Alimentary TractRebound hypersecretion after omeprazole and its relation to on-treatment acid suppression and Helicobacter pylori status☆
Section snippets
Subjects
Twelve H. pylori–negative healthy volunteers (6 men; 3 smokers; mean age, 28.3 years; mean weight, 71.4 kg) and 9 H. pylori–positive healthy volunteers (3 men; 1 smoker; mean age, 30.6 years; mean weight, 70.2 kg) were studied before, during treatment, and at day 15 after omeprazole. Additionally, 7 H. pylori–negative healthy volunteers (4 men; 2 smokers; mean age, 27.4 years; mean weight, 83.1 kg) were studied before, during treatment, and at day 6 after omeprazole. None of the volunteers was
Basal acid output (day 15)
Before omeprazole treatment, median basal acid output (BAO) of the H. pylori–negative subjects was 3.0 mmol · h−1 (range, 0.0–9.7), which was the same as that of H. pylori–positive subjects, 3.0 mmol · h−1 (range, 0.7–14.7) (P < NS) (Figure 1).
At day 15 postomeprazole, BAO of the H. pylori–negative subjects was 6.8 mmol · h−1 (range, 0.6–17.0), which
Discussion
This study shows that a 2-month course of 40 mg/day omeprazole induces marked rebound hypersecretion of gastric acid in H. pylori–negative subjects and that the degree of rebound hypersecretion is related to the elevation of intragastric pH and fasting plasma gastrin during the treatment. H. pylori–positive subjects show a heterogenous response after omeprazole treatment with a proportion showing persisting suppression of acid secretion.
In the H. pylori–negative subjects, there was a median
Acknowledgements
The authors thank Dr. Andrew Kelman for his kind advice on the appropriate pharmacokinetic analysis of the data and the Scottish National Blood Transfusion Service for the provision of human serum albumin.
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Address requests for reprints to: Kenneth E. L. McColl, M.D., University Department of Medicine & Therapeutics, Western Infirmary, Glasgow, G11 6NT Scotland. Fax: (44) 141-339-2800.