Abstract
Nonsteroidal anti-inflammatory medicines, collectively referred to as NSAIDs in academic context, exhibit chemical diversity while concurrently manifesting comparable therapeutic and harmful effects. All pharmaceutical substances under this particular category function by diminishing inflammation, alleviating pain, and reducing fever by means of inhibiting enzymes responsible for the creation of endoperoxides, often referred to as cyclooxygenase (COX) enzymes. The two cyclooxygenase isozymes, COX-1 and COX-2, are responsible for the conversion of arachidonic acid into its endoperoxide metabolites. These metabolites include prostacyclin, prostaglandins, and thromboxane, each exhibiting a wide range of biological activities such as inflammation, regulation of smooth muscle tone, and promotion of thrombosis. The COX-1 enzyme is consistently produced and is recognized as the main provider of prostanoids required for maintaining physiological balance, such as safeguarding the stomach epithelium. In contrast, the COX-2 enzyme is capable of being induced, leading to a substantial increase in the synthesis of prostanoids in circumstances characterized by stress and inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs) may induce toxicity via the same pharmacological mechanisms that contribute to their therapeutic efficacy. This review aims to discuss NSAIDs toxicity in details, its symptoms, and possible management in the emergency room.
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