ERADICATION OF HELICOBACTER-PYLORI AND GASTRIN SOMATOSTATIN LINK IN DUODENAL-ULCER PATIENTS

Helicobacter pylori (Hp) infection may be associated with duodenal ulc er (DU) and accompanied by increased release of gastrin and deficiency of somatostatin (S-S) but the mechanisms of these changes in DU patie nts after eradication of Hp have been little studied. Cholecystokinin (CCK) has been implicated in the feedback control of gastric acid secr etion in healthy subjects but its contribution to secretory disorders in DU patients has been little examined. This study, therefore, invest igated whether CCK participates in the impairment of postprandial gast rin release and gastric acid secretion in active DU patients. Tests we re undertaken in 10 DU patients without or with elimination of the act ion of endogenous CCK using loxiglumide (LOX), a selective CCK-A recep tor antagonist, before and 4 wk, after eradication of Hp with triple t herapy (omeprazole, amoxycillin and bismuth). In Hp positive DU patien ts, the postprandial acid secretion (measured by continuous intragastr ic pH monitoring) was accompanied by a pronounced increment in plasma gastrin with negligible increase of intraluminal release of S-S. The a dministration of LOX in these patients did not affect significantly th e postprandial pH profile and the rise in plasma gastrin. After eradic ation of Hp the median postprandial intragastric pH increased to about 4.3 (compared to 3.5 before the Hp eradication); the postprandial gas trin concentration was reduced by about 40%, while luminal release of S-S was increased 2 folds. The administration of LOX resulted in signi ficantly greater decrease in median pH (3.1) and higher rise in postpr andial plasma gastrin in these patients. Also the postprandial plasma S-S showed a small, but significant decline (by about 25%) as compared to that in placebo treated patients. This study provides evidence tha t: (1) Hp infection in DU patients is accompanied by enhanced gastrin release and the reduction in luminal release of S-S; (2) The failure o f LOX to affect gastric secretion and plasma gastrin DU Hp infected pa tients could be attributed, at least in part, to the failure of endoge nous CCK to control gastric acid secretion via release of S-S; (3) Hp infected patients appear to exhibit a deficiency of S-S release that c an be reversed by the eradication of Hp indicating that both peptides may contribute to the acceleration of the ulcer healing following Hp e radication in DU patients; (4) The test with LOX and gastric luminal S -S assay may be useful in identification of Hp positive DU patients wi th CCK-mediated impaired feedback control of gastric secretion and def iciency of S-S caused by Hp infection.