Abstract
Fasting and meal-stimulated NH2-terminal gastrin concentrations in serum were significantly higher in patients with active duodenal ulcer than in control subjects and in patients with inactive duodenal ulcer (p <0.05). In contrast, the COOH-terminal gastrin concentrations (the bioactive gastrins) did not differ among the groups. Parallel variation in the NH2-and COOH-terminal gastrin concentrations occurred both during meal stimulation and as response to adrenalin or secretin infusion. In a longitudinal study of duodenal ulcer patients, higher NH2-than COOH-terminal gastrin concentrations were associated with the active phase of the disease, whereas this seldom occurred during the inactive phase (p <0.001). These data suggest that abnormally large amounts of the NH2-terminal fragment of gastrin-17 are released to the circulation during the active phase of duodenal ulcer.