ERADICATING HELICOBACTER-PYLORI REDUCES HYPERGASTRINEMIA DURING LONG-TERM OMEPRAZOLE TREATMENT

Background-Both proton pump inhibitor drug treatment and Helicobacter pylori infection cause hypergastrinaemia in man. Aims-To determine whe ther eradicating H pylori is a means of reducing hypergastrinaemia dur ing subsequent proton pump inhibitor treatment. Methods-Patients with Pi pylori were randomised to treatment with either anti-ii pylori or s ymptomatic treatment. One month later, all received four weeks treatme nt with omeprazole 40 mg/day for one month followed by 20 mg/day far s ix months. Serum gastrin concentrations were measured before and follo wing each treatment, Results-In the patients randomised to anti-hi pyl ori treatment, eradication of the infection lowered median fasting gas trin by 48% and meal stimulated gastrin by 46%. When gastrin concentra tions one month following anti-hi pylori/symptomatic treatment were us ed as baseline, omeprazole treatment produced a similar percentage inc rease in serum gastrin in ;he ii pylori infected and hi pylori eradica ted patients. Consequently, in the patients in which H pylori was not eradicated, median fasting gastrin concentration was 38 ng/l (range 26 -86) at initial presentation and increased to 64 ng/l (range 29-271) a fter seven months omeprazole, representing a median increase of 68% (p <0.005). In contrast, In the patients randomised to Hi pylori eradicat ion, median fasting gastrin at initial presentation was 54 ng/l (range 17-226) and was unchanged after seven months omeprazole at 38 ng/l (r ange 17-95). Conclusion-Eradicating hi pylori is a means of reducing t he rise in gastrin during subsequent long term omeprazole treatment. I n view of the potential deleterious effects of hypergastrinaemia it ma y be appropriate to render patients H pylori negative prior to commenc ing long term proton pump inhibitor treatment.