Systematic review: the effects of long‐term proton pump inhibitor use on serum gastrin levels and gastric histology. Issue 6 (16th July 2015)

• Record Type: Journal Article
• Authors: Lundell, L.; Vieth, M.; Gibson, F.; Nagy, P.; Kahrilas, P. J.
• Is Part Of: Alimentary pharmacology & therapeutics. Volume 42:Issue 6(2015)
• Page Start: 649
• Page End: 663
• Publication Date: 2015-07-16
• Subjects: Digestive organs -- Diseases -- Treatment -- Periodicals; Digestive organs -- Effect of drugs on -- Periodicals; Gastrointestinal system -- Diseases -- Treatment -- Periodicals; Gastrointestinal system -- Effect of drugs on -- Periodicals; 615.73
• DOI: 10.1111/apt.13324
• Languages: English
• ISSNs: 0269-2813

Abstract

<abstract abstract-type="main" id="apt13324-abs-0001"> <title>Summary</title> <sec id="apt13324-sec-0001" sec-type="section"> <title>Background</title> <p>Proton pump inhibitors (PPIs) have a well‐established safety profile. However, concerns have been raised about a potential relationship between PPI‐induced hypergastrinaemia and the development of enterochromaffin‐like (ECL) cell hyperplasia, neuroendocrine tumours and gastric cancer during long‐term therapy.</p> </sec> <sec id="apt13324-sec-0002" sec-type="section"> <title>Aim</title> <p>To review the effects of long‐term PPI use on serum gastrin levels and gastric histopathology.</p> </sec> <sec id="apt13324-sec-0003" sec-type="section"> <title>Methods</title> <p>A systematic literature search was conducted in PubMed on 21 April 2015 to identify studies reporting the effects of long‐term (defined as >3 years) PPI use on gastrin levels and gastric histopathology.</p> </sec> <sec id="apt13324-sec-0004" sec-type="section"> <title>Results</title> <p>A total of 16 studies (1920 patients) met the inclusion criteria. During long‐term PPI therapy, mean gastrin levels rose to one to three times the upper limit of the normal range (~100 pg/mL), and an increased prevalence of ECL cell hyperplasia was observed (+7.8–52.0%). <italic>Helicobacter pylori</italic>‐positive patients had a significantly increased risk of developing ECL linear/micronodular hyperplasia compared with <italic>H. pylori</italic>‐negative patients [OR: 2.45 (95% CI: 1.47–4.10), <italic>P </italic>=<italic> </italic>0.0006]; however, no evidence of neoplastic changes was found. The risk of corpus atrophy was markedly higher in <italic>H. pylori</italic>‐positive patients than in <italic>H. pylori</italic>‐negative patients [OR: 11.45 (95% CI: 6.25–20.99), <italic>P </italic><<italic> </italic>0.00001]. Not a single case of gastric adenocarcinoma was found.</p> </sec> <sec id="apt13324-sec-0005" sec-type="section"> <title>Conclusions</title> <p>Long‐term PPI therapy induced moderate hypergastrinaemia in most patients and an increased prevalence of ECL cell hyperplasia. <italic>H. pylori</italic>‐positive patients receiving long‐term PPI therapy were exposed to a higher risk of corpus atrophy than <italic>H. pylori</italic>‐negative patients. No neuroendocrine tumours or gastric cancers were found.</p> </sec> </abstract>