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Proton pump inhibitors and gastric neoplasia
  1. Helge L Waldum,
  2. Gunnar Qvigstad
  1. Department of Gastroenterology and Hepatology, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway
  1. Correspondence to:
    Professor H L Waldum
    Department of Gastroenterology and Hepatology, St Olavs Hospital, Trondheim University Hospital, Olav Kyrres gt., N-7006 Trondheim, Norway; helge.waldum{at}ntnu.no

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We read the leading article by Kuipers (Gut 2006;55:1217–21) with great interest. The conclusion that proton pump inhibitor (PPI) treatment does not increase the risk of gastric neoplasia is reassuring. The overview by Kuipers, however, lacks a few important points:

  1. Hypergastrinaemia. The maximal trophic effect of gastrin is reached at concentrations lower than that realised by most clinicians, both in rats and in humans.1 A concentration of 400 ng/ml or 200 pM induces nearly maximal effect.

  2. Hypergastrinaemia and gastric carcinoids. Kuipers claims that prolonged hypergastrinaemia leads to enterochromaffin-like (ECL) cell carcinoids only in rats.2 This is not correct. Mice also develop gastric carcinoids when treated with insurmountable histamine 2 antagonists.3 PPIs have low potency in this species, which is the cause of the widespread misunderstanding that hypergastrinaemia in mice does not induce ECL cell carcinoids. Moreover, long term treatment of dogs with PPI was reported not to induce any changes in the gastric mucosa.4 Unfortunately, the dose used was not sufficient to induce hypoacidity and accompanying hypergastrinaemia. Even in humans gastric endocrine tumours have been described after PPI …

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Linked Articles

  • Leading article
    E J Kuipers
  • Digest
    Robin Spiller Alastair Watson