Abstract Preliminary data showed that bombesin stimulated serum gastrin levels in patients with the Zollinger—Ellison syndrome (ZES). In this study, the total immunoreactive gastrin and the different molecular forms of gastrin were measured in 16 patients with ZES (11 with proved pancreatic gastrinoma, 2 with proved duodenal gastrinoma and 3 with uncertain tumour localization) following bombesin infusion and following calcium infusion in 13 patients. In all patients with gastrinoma (both pancreatic and duodenal) bombesin augmented serum gastrin levels. In patients with pancreatic gastrinoma calcium infusion was a more potent stimulator of gastrin secretion than bombesin. In the 2 patients with duodenal gastrinoma bombesin was more potent than calcium in stimulating serum gastrin levels with a basal/stimulated gastrin level ratio similar to the ratio found in patients with incomplete antrectomy. These data suggest that gastrin-producing cells from duodenal gastrinomas may be more closely related to the normal antral G cells than to the gastrin-producing cells from pancreatic gastrinomas. Furthermore, the comparison between the basal/calcium and the basal/bombesin stimulated gastrin levels may help in differentiating preoperatively patients with pancreatic gastrinoma from patients with retained antral mucosa. In all the patients studied, bombesin augmented the concentration of all of the gastrin components considered. These data support the hypothesis that G 34, G 17 and the N-terminal G 17 fragment are all present in gastrinomas.
The role of prostaglandins in peptic ulcer disease and their relation to Helicobacter pylori infection remain controversial. This study sought to compare the effects of oral nizatidine and ranitidine on the gastric mucosal release of prostanoids in duodenal ulcer (DU) patients and to correlate prostanoid concentrations with H. pylori status. Twenty-eight patients with DUs were randomized to receive either nizatidine or ranitidine. Nizatidine 300 mg at night elevated intraluminal PGE2 concentrations; 6-keto-PGF1α, concentrations also rose, but did not reach statistical significance. Ranitidine induced nonsignificant falls in PGE2 and 6-keto-PGE1α concentrations. Patients with H. pylori infection had lower PGE, and 6-keto-PGF1α concentrations than non-infected patients, but nizatidine was equally effective in increasing prostanoid levels in both groups. These findings may be considered as favourable side effects of nizatidine with uncertain clinical significance. Further studies are needed to elucidate the synergism between prostanoids, eradication of H. pylori and nizatidine in the treatment of DU.
