Eradicating Helicobacter pylori reduceshypergastrinaemia during long term omeprazole treatment

Background—Both proton pump inhibitor drugtreatment and Helicobacter pylori infection causehypergastrinaemia in man.
Aims—To determine whether eradicating Hpylori is a means of reducing hypergastrinaemia duringsubsequent proton pump inhibitor treatment.
Methods—Patients with H pylori wererandomised to treatment with either anti-H pylori orsymptomatic treatment. One month later, all received four weekstreatment with omeprazole 40 mg/day for one month followed by 20 mg/dayfor six months. Serum gastrin concentrations were measured before andfollowing each treatment.
Results—In the patients randomised toanti-H pylori treatment, eradication of the infectionlowered median fasting gastrin by 48% and meal stimulated gastrin by46%. When gastrin concentrations one month following anti-Hpylori/symptomatic treatment were used as baseline,omeprazole treatment produced a similar percentage increase in serumgastrin in the H pylori infected and H 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 amedian increase of 68% (p<0.005). In contrast, in the patients randomised to H pylori eradication, median fasting gastrinat 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 H pylori is ameans of reducing the rise in gastrin during subsequent long termomeprazole treatment. In view of the potential deleterious effects ofhypergastrinaemia it may be appropriate to render patients Hpylori negative prior to commencing long term proton pumpinhibitor treatment.

Keywords:hypergastrinaemia; Helicobacter pylori; omeprazole