Nonselective (ie, inhibiting both cyclooxygenase [COX]-1 and COX-2) nonsteroidal antiinflammatory drugs (NSAIDs), including aspirin, cause considerable morbidity and mortality related to gastric and duodenal ulcer disease, particularly gastrointestinal (GI) bleeding . Even low-dose aspirin is associated with an increase in risk .
The prevention of recurrent gastroduodenal toxicity associated with NSAID therapy (secondary prevention) will be reviewed here. Primary prevention and treatment of NSAID-related gastroduodenal toxicity are discussed separately as is the pathogenesis of the gastroduodenal toxicity. (See "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity" and "NSAIDs (including aspirin): Treatment of gastroduodenal toxicity" and "NSAIDs (including aspirin): Pathogenesis of gastroduodenal toxicity".)
SECONDARY PREVENTION OF GASTRODUODENAL TOXICITY
Prevention of ulcer disease becomes important in patients with a history of gastroduodenal toxicity from nonsteroidal antiinflammatory drugs (NSAIDs) who require continued NSAID therapy, including those treated with low-dose aspirin for cardiovascular protection.
With continued NSAID therapy — There are some patients who must resume or continue NSAID therapy despite prior development of gastroduodenal ulcers or erosions. Several randomized trials have evaluated various strategies for treating such patients [3-7]. Considered together they suggest that patients with gastroduodenal ulcers or numerous erosions who must continue NSAID therapy should be treated with a proton pump inhibitor (PPI) for as long as the NSAID or aspirin is used.
●Omeprazole was found to be superior to ranitidine, misoprostol, and placebo in maintaining remission [3,4].