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Hypergastrinaemia during long‐term omeprazole therapy: influences of vagal nerve function, gastric emptying and Helicobacter pylori infection
Author(s) -
B.E. Schenk,
E.J. Kuipers,
Elly C. KlinkenbergKnol,
Elisabeth Bloemena,
G. F. Nelis,
H. P. M. Festen,
Erik Jansen,
I. Biemond,
C. B. H. W. Lamers,
S. G. M. Meuwissen
Publication year - 1998
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.1998.00349.x
Subject(s) - gastroenterology , medicine , helicobacter pylori , gastrin , gastric emptying , gerd , omeprazole , gastritis , atrophic gastritis , stomach , antrum , endocrinology , reflux , disease , secretion
Aim: 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). Results: 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. Conclusion: 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.