The somatostatin-gastrin link of Helicobacter pylori infection.
Helicobacter pylori is the new-found cause of duodenal ulcers (DU), but acid secretion remains necessary and is elevated in DU patients. My group and others have asked whether H. pylori itself alters gastric physiology. This infection has been found to decrease local expression of the inhibitory peptide somatostatin, and to increase release of the acid-stimulating hormone gastrin. H. pylori infection can alter acid secretion in both directions. Acid disappears temporarily on first infection, and may dwindle later if H. pylori causes gastric atrophy. DU patients have approximately twice the normal parietal cell mass, which increases their maximal secretory capacity, but it is not clear whether or not this is due to H. pylori. However, the infection certainly does change physiological control of acid secretion, as expected from the endocrine changes. Acid secretion is elevated during fasting, during stimulation with an acidic meal and during infusions of gastrin-releasing peptide. The balance between these opposing effects of H. pylori on acid may be crucial in determining the clinical outcome of H. pylori infection. High-acid secretion leads to DUs whilst low acid secretion is found in patients with gastric ulcers and gastric cancer. Inflammatory cytokines released in H. pylori gastritis may cause some of these changes in gastric physiology.
Calam
J
J
Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
D000818:Animals; D016207:Cytokines / Q000502:physiology; D004381:Duodenal Ulcer / Q000382:microbiology / Q000503:physiopathology*; D005744:Gastric Acid / Q000378:metabolism; D005755:Gastrins / Q000378:metabolism*; D016481:Helicobacter Infections / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000201:enzymology; D006801:Humans; D013004:Somatostatin / Q000378:metabolism*; D014510:Urease / Q000502:physiology
D016207:Cytokines; D005755:Gastrins; D013004:Somatostatin; D014510:Urease