Gastric Bicarbonate Secretion and Release of Prostaglandin E₂ Are Increased in Duodenal Ulcer Patients But Not in Helicobacter pylori-Positive Healthy Subjects

Abstract

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) E₂ 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 PGE₂ were performed in 16 healthy volunteers (5 Helicobacter pylori-positive) and 8 inactive DU patients (all H. pylori-positive). Results: In healthy volunteers the rates of gastroduodenal bicarbonate secretion and the release of PGE₂ were not influenced by H. pylori status. In inactive DU patients the rates of basal (704 ± 84 versus 356 ± 40 μmol/h; mean ± SEM) and vagally stimulated (modified sham feeding) (1724 ± 376 versus 592 ± 52 μmol/h) gastric bicarbonate secretion were higher (p < 0.05) than in the health, whereas the corresponding rates (339 ± 42 versus 591 ± 51 μmol/h and 543 ± 99 versus 778 ± 69 μmol/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 PGE₂, but only the basal release of PGE₂ into the duodenum was significantly increased (20 ± 3 versus 5 ± 1 ng/h; p < 0.05). Conclusion: Increased mucosal production of PGE₂ may be responsible for the abnormally high gastric secretion of bicarbonate in inactive DU patients. The 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.

Key Words:

• Bicarbonate secretion
• duodenal ulcer
• duodenum
• Helicobacter pylori
• prostaglandins
• stomach