Gastric histology in children treated with proton pump inhibitors long term, with emphasis on enterochromaffin cell-like hyperplasia
Version of Record online: 14 FEB 2011
© 2011 Blackwell Publishing Ltd
Alimentary Pharmacology & Therapeutics
Volume 33, Issue 7, pages 829–836, April 2011
How to Cite
Hassall, E., Owen, D., Kerr, W., Sturby, T., Richardson, P. and El-Serag, H. (2011), Gastric histology in children treated with proton pump inhibitors long term, with emphasis on enterochromaffin cell-like hyperplasia. Alimentary Pharmacology & Therapeutics, 33: 829–836. doi: 10.1111/j.1365-2036.2011.04592.x
- Issue online: 2 MAR 2011
- Version of Record online: 14 FEB 2011
- Publication data Submitted 23 October 2009 First decision 17 November 2009 Resubmitted 13 January 2011 Accepted 18 January 2011
Aliment Pharmacol Ther 2011; 33: 829–836
Background There are longstanding concerns that carcinoid tumours or atrophic gastritis might develop in children receiving proton pump inhibitors (PPIs) long term. In children, this has not been studied using stains sensitive and specific for enterochromaffin-like (ECL) cells.
Aim To evaluate gastric biopsies for ECL hyperplasia or gastric atrophy, in children treated long-term with PPIs.
Methods Synaptophysin and chromogranin immunostaining, biopsies read anonymised, blinded. Endocrine cell numbers graded according to Rindi and Solcia.
Results Of 130 children with gastro-oesophageal reflux disease (GERD), 65 had sequential gastric biopsies, starting at median 8.2 years (<1 to 17). Of the 65, 83% had GERD-predisposing conditions, mostly neurological impairment or repaired oesophageal atresia. Four hundred and fifty-eight tissue blocks (208 antrum, 250 body) were available from a mean of 5.8 endoscopies (2–14). Of 82 gastric body biopsies in 40 patients with ECL hyperplasia, 67 had grade 1 hyperplasia, 15 grade 2. Of the 40, nine had ECL hyperplasia before PPI use; all nine had received H2-receptor antagonists. Median duration of PPI use was 3.17 years in patients with ECL hyperplasia, 2.20 years in those without (P = 0.16). Helicobacter pylori was present in four patients; two had ECL hyperplasia. PPI duration was >3 years in 24 patients. In nine patients who received H2-receptor antagonists, changes were present before PPI use. No patient had atrophic gastritis.
Conclusions A high percentage of children (61%) receiving long-term PPI continuously for up to 10.8 years (median 2.84 years) develop minor degrees of ECL hyperplasia. This has no known clinical significance. Children on PPIs for this duration do not appear to develop atrophic gastritis or carcinoid tumours.