Is Helicobacter pylori associated hypergastrinaemia due to the bacterium's urease activity or the antral gastritis?

Abstract

There is now convincing evidence that Helicobacter pylori infection plays an important part in the pathogenesis of duodenal ulcer disease. The way in which the chronic antral infection predisposes to duodenal ulceration is unclear but stimulation of excessive gastrin release may be important.A`Eradication of H pylori infection results in a fall in the basal gastrin concentration of 27-33% and a fall of 30-58% in the integrated gastrin response to a meal.5 The mechanism by which H pylori infection raises plasma gastrin concentration is unclear.The hypergastrinaemia might be related to the organism's high urease activity. The production of ammonia at the antral epithelial surface could raise the local pH, resulting in loss of the physiological inhibition of gastrin release by intragastric acid.67 The ammonia might also increase gastrin release by directly stimulating the G cells as has been shown to occur in rats.8 A second explanation for the hypergastrinaemia is that it might be due to the chronic inflammation which H pylon induces in the underlying antral mucosa and which resolves on eradication of the infection. Wyatt et al have shown that antral gastritis, irrespective ofH pylon status, is associated with raised plasma gastrin concentration.9 In addition the T lymphocyte products, interleukin-2 and gamma interferon, have been shown to stimulate gastrin release in studies on isolated perfused canine antrum.'°I n an attempt to differentiate between the effects of the H pylon urease activity and the antral gastritis we decided to examine serum gastrin concentrations soon after starting H pylon eradication treatment. At this early time we hoped to achieve complete suppression of bacterial urease activity without appreciable resolution of the antral gastritis. PatientsTen patients (seven men, age range 31-65 years) with a history of endoscopically confirmed duodenal ulcer were studied. In each H pylon infection had been shown by histology of antral biopsy specimen and rapid urease test (CLO

Effect of Helicobacter pylori on Parietal Cell Sensitivity to Pentagastrin in Duodenal Ulcer Subjects

“…(13) noted that healthy volunteers with H . pylori had increased basal and meal-stimulated gastrin concentrations compared with uninfected volunteers, yet there was no difference between the two groups with regard to (5)(6)(7). basal, maximal, or meal-stimulated acid outputs.…”

Diversity in bacterium-host interactions within the species Helicobacter heilmannii sensu stricto

“…H. pylori infection in human patients and animal models is commonly associated with increased gastrin levels and is considered to be a reaction to the H. pylori- induced hypochlorhydria [47,48]. In an attempt to repair acid homeostasis, gastrin stimulates histamine release from enterochromaffin-like (ECL) cells, inducing acid secretion [49-51].…”

Helicobacter pylori eradication induces marked increase in H+/K+-adenosine triphosphatase expression without altering parietal cell number in human gastric mucosa

“…Antibacterial treatment is known to induce resolution of the acute component of H pylori gastritis within a few days after treatment. 21 IL-1b is important in initiating and amplifying the inflammatory response against bacteria and is also a potent inhibitor of gastric acid secretion. [22][23][24][25][26] Indeed, our data showed a negative association between H + /K + -ATPase and IL-1b, supporting this notion.…”