Gastric bicarbonate secretion and release of prostaglandin E2 are increased in duodenal ulcer patients, but not in Helicobacter pylori positive healthy subjects.

Background: Duodenal ulcer (DU) patients have impaired proximal duodenal mucosal bicarbonate secretion at rest and in response to luminal acid with higher acid-stimulated mucosal release of prostaglandin (PG) E(2) than healthy subjects. Our purpose was to determine whether this abnormality was present also in the stomach of DU patients. Methods: Simultaneous determinations of gastric and duodenal bicarbonate secretion and luminal release of PGE(2) were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positivr). Results: In healthy volunteers the rates of gastroduodenal bicarbonate secretion and the release of PGE(2), were not influenced by H. pylori status. In inactive DU patients the rates of basal (704 +/- 84 versus 356 +/- 40 mu mol/h: mean +/- SEM) and vagally stimulated (modified sham feeding) (1724 +/- 376 versus 592 +/- 52 mu mol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 +/- 42 versus 591 +/- 51 mu mol/h and 543 +/- 99 versus 778 +/- 69 mu mol/h) in duodenal bicarbonate secretion were lower (p < 0.05). In addition, inactive DU patients had higher basal (148 +/- 32 versus 53 +/- 5 ng/h) and stimulated (291 +/- 84 versus 131 +/- 25 ng/h) gastric release of PGE(2), but only the basal release of PGE(2) into the duodenum was significantly increased (20 +/- 3 versus 5 +/- 1 ng/h; p < 0.05). Conclusion: Increased mucosal production of PGE(2) may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. Th; defective duodenal secretion of bicarbonate observed in these patients may be a consequence of previous ulceration rather than the mere presence of H. pylori infection.