D Varaprada and K Blessi Priyanka
Nonsteroidal anti-inflammatory drugs (NSAIDs) represent a widely utilized class of agents for the treatment of pain, inflammation, and various medical conditions [1]. This overview summarizes their mechanism of action, clinical applications, and associated risks. NSAIDs exert their effects by inhibiting cyclooxygenase (COX) enzymes, which mediate prostaglandin synthesis, with varying selectivity toward COX-1 and COX-2 isoforms [8, 15]. Clinically, they are employed for analgesia, antipyresis, anti-inflammatory purposes, and in certain cardiovascular settings [1]. However, NSAID use is linked to adverse effects, including gastrointestinal irritation, renal impairment, cardiovascular complications, bleeding tendencies, hypersensitivity reactions, and hepatic toxicity[2].The pharmacokinetic and pharmacodynamic profiles of NSAIDs vary widely, influencing their clinical applications and safety profiles. Recent advancements include the investigation of COX-3 as a novel target and the integration of personalized medicine to improve therapeutic safety and efficacy [14]. The use of willow leaves containing salicylate, highly selective cyclooxygenase-2 (COX-2) inhibitors, and the newest dual-acting anti-inflammatory drugs have all undergone rapid and continuous change [7]. Even with the tremendous progress made over the past two decades, researchers continue to strive for the creation of safer and more effective treatments for inflammatory diseases. For NSAID therapy to reduce risk and maximize results, a patient-specific strategy is necessary. Ongoing research aims to develop more selective and safer NSAID options to enhance clinical benefit while reducing harm.
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