Abstract
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) which are widely used in clinical practice are also very well-known for their various adverse reactions. Each NSAID has its own unique safety profile and selecting an appropriate NSAID m ust be individualized for each patient based on his or her medical needs and risk factors. We reviewed literatures on NSAIDs, focusing on their adverse reaction profile. We reviewed and compared the inci dence of adverse reaction from individual NSAIDs according to organ systems. This review includes both selective COX-2 inhibitors and non- selective NSAIDs. Based on the most up-to-date evidence, ibuprofen appears to be the preferred NSAIDs based on its favorable GI and nephrotoxicity profiles. Naproxen might be considered in patients who have greater cardiac risk. Celecoxib, at the do se of less than or equal to 200 mg day -1 , might be an option in the patients who are at high risk for GI bleeding. Key word: Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), COX-2 inhibitor, adverse drug reaction, adverse reactions, safety profile, clinic al practice, organ systems
Highlights
Generic name Usual doseNon-Steroidal Anti-Inflammatory Drugs (NSAIDs) are the most commonly used medications in the United States (Laine, 2001)
With the continued aging of our population, the Center for Disease Control predicts that the prevalence of painful degenerative joint disease will increase, which will probably lead to an increase in the use of NSAIDs
A possible explanation for the disparate result is that diclofenac is the most selective for COX-2 compared with other conventional NSAIDs
Summary
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) are the most commonly used medications in the United States (Laine, 2001). A possible explanation for the disparate result is that diclofenac is the most selective for COX-2 compared with other conventional NSAIDs. This study showed a slight cardioprotective effect of naproxen but without statistical significance (Table 2). As a result of COX-1 inhibition and subsequent reduction of prostaglandins synthesis, gastric and duodenal mucosa which appears to be more vulnerable to luminal acid and pepsin (Cryer and Feldman, 1998; Jick, 1981) These gastrointestinal toxicities result in more than 100,000 hospital admissions and 7,000-10,000 deaths per year in the United States. One study in healthy human subjects found that aspirin at a dose of 10 mg day−1 reduced gastric mucosal prostaglandins to 40% of baseline level and induced significant gastric mucosa injury (Cryer and ibuprofen, diclofenac and naproxen) significantly Feldman, 1999). The mechanism by which NSAIDs can cause and the dose of aspirin (Jick, 1981; Farrell et al, 1991; exacerbation of heart failure is related to their Weil et al, 1995; Singh and Triadafilopoulos 1999)
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