  • D, somatostatin
  • G, gastrin
  • gastritis
  • Helicobacter pylori
  • gastrin
  • somatostatin
  • chromogranin

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