HELICOBACTER-PYLORI AND IMPAIRED GASTRIC SECRETORY FUNCTIONS ASSOCIATED WITH DUODENAL-ULCER AND ATROPHIC GASTRITIS

Previous study shelved that duodenal ulcer (DU) patients infected with Helicobacter. pylori (H. pylori) have increased basal and pentagastri n-or GRP-induced gastric acid secretion and that these disturbances re versed fully after eradication of H. pylori. This study was designed t o compare the gastric acid secretory profile, plasma gastrin levels an d growth factors (EGF and TGF alpha) expression in gastric mucosa in D U patients with those in atrophic gastritis patients before and six mo nths after verified eradication of H. pylori. In DU patients, basal an d stimulated (GRP and pentagastrin) gastric acid secretion was signifi cantly higher than in healthy controls. Six months following the eradi cation of H. pylori with triple therapy (omeprazole + clarithromycin amoxicillin), this secretion returned to normal value. In contrast, i n patients with atrophic gastritis, such eradication of H. pylori resu lted in a significant increase in basal and pentagastrin-and GRP-stimu lated acid secretion. Mucosal expression of immunoreactive EGF and TGF alpha was significantly enhanced in Ei. pylori positive DU and atroph ic gastritis patients but this elevation disappeared or was markedly d ecreased 6 months upon the eradication of H. pylori. We conclude that 1) H. pylori infection is accompanied both in DU and atrophic gastriti s patients by an enhanced plasma gastrin and increased mucosal express ion of EGF and TGF alpha, 2) basal and GRP-induced acid secretion is s ignificantly elevated in DU, whereas that in atrophic gastritis patien ts is greatly reduced, and 3) the H. pylori eradication restores gastr ic acid and plasma gastrin release as well as the mucosal expression o f growth factors in DU and atrophic gastritis.