Gout is a crystal-associated arthropathy caused by urate deposition, and its onset is directly related to hyperuricemia due to disorders of purine metabolism and/or reduced uric acid excretion. Purine is one of the constituent substances of the human body, mainly in the form of purine nucleotides, and has an important role in energy supply and metabolic regulation in the human body. Purines are metabolized in the human body and eventually converted into uric acid, which is the final metabolite of purines. In the human body, 80% of uric acid is produced by endogenous purine metabolism, and 20% comes from external high purine diet intake. The body has a self-regulatory function for uric acid, which can maintain it at a certain stable level. If the endogenous purine production is excessive or the uric acid excretion is reduced, the blood uric acid level will be increased, resulting in hyperuricemia. If the blood uric acid level is elevated for a long time, the concentration of uric acid salts will increase and crystals will be deposited in joints and kidneys, leading to gout attacks. However, it is important to note that elevated blood uric acid alone does not equal gout; gout must occur with the formation and deposition of urate crystals. It follows that hyperuricemia is the basis for the development of gout, and uric acid is the final metabolite of purines. Therefore, both endogenous and exogenous causes of elevated purine levels in the body may lead to gout attacks.