Increased risk of fundic gland polyps during long-term proton pump inhibitor therapy
Article first published online: 16 OCT 2006
Alimentary Pharmacology & Therapeutics
Volume 24, Issue 9, pages 1341–1348, November 2006
How to Cite
JALVING, M., KOORNSTRA, J. J., WESSELING, J., BOEZEN, H. M., DE JONG, S. and KLEIBEUKER, J. H. (2006), Increased risk of fundic gland polyps during long-term proton pump inhibitor therapy. Alimentary Pharmacology & Therapeutics, 24: 1341–1348. doi: 10.1111/j.1365-2036.2006.03127.x
- Issue published online: 16 OCT 2006
- Article first published online: 16 OCT 2006
- Publication data Submitted 29 June 2006 First decision 11 July 2006 Resubmitted 8 August 2006 Accepted 14 August 2006
It is controversial whether proton pump inhibitor use leads to fundic gland polyp development.
To determine whether fundic gland polyp development is due to proton pump inhibitor use and to investigate mechanisms involved.
Proton pump inhibitor use and the presence of fundic gland polyps were assessed in consecutive patients undergoing oesophagogastroduodenoscopy. Biopsies from fundic gland polyps and gastric mucosa were taken. Dysplasia was graded as negative, low or high grade. Prevalence of parietal cell hyperplasia and parietal cell protrusions and the proportional cystic area were assessed.
599 patients participated, 322 used proton pump inhibitors, 107 had fundic gland polyps. Long-term proton pump inhibitor use was associated with an increased risk of fundic gland polyps (1–4.9 years use: OR 2.2, 95% CI: 1.3–3.8; ≥5 years: OR 3.8, 95% CI: 2.2–6.7) while short-term therapy (<1 year) was not (OR 1.0, 95% CI: 0.5–1.8). Low-grade dysplasia was found in one fundic gland polyp. Fundic gland polyps associated with long-term proton pump inhibitor use had a larger proportional cystic area and higher frequency of parietal cell hyperplasia and parietal cell protrusion.
Long-term proton pump inhibitor use is associated with an up to fourfold increase in the risk of fundic gland polyps. Risk of dysplasia is negligible. Aetiologically, these polyps seem to arise because of parietal cell hyperplasia and parietal cell protrusions resulting from acid suppression.