Clinical and pathophysiological consequences of on-demand treatment with PPI in endoscopy-negative reflux disease. Is rebound hypersecretion of acid a problem?

Abstract

Objective. Rebound acid hypersecretion after withdrawal of proton pump inhibitor (PPI) may lead to symptom aggravation and difficulties in withdrawing anti-reflux medication. The aim was to investigate pathophysiological and clinical consequences of on-demand treatment with PPI in patients with endoscopy-negative reflux disease. Material and methods. Twenty-six patients with endoscopy-negative reflux disease were investigated for rebound effects of lansoprazole 15 mg, used on-demand, maximum 4 capsules daily during a 6-month period. P-CgA and s-gastrin were measured before, at termination and 2 weeks after stopping treatment. Symptom score was performed the week before and the second week after treatment, 24-h pH-metry after both periods. Results. Median daily consumption of lansoprazole was 15.1 mg (95% CI: 10.5; 18.8). S-gastrin before treatment was 31.2 pmol/l, 54.8 at the end (p < 0.01), 31.7 two weeks after withdrawal. P-CgA was 16.7 u/l before treatment, 37.5 at the end (p < 0.01), 17.7 two weeks after withdrawal (p = 0.35). A positive correlation was found between total consumption of lansoprazole and CgA increase during treatment (r = 0.44 p = 0.03). There was a reduction in symptom score during the treatment period from 30 (24–38) before, to 20 (15–36) the second week after treatment, p = 0.06. 32% had increase in symptoms. Conclusions. Rebound acid hypersecretion is probably an infrequent problem in on-demand treatment with PPI in patients with endoscopy-negative reflux disease. A significant increase in p-CgA and s-gastrin was found after 6 months treatment. Fourteen days after withdrawal, CgA and gastrin returned to pretreatment levels. Overall, no aggravation of symptoms was found, but 1/3 experienced increased symptoms.

Key Words::

• Gastro-esophageal reflux
• heartburn
• lansoprazole
• esophagitis
• proton pump inhibitors

Acknowledgements

The authors thank Mr. Torfinn Hansen, who is an employee of Wyeth Norway, for his help in the statistical analysis and interpretation of data. We also thank the Research Institute of Internal Medicine, Rikshospitalet, Oslo, Norway, for carrying out the gastrin and CgA analysis.

Declaration of interest: Torfinn Hansen in Wyeth Norway has assisted in the statistical analysis and interpretation of data. The study has been supported by a grant from Wyeth Norway. The authors alone are responsible for the content and writing of the paper.