Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid Suppression

One major cause of peptic ulceration is the use of nonsteroidal anti-inflammatory drugs (NSAIDs). The precise mechanisms through which NSAIDs cause peptic ulceration are unknown, but the discovery that they reduce the production of ‘cytoprotective’ prostaglandins led to the hypothesis that coadminis...

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Main Authors: R Lad, D Armstrong
Format: Article
Language:English
Published: Wiley 1999-01-01
Series:Canadian Journal of Gastroenterology
Online Access:http://dx.doi.org/10.1155/1999/715703
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author R Lad
D Armstrong
author_facet R Lad
D Armstrong
author_sort R Lad
collection DOAJ
description One major cause of peptic ulceration is the use of nonsteroidal anti-inflammatory drugs (NSAIDs). The precise mechanisms through which NSAIDs cause peptic ulceration are unknown, but the discovery that they reduce the production of ‘cytoprotective’ prostaglandins led to the hypothesis that coadministration of exogenous prostaglandins heals and prevents NSAID-induced gastroduodenal ulcers and other mucosal lesions. Studies using high doses of misoprostol have shown that it does have a protective effect; however, gastrointestinal intolerance of this prostaglandin E2 analogue is common. Early indications that acid suppression was effective in the management of NSAID-related peptic ulcers came from studies showing that gastric ulcers could be healed by omeprazole in patients who continued to take NSAIDs. Other studies suggested that acid suppression reduces the incidence of mucosal lesions but that standard dose ranitidine protects only against duodenal lesions. Subsequent studies reported that higher dose H2 receptor antagonist therapy can protect against both gastric and duodenal ulcers during continued NSAID therapy. An ideal therapeutic strategy would heal NSAID-related ulcers and prevent the development of new NSAID-related lesions and complications in patients who are unable to discontinue NSAID therapy. A number of recent studies indicate that effective acid-suppressive treatment with the proton pump inhibitor omeprazole can achieve these aims. Overall, data from recent studies show that acid suppression with the proton pump inhibitor omeprazole at a dose of 20 mg daily is the most effective means of healing NSAID-associated gastroduodenal lesions and that it is the most effective prophylactic therapy. In the long run, the role of omeprazole will have to be evaluated with respect to its cost effectiveness compared with other strategies and with respect to the development of less damaging NSAIDs.
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spelling doaj-art-30b5c4d5c68b4c6696e79b7970571f752025-02-03T05:47:04ZengWileyCanadian Journal of Gastroenterology0835-79001999-01-0113213514210.1155/1999/715703Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid SuppressionR Lad0D Armstrong1Division of Gastroenterology, McMaster University, Hamilton, Ontario, CanadaDivision of Gastroenterology, McMaster University, Hamilton, Ontario, CanadaOne major cause of peptic ulceration is the use of nonsteroidal anti-inflammatory drugs (NSAIDs). The precise mechanisms through which NSAIDs cause peptic ulceration are unknown, but the discovery that they reduce the production of ‘cytoprotective’ prostaglandins led to the hypothesis that coadministration of exogenous prostaglandins heals and prevents NSAID-induced gastroduodenal ulcers and other mucosal lesions. Studies using high doses of misoprostol have shown that it does have a protective effect; however, gastrointestinal intolerance of this prostaglandin E2 analogue is common. Early indications that acid suppression was effective in the management of NSAID-related peptic ulcers came from studies showing that gastric ulcers could be healed by omeprazole in patients who continued to take NSAIDs. Other studies suggested that acid suppression reduces the incidence of mucosal lesions but that standard dose ranitidine protects only against duodenal lesions. Subsequent studies reported that higher dose H2 receptor antagonist therapy can protect against both gastric and duodenal ulcers during continued NSAID therapy. An ideal therapeutic strategy would heal NSAID-related ulcers and prevent the development of new NSAID-related lesions and complications in patients who are unable to discontinue NSAID therapy. A number of recent studies indicate that effective acid-suppressive treatment with the proton pump inhibitor omeprazole can achieve these aims. Overall, data from recent studies show that acid suppression with the proton pump inhibitor omeprazole at a dose of 20 mg daily is the most effective means of healing NSAID-associated gastroduodenal lesions and that it is the most effective prophylactic therapy. In the long run, the role of omeprazole will have to be evaluated with respect to its cost effectiveness compared with other strategies and with respect to the development of less damaging NSAIDs.http://dx.doi.org/10.1155/1999/715703
spellingShingle R Lad
D Armstrong
Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid Suppression
Canadian Journal of Gastroenterology
title Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid Suppression
title_full Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid Suppression
title_fullStr Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid Suppression
title_full_unstemmed Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid Suppression
title_short Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid Suppression
title_sort management of nonsteroidal anti inflammatory drug induced gastroduodenal disease by acid suppression
url http://dx.doi.org/10.1155/1999/715703
work_keys_str_mv AT rlad managementofnonsteroidalantiinflammatorydruginducedgastroduodenaldiseasebyacidsuppression
AT darmstrong managementofnonsteroidalantiinflammatorydruginducedgastroduodenaldiseasebyacidsuppression