Eradicating Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer.

Abstract

Helicobacter pylori (H pylori) raises serum gastrin but it is unclear whether this stimulates increased acid secretion. Gastrin mediated acid secretion and plasma gastrin after the intravenous infusion of gastrin releasing peptide was studied in nine H pylon negative and nine H pylon positive healthy volunteers, and in 11 duodenal ulcer patients. Nine of the last group were re-examined one month after eradication of H pylon.

Helicobacter pylori

“…Decreased expression of somatostatin also explains the increased gastrin-releasing peptide (GRP)-stimulated acid secretion found in H . pylori infection by ElOmar et al [93], because GRP normally stimulates release of somatostatin as well as gastrin (Fig. 1) [94].…”

“…Another possibility is that ulceration itself causes elevated basal acid secretion. However, this cannot be the whole story because H. pylori infection is associated with elevated acid secretion during stimulation with acid-peptone and GRP, even in patients without ulcers [84,93].…”

Pathogenesis of duodenal ulcer disease: the rest of the story

“…They showed that GRP-stimulated acid secretion was exaggerated in patients with duodenal ulcer compared with uninfected patients or those with H. pylori infection without duodenal ulcer disease. 32,34,35 The results of these experiments illustrate the pitfalls that arise in attempting to identify speci®c dysregulations of gastric physiology relating H. pylori and duodenal ulcer disease without including what are now recognized as the controls needed to place the physiological observations into perspective (Table 2). For example, GRP-stimulated acid secretion has been reported to be exaggerated in duodenal ulcer patients compared with those with H. pylori infection without duodenal ulcer, or uninfected individuals.…”

Ecology of Helicobacter pylori in the human stomach.

“…In this model, the equilibrium established by the colonizing population in each host is dynamic and unique. A consequence of these interactions is that the nature of the equilibrium would determine such characteristics as epithelial cell proliferation and apoptosis (14), gastric secretion (15), and antigenic stimulation of lymphoid cell populations (16). These in turn, would be determinants of the likelihood of disease under differing environmental circumstances.…”