Nonsteroidal anti-inflammatory drugs and upper and lower gastrointestinal mucosal damage

Abstract

NSAIDs are among the most commonly used drugs worldwide and their beneficial therapeutic properties are thoroughly accepted. However, they are also associated with gastrointestinal (GI) adverse events. NSAIDs can damage the whole GI tract including a wide spectrum of lesions. About 1 to 2% of NSAID users experienced a serious GI complication during treatment. The relative risk of upper GI complications among NSAID users depends on the presence of different risk factors, including older age (>65 years), history of complicated peptic ulcer, and concomitant aspirin or anticoagulant use, in addition to the type and dose of NSAID. Some authors recently reported a decreasing trend in hospitalizations due to upper GI complications and a significant increase in those from the lower GI tract, causing the rates of these two types of GI complications to converge. NSAID-induced enteropathy has gained much attention in the last few years and an increasing number of reports have been published on this issue. Current evidence suggests that NSAIDs increase the risk of lower GI bleeding and perforation to a similar extent as that seen in the upper GI tract. Selective cyclooxygenase-2 inhibitors have the same beneficial effects as nonselective NSAIDs but with less GI toxicity in the upper GI tract and probably in the lower GI tract. Overall, mortality due to these complications has also decreased, but the in-hospital case fatality for upper and lower GI complication events has remained constant despite the new therapeutic and prevention strategies.

A wider view on gastric erosion: detailed evaluation of complex somatic and behavioral changes in rats treated with indomethacin at gastric ulcerogenic dose

“…Approximately 1-2% of NSAID users develop upper GI complications per year, a rate 3-5 times higher than in non-NSAID users (Targownik et al 2008). Experimental studies with NSAIDs confirm the clinical data that NSAIDs cause damage to the up-per GI tract and also affect the lower GI tract (Sostres et al 2013). …”

Dual cyclooxygenase–fatty acid amide hydrolase inhibitor exploits novel binding interactions in the cyclooxygenase active site

“…A major limitation to the use of most NSAIDs is gastrointestinal toxicity due to blockade of the biosynthesis of cytoprotective PGs (8,9). This problem was addressed by the development of COX-2-selective inhibitors that preserved COX-1-dependent gastrointestinal PGE2 production.…”

Starz-Drp: A Tool for Pharmacy Triage Services

“…This study is revealing that CPs must be cautious with patients who ask for selfcare medications as their symptoms might hide actual or potential problems. Other studies, for example, reveal non-steroidal antiinflammatory drugs (NSAIDs) induced upper and lower gastrointestinal symptoms [29][30][31][32] and cardiovascular risk [32] and the patients might need to stop the medications before it becomes worse. Certainly, most of NSAIDs are reachable in the pharmacy, requiring CPs to take the role to counsel their patients about the potential side effects [33,34].…”