MECHANISMS OF HYPERGASTRINEMIA IN PERNICI OUS-ANEMIA 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 is a complex mechani sm involving inhibition by a low gastric pH and several peptides inclu ding somatostatin, and stimulation by different factors, mainly alimen tary peptides and amino-acids. The hypergastrinaemia observed in patie nts with Helicobacter pylori infection occurs despite a normal intralu minal pH. This may be through alcalinisation of the gastric mucus laye r due to the production of ammonia by the bacterial urease or through local release of inflammatory mediators. In pernicious anaemia a facto r present in the anacid gastric juice could explain the important hype rgastrinaemia observed. The gastrin releasing activity of the gastric juice itself was demonstrated by a decrease of the patients' plasma ga strin concentration during a neutral gastric lavage and by a rise of t he gastrin levels in rats whose stomachs were perfused with gastric ju ice from pernicious anaemia patients. A better understanding of the re lation between gastric pH and gastrin release is important not only fo r these pathological states but also for treatments which suppress aci d secretion.