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Rebound acid hypersecretion after acid-suppressive therapy

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Helicobacter pylori

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Abstract

Early studies suggested that there were no physiological sequelae to H2-receptor antagonist-induced acid suppression after treatment was discontinued1,2. However, these early studies focused primarily on pentagastrin-stimulated maximal acid secretion. Since that time a number of studies have shown that there is significant rebound hypersecretion of gastric acid after H2-receptor antagonist treatment, both basally3–6 and in response to meal7 and gastrin-releasing peptide (GRP) stimulation6.

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Authors
  1. D. Gillen
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  2. K. E. L. Mccoll
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Editor information

Editors and Affiliations

  1. Division of Gastroenterology, McMaster University Medical Centre, 1200 Main Street West, Hamilton, Ontario, L8N 3Z5, Canada

    Richard H. Hunt (Professor of Medicine Director) (Professor of Medicine Director)

  2. Department of Gastroenterology and Hepatology, Academic Medical Centre, 9 Meibergdreef, 1105 AZ, Amsterdam, The Netherlands

    Guido N. J. Tytgat (Professor) (Professor)

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© 2000 Springer Science+Business Media Dordrecht

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Gillen, D., Mccoll, K.E.L. (2000). Rebound acid hypersecretion after acid-suppressive therapy. In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3927-4_41

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  • DOI: https://doi.org/10.1007/978-94-011-3927-4_41

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-5753-0

  • Online ISBN: 978-94-011-3927-4

  • eBook Packages: Springer Book Archive

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