Eradicating Helicobacter pylori reduces hypergastrinaemia during long term omeprazole treatment

Background-Both proton pump inhibitor drug treatment and Helicobacter pylori infection cause hypergastrinaemia in man. Aims-To determine whether eradicating H pylori is a means of reducing hypergastrinaemia during subsequent proton pump inhibitor treatment. Methods-Patients with Pi pylori were randomised to treatment with either anti-ii pylori or symptomatic treatment. One month later, all received four weeks treatment with omeprazole 40 mg/day for one month followed by 20 mg/day far six months. Serum gastrin concentrations were measured before and following each treatment, Results-In the patients randomised to anti-hi pylori treatment, eradication of the infection lowered median fasting gastrin by 48% and meal stimulated gastrin by 46%. When gastrin concentrations one month following anti-hi pylori/symptomatic treatment were used as baseline, omeprazole treatment produced a similar percentage increase in serum gastrin in ;he ii pylori infected and hi pylori eradicated 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) after seven months omeprazole, representing a median increase of 68% (p<0.005). In contrast, In the patients randomised to Hi pylori eradication, median fasting gastrin at initial presentation was 54 ng/l (range 17-226) and was unchanged after seven months omeprazole at 38 ng/l (range 17-95). Conclusion-Eradicating hi pylori is a means of reducing the rise in gastrin during subsequent long term omeprazole treatment. In view of the potential deleterious effects of hypergastrinaemia it may be appropriate to render patients H pylori negative prior to commencing long term proton pump inhibitor treatment.