Uric acid is the end product of purine metabolism and is mainly produced by the enzymatic breakdown of nucleic acids and other purine analogues from cellular metabolism as well as purines from food. Clinically, hyperuricemia (HUA) is defined as a fasting blood uric acid level higher than 420 μmol/L in men and 357 μmol/L in women on two non-same days under a normal purine diet. There are two main causes of hyperuricemia: increased uric acid production and decreased uric acid excretion, and sometimes both of them coexist. Increased uric acid production: This includes both high purine dietary intake and increased metabolic production of endogenous purines. Food-induced uric acid production is proportional to the purine content of food, and purine-rich foods include mainly animal offal such as liver, pancreas, kidney and seafood. The increase of endogenous purine metabolism in the body is mainly related to the abnormal synthesis and decomposition of purine. Decreased uric acid excretion: About 2/3 of uric acid is excreted through the kidneys, while the remaining 1/3 is excreted through extrarenal pathways such as the intestine and biliary tract. About 90% of patients with persistent hyperuricemia have defects in renal processing of uric acid and show reduced uric acid excretion, including reduced glomerular filtration rate, increased tubular reabsorption, reduced tubular secretion and impaired renal function due to urate crystallization in the kidney. The treatment of primary hyperuricemia and gout includes the following: 1. General treatment: low purine diet and control of total dietary calories; restrict alcohol consumption; drink plenty of water to increase uric acid excretion; use drugs that inhibit uric acid excretion such as thiazide diuretics with caution; avoid gout attacks as much as possible. Avoid the triggering factors of gout attack and actively treat the related diseases that cause high uric acid. 2. Treatment of hyperuricemia: The aim is to maintain uric acid at normal level. Mainly include: uric acid detoxifying drugs such as benzbromarone, drugs that inhibit uric acid production such as allopurinol and febuxostat, alkaline drugs such as sodium bicarbonate, new uric acid lowering drugs such as selective uric acid reabsorption inhibitors, etc. 3.Treatment of acute gouty arthritis: Colchicine, non-steroidal anti-inflammatory drugs and glucocorticoids are the first-line drugs for the treatment of acute gouty arthritis and should be used early. 4. Treatment of intermittent and chronic gout attacks: For patients with frequent attacks of acute gouty arthritis, chronic gouty arthritis or gout stones, uric acid-lowering therapy should be performed. Treatment principles for secondary hyperuricemia: actively treat the primary disease; try to avoid or reduce the use of drugs and methods that may trigger and/or aggravate hyperuricemia; control acute gouty arthritis attacks as soon as possible. In addition, hyperuricemia and gout are often associated with metabolic syndrome, and should be actively treated with a combination of antihypertensive, lipid-lowering, weight reduction and improvement of insulin resistance. Therefore, the causes of high uric acid include two main categories: increased uric acid production and decreased uric acid excretion. The treatment is based on the cause and condition of the patient, and the combination of drug treatment and general treatment can achieve better results.