NSAIDs (including aspirin): Treatment of gastroduodenal toxicity
- Mark Feldman, MD, MACP, AGAF, FACG
Mark Feldman, MD, MACP, AGAF, FACG
- Section Editor — Acid Peptic Disease
- Texas Health Presbyterian Hospital Dallas
- Clinical Professor of Internal Medicine
- University of Texas Southwestern Medical School at Dallas
Nonsteroidal antiinflammatory drugs (NSAIDs), including aspirin, cause considerable morbidity and mortality related to gastric and duodenal ulcer disease, particularly by causing gastrointestinal (GI) bleeding .
The treatment of gastroduodenal toxicity associated with NSAID therapy will be reviewed here. Modalities used for primary and secondary prevention of gastroduodenal toxicity, including the role of cyclooxygenase (COX)-2 selective NSAIDs, are discussed separately as is the pathogenesis of the gastroduodenal toxicity. The prevention of recurrent gastroduodenal toxicity is also discussed separately. (See "NSAIDs (including aspirin): Pathogenesis of gastroduodenal toxicity" and "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity" and "NSAIDs (including aspirin): Secondary prevention of gastroduodenal toxicity".)
If a patient develops an ulcer while on a nonsteroidal antiinflammatory drug (NSAID) or aspirin, the NSAID or aspirin should be stopped if at all possible and traditional ulcer therapy with a proton pump inhibitor or an H2 antagonist started . Proton pump inhibitors are generally preferred because they are associated with more rapid ulcer healing. (See "Overview of the natural history and treatment of peptic ulcer disease".) If the patient has been taking low-dose aspirin for cardiovascular prophylaxis, there is no consensus as to when to resume the aspirin. The indication for the low-dose aspirin should be reviewed and the severity of the ulcer presentation considered. For most patients, the author recommends low-dose aspirin, if still indicated, be restarted one to two weeks after initiating therapy with a proton pump inhibitor.
As in all patients with peptic ulcers, the patient's H. pylori status should also be assessed (if not done previously); if positive, appropriate therapy for H. pylori should be instituted . However, the sensitivity of H. pylori testing in the setting of acute GI bleeding is significantly reduced. (See "Indications and diagnostic tests for Helicobacter pylori infection", section on 'Peptic ulcers' and "Treatment regimens for Helicobacter pylori" and "Management of duodenal ulcers in patients infected with Helicobacter pylori".)
For patients who must remain on low-dose aspirin or NSAID therapy, randomized trials have shown that ulcer healing occurs more rapidly with a proton pump inhibitor than an H2 antagonist [4,5], misoprostol , or sucralfate :
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