HELICOBACTER-PYLORI INFECTION AND EXAGGERATED GASTRIN-RELEASE - EFFECTS OF INFLAMMATION AND PROGASTRIN PROCESSING

Helicobacter pylori infection is associated with exaggerated gastrin r elease. We investigated whether this abnormality was due to the bacter ia or the immune response. Fasting and meal-stimulated 'total' and ami dated gastrin were measured in 10 H. pylori-infected volunteers before eradication therapy, after 2 and 14 days of therapy, and 4 weeks afte r completion of therapy. The exaggerated meal-stimulated gastrin conce ntration remained unchanged after 2 days of therapy, although the poly morphonuclear cell infiltrate and H. pylori bacteria were no longer ev ident. The expected fall in gastrin concentration after 14 days of the rapy was associated with a reduction in the density of mucosal mononuc lear cells, suggesting exaggerated gastrin release was related to chro nic inflammation or to H. pylori or its products. The effect of H. pyl ori on normal progastrin processing was also assessed; 2 control group s were included: 10 H. pylori-uninfected volunteers and 13 patients wi th H. pylori peptic ulcers. There was a significant difference in the proportion of circulating gastrins that were biologically active amida ted gastrins between ulcer patients and uninfected controls (56,7 +/- 4% versus 33.8 +/- 4%, p < 0.001). The proportion of amidated to total gastrins did not increase after successful eradication.