Effect of Helicobacter pylori Eradication on Antral Gastrin- and Somatostatin-Immunoreactive Cell Density and Gastrin and Somatostatin Concentrations

Abstract

The density of antral gastrin (G)- and somatostatin (D)-immunoreactive cells and the contents of antral gastrin and somatostatin were investigated in endoscopic antral biopsy specimens from patients with duodenal ulcer before and after eradication of Helicobacter pylori. After H. pylori eradication both antral somatostatin concentration (p = 0.0002) and antral D-cell density (p = 0.01) increased significantly. Conversely, although the number of G-cells was unchanged, antral (p = 0.0002) and serum (p = 0.001) gastrin contents decreased significantly. The number of oxyntic D-cells did not change significantly. These results strongly suggest that the hypergastrinaemia observed in H. pylori-positive patients may be due to a deficiency in antral somatostatin, which normally inhibits the synthesis and release of gastrin.

Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection

“…This study showed for the first time that the levels of EGF in duodenal ulcer patients with H. pylori infection were much lower than those of the healthy volunteers and chronic gastritis patients with H. pylori infection, and also confirmed the previous fingings that H. pylori infection can enhance gastrin secretion and lower somatostatin level, which can cause abnormal secretion of gastric acid [4,[7][8][9][10] . A strong association between H. pylori and diseases of upper gastrointestinal tract has been reported [1,2] .…”

“…The patients also have a decreased somatostatin level in gastric juice and antral mucosal tissue [7] . Eradication of H. pylori may decrease hypergastrinemia, enhance antral somatostatin secretion, and then reduce gastric acid secretion [8][9][10] . However, hypergastrinemia and decreased antral somatostatin secretion cannot explain the relation between H. pylori and duodenal ulcer, because there was no consistent relationship between chronic H. pylori infection and acid secretion (either basal or stimulated) observed [11,12] .…”

Increased gastric emptying induced by Helicobacter heilmannii type 1 infection in rats

“…As observed in human patients infected with H. pylori [3,4,41], Hh1 induced a signi®cant increase in serum gastrin concentration in rats. The hypergastrinaemia that occurs in H. pylori-infected patients may be secondary to a reduction in antral somatostatin levels [3,4,41], as observed in the infected animals.…”

“…As observed in human patients infected with H. pylori [3,4,41], Hh1 induced a signi®cant increase in serum gastrin concentration in rats. The hypergastrinaemia that occurs in H. pylori-infected patients may be secondary to a reduction in antral somatostatin levels [3,4,41], as observed in the infected animals. Possible explanations for the reduction in somatostatin concentration in the antrum of H. pylori-infected individuals include alkalinisation of the environment as a result of the production of ammonia from urea by the action of the potent urease produced by the bacteria.…”

“…Several factors have been implicated in the pathogenesis of the diseases associated with the micro-organism, such as a decrease in antral somatostatin content and an increase in serum and antral gastrin concentrations observed in H. pylori-infected patients [3,4]. The mechanism by which H. pylori changes gastric hormone metabolism has been only partially elucidated.…”