Gastroenterology

Gastroenterology

Volume 116, Issue 2, February 1999, Pages 239-247
Gastroenterology

Alimentary Tract
Rebound hypersecretion after omeprazole and its relation to on-treatment acid suppression and Helicobacter pylori status

https://doi.org/10.1016/S0016-5085(99)70118-6Get rights and content

Abstract

Background & Aims: There have been conflicting reports regarding acid secretion after treatment with omeprazole. This study examined acid secretion after treatment with omeprazole and its relation to Helicobacter pylori status and on-treatment gastric function. Methods: Twelve H. pylori–negative and 9 H. pylori–positive subjects were examined before, on, and at day 15 after an 8-week course of 40 mg/day omeprazole. On each occasion, plasma gastrin, intragastric pH, and acid output were measured basally and in response to increasing doses of gastrin 17. Results: In the H. pylori–negative subjects at day 15 after omeprazole treatment, basal acid output was 82% higher (P < 0.007) and maximal acid output 28% higher (P < 0.003) than before omeprazole. The degree of increase in maximal acid output was related to both on-treatment pH and on-treatment fasting gastrin levels, being 48.0% in subjects with an on-treatment pH of >4 vs. 21.0% in those with a pH of <4 (P < 0.02) and 49.2% in subjects with an on-treatment gastrin of >25 ng · L−1 vs. 19.8% in those with a fasting gastrin of <25 ng · L−1 (P < 0.006). At day 15 after omeprazole treatment, the H. pylori–positive subjects showed a heterogeneous response with some having increased acid output and others persisting suppression. Conclusions: Rebound acid hypersecretion occurs in H. pylori–negative subjects after omeprazole treatment. Its severity is related to the degree of elevation of pH on treatment. Persisting suppression of acid secretion masks the phenomenon in H. pylori–positive subjects.

GASTROENTEROLOGY 1999;116:239-247

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).

. BAO in H. pylori–negative and –positive subjects before commencing a 2-month course of 40 mg/day omeprazole and 15 days after completing it.

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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