Aliment Pharmacol Ther 1995; 9: 575-579. Do non-steroidal anti-injlammatorg drugs have an eflect on gastric cell turnover ? S. M. SANT, R. J. CAHILL, J. GILVARRY & C. A. O'MORAIN Department of Gastroenterology, Meath/Adelaide Hospitals, Trinity College, Dublin, Ireland Accepted for publication 24 February 1995 SUMMARY Aim: To study the effect of non-steroidal anti- inflammatory drugs (NSAIDs) on gastric cell turnover using an in vitro immunohistochemical method of bromodeoxyuridine (BrDU) uptake. Methods : Thirty patients undergoing routine upper gastrointestinal endoscopy were studied. Sixteen had taken NSAIDs daily for more than 3 months and there were 14 age-matched controls. Endoscopic gastric antral biopsies were obtained and stained immediately using the BrDU technique. Cell proliferation was expressed as a labelling index percentage (LI%) defined as the number of BrDU-labelled nuclei in 10 gastric glands, expressed as a percentage of the total cells in the gastric gland. Results : Gastric infection with Helicobacter pylori was INTRODUCTION Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used and are therapeutically effective.' Their use, however, is limited by gastrointestinal side-effects that can be life threatening especially in the elderly and may occur without warning.'-* NSAID gastropathy describes the unique range of gastric lesions typically situated in the antrum or prepyloric region, which ranges from erythema or mucosal haemorrhage to erosions and frank ulceration. Patients most at risk for NSAID gastric damage are eIderIy (> 65 years) fern ale^,^ those on combination NSAID therapy, those with a history of ulcers or gastric bleeding or patients with large ulcers.6 Correspondence to: Dr S. M. Sant, Department of Rheumatology, Mater Misericordiar Hospital, Ercles Street, Dublin 7, Ireland. excluded in all patients. Of the 16 patients on NSAIDs, four had gastritis, four had erosions or ulceration and eight had a normal examination. Endoscopy was normal in all patients in the control group. The LI% (mean & S.E.M.) in the entire NSAID group was 4.09f0.29 and in the control group 3.57k0.29. No significant difference was observed. In the NSAID patients with gastritis and erosions or ulceration, the LI% was 4.99 f0.61 and 3.07k0.32, respectively. There was no significant difference in LI% between the endoscopic subgroups of patients on NSAIDs or between patients on NSAIDs who had normal endoscopy and the control patients. Conclusion : These results provide evidence that refutes the hypothesis that the prevalence of NSAID gastropathy is due to an effect on gastric cell turnover. Several mechanisms of gastric damage by NSAIDs have been identified and one of these includes inhibition of gastric epithelial cell regeneration by chronic use of NSAIDS.'.~ Previous cell kinetic studies of the effect of NSAIDs on human gastric epithelial cell proliferation have employed tritiated thymidine (3H-thymidine)7 and microdissection A more recent technique uses the immuno- histochemical method of bromodeoxyuridine (BrDU) uptake." BrDU is a pyridine analogue of thymidine that incorporates into DNA during the S-phase of cell division. It is demonstrated in dividing cells by immunostaining using a specific monoclonal antibody to BrDU. The BrDU technique for measurement of cell prolifer- ation carries several advantages over those of [3H]- thymidine or microdissection. Its main advantage over 0 1995 Blackwell Science Ltd 5 75