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Do non‐steroidal anti‐inflammatory drugs have an effect on gastric cell turnover?
Author(s) -
SANT S. M.,
CAHILL R. J.,
GILVARRY J.,
O'MORAIN C. A.
Publication year - 1995
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.1995.tb00424.x
Subject(s) - medicine , gastroenterology , bromodeoxyuridine , antrum , gastritis , endoscopy , helicobacter pylori , stomach , spirillaceae , atrophic gastritis , immunohistochemistry
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 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 4.09 ± 0.29 and in the control group 3.57 ± 0.29. No significant difference was observed. In the NSAID patients with gastritis and erosions or ulceration, the LI% was 4.99 ± 0.61 and 3.07 ± 0.32, 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.