Abstract
The incidence of gout and the clinical manifestation of hyperuricemia continue to rise. In addition to painful acute attacks, chronic gout can lead to the development of crystal arthropathy, tophi, and renal lithiasis, coincidental with declines in quality of life. As a greater appreciation for the associations between hyperuricemia, gout, and certain comorbidities, such as renal impairment and cardiovascular diseases, grows, so does the search for new therapeutic options to both alleviate the painful symptoms of acute gout attacks and reduce the underlying hyperuricemia. This manuscript reviews the pathophysiology of hyperuricemia and gout, and associated comorbidities, and then discusses traditional therapeutic options, newly available agents, and future targets for pharmacologic management.
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