Uric acid metabolism

\"Uric acid metabolism\" refers to the **biochemical pathway by which purine nucleotides are degraded to produce uric acid as an end product in humans**[1][3][5]. Uric acid metabolism involves key enzymes such as xanthine oxidase and includes the transformation of hypoxanthine to xanthine and then to uric acid, which is then excreted primarily via the kidneys[3][5]. Unlike most other mammals, humans lack uricase, the enzyme that would further convert uric acid to allantoin, resulting in higher uric acid levels in humans[3][5]. Dysregulation of uric acid metabolism leads to hyperuricemia, gout, and is implicated in a variety of diseases including metabolic syndrome, cardiovascular disease, renal disorders, and nonalcoholic fatty liver disease[4][6]. Serum uric acid is a key biomarker used clinically to monitor these conditions[10]. Drugs targeting enzymes or transporters in the uric acid metabolic pathway—including xanthine oxidase inhibitors (such as allopurinol or febuxostat) or uricosurics—are used to treat hyperuricemia but interact primarily with the enzymes, not the pathway as a whole[4][2][10].