HYPERGASTRINEMIA DURING LONG-TERM OMEPRAZOLE THERAPY - INFLUENCES OF VAGAL NERVE FUNCTION, GASTRIC-EMPTYING AND HELICOBACTER-PYLORI INFECTION

Aim: To elucidate the mechanisms that lead to severe hypergastrinaemia during long-term omeprazole therapy for gastro-oesophageal reflux dis ease (GERD). Patients and methods: A total of 26 GERD patients were st udied during omeprazole maintenance therapy. Twelve patients with seve re hypergastrinaemia (gastrin > 400 ng/L) were compared with 14 contro l patients (gastrin < 300 ng/L). Helicobacter pylori serology and a la boratory screen were obtained in all patients. Gastric emptying was sc ored by the evidence of food remnants upon endoscopy 12 h after a stan dardized meal. Gastric antrum and corpus biopsies were analysed for hi stological parameters, as well as somatostatin and gastrin concentrati ons. All patients underwent a meal-stimulated gastrin test and the hyp ergastrinaemia patients also underwent a vagal nerve integrity assessm ent by pancreatic polypeptide testing (PPT). Results: Severe hypergast rinaemia patients had a longer duration of treatment (80 vs. 55 months ; P = 0.047) and were characterized by a higher prevalence of H. pylor i infection (9/12 vs. 2/14, P = 0.004), corpus mucosal inflammation an d atrophic gastritis (P < 0.04). This was reflected in lower serum pep sinogen A concentrations (mean +/- S.E.M. 53.6 +/- 17.9 vs. 137 +/- 16 .0 mg/L, P = 0.03), pepsinogen A/C ratio (1.8 +/- 0.3 vs. 4.1 +/- 0.6, P = 0.005) and mucosal somatostatin concentrations (2.75 +/- 0.60 vs. 4.48 +/- 1.08 mg/g protein, P = 0.038). Two patients in the hypergast rinaemia group had signs of delayed gastric emptying, but none in the normogastrinaemia group did (P = N.S.). In addition, both groups had a normal meal-stimulated gastrin response. Conclusion: Severe hypergast rinaemia during omeprazole maintenance therapy for GERD is associated with the duration of therapy and H. pylori infection, but not with abn ormalities of gastric emptying or vagal nerve integrity.