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Gout is a prevalent inflammatory arthritis resulting from the deposition of monosodium urate (MSU) crystals in tissues, typically characterized by severe pain and swelling at the affected joints. This review article aims to understand the reasons for the global rise in gout cases through examining the underlying mechanism and evaluating available treatments. Four treatmentsNSAIDs, colchicine, glucocorticoids, and xanthine oxidase inhibitorsare evaluated based on mechanisms of action, commonly used drugs, and associated safety issues. NSAIDs, with ibuprofen, aspirin, and naproxen sodium as the most used drugs, exert their effect by inhibiting prostaglandin production from the COX enzyme, although their adverse effects of gastrointestinal disorders warrant attention. Colchicine has long been used to relieve joint pain and swelling by inhibiting microtubules, blocking NLRP3 activation, and reducing neutrophil recruitment. However, it has comparatively narrow therapeutic uses as high doses may lead to severe toxicity. Glucocorticoids relieve acute gout by inhibiting leukocyte recruitment and by suppressing inflammation and vascular permeability. Prednisone, methylprednisolone, and triamcinolone are used depending on disease severity and sites of onset. They are recommended only for short-term treatment due to the risks of ulcers. Lastly, xanthine oxidase inhibitors, allopurinol and febuxostat, focus on maintaining serum urate levels to prevent crystal formation. However, side effects include allopurinol leading to allopurinol hypersensitivity syndrome and febuxostat causing cardiovascular events. The major issues lie in drug safety and knowledge gaps. Future research should focus on eliminating side effects; professionals and patients should be educated on gout treatment and prevention.
Published in: Theoretical and Natural Science
Volume 144, Issue 1, pp. 178-186