[Mechanisms in hypergastrinemia in autoimmune atrophic gastritis and Helicobacter pylori infection].
The authors review recent progresses made in the understanding of the disturbed gastrin homeostasis in Helicobacter pylori infection and in pernicious anaemia. Regulation of gastrin release in a complex mechanism involving inhibition by a low gastric pH and several peptides including somatostatin, and stimulation by different factors, mainly alimentary peptides and amino-acids. The hypergastrinaemia observed in patients with Helicobacter pylori infection occurs despite a normal intraluminal pH. This may be through alkalinisation of the gastric mucus layer due to the production of ammonia by the bacterial urease or through local release of inflammatory mediators. In pernicious anaemia a factor present in the antacid gastric juice could explain the important hypergastrinaemia observed. The gastrin releasing activity of the gastric juice itself was demonstrated by a decrease of the patients' plasma gastrin concentration during a neutral gastric lavage and by a rise of the gastrin levels in rats whose stomachs were perfused with gastric juice from pernicious anaemia patients. A better understanding of the relation between gastric pH and gastrin release is important not only for these pathological states but also for treatments which suppress acid secretion.
Deprez
P
P
Département de Médecine Interne, Cliniques Universitaires Saint-Luc, Bruxelles, Belgique.
Calam
J
J
D000752:Anemia, Pernicious / Q000097:blood*; D000818:Animals; D005744:Gastric Acid / Q000378:metabolism; D005755:Gastrins / Q000097:blood*; D016481:Helicobacter Infections / Q000097:blood*; D016480:Helicobacter pylori; D006801:Humans; D006863:Hydrogen-Ion Concentration; D051381:Rats
D005755:Gastrins
Nouveaux mécanismes d'hypergastrinémie en rapport avec la gastrite atrophique auto-immune et l'infection à Helicobacter pylori.