DUODENAL BICARBONATE SECRETION - ERADICATION OF HELICOBACTER-PYLORI AND DUODENAL STRUCTURE AND FUNCTION IN HUMANS

Background & Aims: Eradication of Helicobacter pylori expedites duoden al ulcer healing and prevents recurrences. Most patients with duodenal ulcers have impaired proximal duodenal mucosal bicarbonate secretion (DMBS). In patients with inactive, healed duodenal ulcers and normal s ubjects, the effect of H. pylori infection on DMBS and proximal duoden al secretory function and structure were examined. Methods: DMBS was q uantitated before and after eradication of H. pylori. Mucosal structur e (duodenal bulb histopathology) and function (DMBS at rest and stimul ated, effect of active vs. healed ulcer and of age) were determined in patients with duodenal ulcers and normal subjects. Results: In patien ts with duodenal ulcers, H. pylori eradication normalized proximal DMB S. Histological examination of duodenal biopsy samples was comparable in patients with duodenal ulcers and normal subjects without apparent relationship between inflammation and DMBS. Significantly impaired DMB S occurred in response to all agonists tested (luminal acid, prostagla ndin E(2), and cephalic-vagal stimulation) in patients with duodenal u lcers, suggesting a generalized secretory defect. Neither the presence of active (vs. inactive) ulcer nor age significantly affected bicarbo nate secretion. Conclusions: In patients with duodenal ulcers, eradica tion of H. pylori normalized proximal DMBS and may thereby reduce ulce r recurrences. Altered DMBS in patients with duodenal ulcers was unrel ated to histopathologic abnormalities. Impaired bicarbonate secretion in patients with duodenal ulcers could be caused by a cellular and/or physiological regulatory transport defect possibly related to H. pylor i.