Salivary and gastric luminal release of epidermal growth factor under basal conditions and after pentagastrin stimulation in healthy subjects and in duodenal ulcer patients before and after eradication of Helicobacter pylori

Epidermal growth factor (EGF) is secreted by salivary and Brunner's glands and shows a potent inhibitory effect on gastric acid and stimulatory influence on mucosal growth and protection but little is known about the effect of the Helicobacter pylori (Hp) infection on the release of EGF. In this study the salivary and gastric concentrations of EGF have been measured and gastric mucosal expression of EGF has been determined in 25 Hp positive duodenal ulcer (DU) patients before and after the eradication of Hp (using triple therapy with omeprazole, 20 mg bd, amoxycillin, 500 mg qd and metronidazole, 500 mg bd for 2 weeks) and in 10 healthy controls under basal conditions and following pentagastrin (2 mu g/kg-h) stimulation. Basal salivary and gastric concentrations of EGF were similar and no significant difference was found between DU patients and healthy controls. Pentagastrin infusion (2 mu g/kg-h) caused a significant increase in EGF release into saliva and gastric juice both in healthy controls and DU patients but in DU patients the Hp eradication resulted in several folds higher basal and pentagastrin-induced gastric EGF content than that before the anti-Hp therapy, whereas such Hp eradication had no significant influence on basal and pentagastrin-induced salivary EGF. Antral mucosal expression of EGF in Hp-positive DU patients was significantly higher than that in healthy Hp-negative controls and this elevation persisted after eradication of Hp. Basal and pentagastrin-induced gastric acid outputs In Hp-positive DU patients were significantly higher than in healthy controls and they were slightly reduced after the triple therapy. In all DU patients, 4 weeks after termination of anti-Hp therapy, a complete ulcer healing occurred. We conclude that (1) the stomach is capable of secreting large amounts of EGF and pentagastrin appears to be a potent stimulus of salivary and gastric EGF release; (2) the Hp infection reduces the release of gastric EGF and the eradication of Hp results in the augmentation of basal and pentagastrin-induced EGF release into the stomach but not into the saliva and (3) since the eradication of Hp infection in DU patients resulted in DU healing and this was accompanied by an increase in EGF release, we conclude that EGF plays a crucial role in the DU healing process.