Hypergastrinaemia during long-term omeprazole therapy: influences of vagal nerve function, gastric emptying and Helicobacter pylori infection
Version of Record online: 25 DEC 2001
Alimentary Pharmacology & Therapeutics
Volume 12, Issue 7, pages 605–612, July 1998
How to Cite
Schenk, Kuipers, Klinkenberg-Knol, Bloemena, Nelis, Festen, Jansen, Biemond, Lamers and Meuwissen (1998), Hypergastrinaemia during long-term omeprazole therapy: influences of vagal nerve function, gastric emptying and Helicobacter pylori infection. Alimentary Pharmacology & Therapeutics, 12: 605–612. doi: 10.1046/j.1365-2036.1998.00349.x
- Issue online: 25 DEC 2001
- Version of Record online: 25 DEC 2001
To elucidate the mechanisms that lead to severe hypergastrinaemia during long-term omeprazole therapy for gastro-oesophageal reflux disease (GERD).
Patients and methods:
A total of 26 GERD patients were studied during omeprazole maintenance therapy. Twelve patients with severe hypergastrinaemia (gastrin > 400 ng/L) were compared with 14 control patients (gastrin < 300 ng/L). Helicobacter pylori serology and a laboratory screen were obtained in all patients. Gastric emptying was scored by the evidence of food remnants upon endoscopy 12 h after a standardized meal. Gastric antrum and corpus biopsies were analysed for histological parameters, as well as somatostatin and gastrin concentrations. All patients underwent a meal-stimulated gastrin test and the hypergastrinaemia patients also underwent a vagal nerve integrity assessment by pancreatic polypeptide testing (PPT).
Severe hypergastrinaemia patients had a longer duration of treatment (80 vs. 55 months; P = 0.047) and were characterized by a higher prevalence of H. pylori infection (9/12 vs. 2/14, P = 0.004), corpus mucosal inflammation and atrophic gastritis (P < 0.04). This was reflected in lower serum pepsinogen 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 hypergastrinaemia 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.
Severe hypergastrinaemia during omeprazole maintenance therapy for GERD is associated with the duration of therapy and H. pylori infection, but not with abnormalities of gastric emptying or vagal nerve integrity.