There are a substantial number of adverse reactions attributable to nonsteroidal anti-inflammatory drug (NSAID) therapy, particularly of the gastrointestinal (GI) tract. The stomach is most commonly affected, although injury may occur from esophagus to colon. The incidence of developing serious GI toxicity seems to be three times as great in users compared with nonusers of NSAIDs. Age greater than 60 years, history of GI problems, previous corticosteroid use, and recency of NSAID use seem to increase the risk of toxicity. Short-term studies have found differences in ulceration or bleeding caused by various NSAIDs. However, there are insufficient long-term clinical trials involving adequate numbers of patients to demonstrate substantial advantages for any particular NSAID based on its toxicity profile. Prostaglandin inhibition seems to be one mechanism responsible for the GI toxicity of NSAIDs, but it is probably not the only mechanism. When serious GI bleeding occurs, the NSAID use must be stopped, although omeprazole and misoprostol have been used successfully to treat gastroduodenal ulcerations in patients while continuing NSAID therapy. Misoprostol and possibly omeprazole have effectively prevented GI ulceration associated with NSAID therapy, but questions remain regarding patient selection, length of therapy, and their utility in preventing serious GI bleeding. At this time, routine prophylaxis for patients receiving long-term NSAID therapy cannot be recommended.
Safety and efficacy of long-term esomeprazole 20 mg in Japanese patients with a history of peptic ulcer receiving daily non-steroidal anti-inflammatory drugs
