Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Agrawal, N. M.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Agrawal, N. M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1995 British Society for Rheumatology

Epidemiology and prevention of non-steroidal anti-inflammatory drug effects in the gastrointestinal tract

N. M. Agrawal

University of Connecticut Health Center 263 Farmington Avenue, Farmington, CT 06030-1845, USA


   Abstract

Lesions of the gastric, duodenal and intestinal mucosae are found in large numbers of patients using non-steroidal anti-inflammatory drugs (NSAIDs); however, no markers have yet been isolated to identify patients at risk for developing gastrointestinal problems or to predict which patients with lesions are at risk for developing catastrophic complications. There appears to be a poor correlation between the presence of ulcer disease and the appearance of symptoms while patients are using NSAIDs. The ideal treatment—namely, withdrawal from NSAIDs—may not always be practicable in patients who require the analgesic benefit of these otherwise generally innocuous agents. It is incumbent on the clinician to identify the agent most appropriate for the needs of the individual, and to supplement NSAID therapy, where appropriate, with a means of preventing or minimizing adverse effects. Four classes of drugs are used to prevent NSAID-related gastric mucosal damage: histamine (H2) preceptor antagonists (ranitidine, cimetidine, nizatidine, famotidine); gastric acid-pump inhibitor (omeprazole); barrier agent (sucralfate); and prostaglandin analogue (misoprostol). The current therapies (H2 antagonists and barriers) have not lived up to their promise for preventing gastroduodenal erosion. Moreover, such protection as they provide is limited to the duodenal mucosa; they afford no protection to the gastric mucosa. Preliminary data indicate that an acid pump inhibitor may be useful, but large-scale studies have yet to be reported. Acute and long-term studies of the prostaglandin analogue misoprostol have shown that this agent has an important role as an adjunctive therapy to prevent both gastric and duodenal ulceration due to NSAIDs.

KEY WORDS: Non-steroidal anti-inflammatory drugs, Duodenal ulcer, Gastric ulcer, Arthritis, Ranitidine, Omeprazole, Misoprostol, Sucralfate


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.