ZOLLINGER-ELLISON SYNDROME AND ANTRAL G-CELL HYPERFUNCTION IN PATIENTS WITH RESISTANT DUODENAL-ULCER DISEASE

We measured basal and pentagastrin-stimulated acid secretion, as well as basal and meal-stimulated plasma gastrin concentration to determine , in 67 patients affected by resistant duodenal ulcer, whether their c ondition could be related to gastric acid secretion and/or gastrin-rel ated syndromes. We then compared them to 46 duodenal ulcer control pat ients. The outpatients were investigated consecutively. The resistant duodenal ulcer patients differed from the controls only in their highe r complication rates (bleeding or perforation, P < 0.05). We identifie d five patients in the resistant duodenal ulcer group with Zollinger-E llison syndrome and 12 with antral G cell hyperfunction, whereas in th e control group only one patient was affected by antral G cell hyperfu nction. IgG anti-Helicobacter pylori antibodies were positive for the presence of infection in 7 of the hypergastrinaemic patients. When Zol linger-Ellison syndrome or antral G cell hyperfunction were excluded, no differences could be found in gastric acid secretion, or basal and meal-stimulated plasma gastrin levels, between the resistant and contr ol duodenal ulcer patients, except for basal acid hypersecretion (resi stant duodenal ulcer 16% vs duodenal ulcer 2% P = 0.0144). In the pres ence of duodenal ulcer disease resistant to H-2-blockers, it is mandat ory to measure basal plasma gastrin concentration since it was possibl e to diagnose the gastrin-related syndromes, Zollinger-Ellison syndrom e and antral G cell hyperfunction, in 26% of this group of patients.