Nonselective (ie, inhibiting both cyclooxygenase [COX]-1 and COX-2) nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, remain popular and effective drugs but can 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 anti-inflammatory drugs (NSAIDs) who require continued NSAID or aspirin therapy.
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 [3-8]. 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 is used.
PPI therapy also appears effective in patients who test positive for H. pylori, and must remain on NSAIDs. In one study of H. pylori positive patients with naproxen- or low dose aspirin-related ulcer disease from Hong Kong, maintenance therapy with omeprazole was more effective in preventing recurrent bleeding than anti-H. pylori therapy alone . In clinical practice, patients who are H. pylori positive are generally treated with a PPI along with H. pylori eradication. (See "Management of duodenal ulcers in patients infected with Helicobacter pylori".)