Gout (gout) is a heterogeneous group of diseases caused by disorders of purine metabolism and impaired uric acid excretion resulting in increased blood uric acid, including hyperuricemia, recurrent monoarthritis, gouty stone deposits, chronic gouty stone arthritis, gouty nephropathy, and bird-acid urinary tract stones. Gout is divided into two categories: primary and secondary. Most primary gout has an unknown cause and is often associated with obesity, hyperlipidemia, diabetes mellitus, hypertension and cardiovascular disease. Secondary gout can be caused by kidney disease, blood disease, certain drugs, tumor radiotherapy and other causes. The saturated concentration of serum uric acid at 37℃ is 420umol/L, higher than this value is considered hyperuricemia. Only 5-12% of patients with hyperuricemia develop gout clinically, and the exact cause is unknown. The natural course of gout can be divided into the following four stages: (1) Hyperuricemia: a clinical manifestation of elevated serum urate concentration without gout symptoms. Most patients with hyperuricemia are asymptomatic for life, but the risk of transition to acute gout increases with increasing serum urate concentrations. (2) Acute gouty arthritis: The typical attack starts rapidly, mostly awakened by midnight foot pain, and the pain reaches its peak in 24-48h, like a knife cut or bite. The joint and surrounding soft tissues show obvious redness, swelling and heat pain. Most of them have no systemic symptoms, but a few may be accompanied by fever, elevated white blood cells and increased blood sedimentation. Gout attacks may last for several days or weeks and resolve on their own. The frequency of gout attacks gradually increases in untreated patients and is characterized by less acute, longer-lasting, mostly arthritic, slow remission after an attack. (3) Gout interval: after the acute attack of gout remission, generally no obvious sequelae symptoms, sometimes only the attack site skin flaking, itching, called asymptomatic interval. (4) Chronic gout stone gout stone gout: repeated deposition of uric acid salts causes local tissue to react with foreign substances, forming gout stone. Gout stones mostly appear 10 years after the onset of the disease, which is a sign that the disease process has entered chronicity and can be seen in joints, peri-articular, subcutaneous tissues and visceral organs. They are typically found in the ears and toes, fingers, wrists, ankles, elbows and other joints, and are raised under the skin. When gouty stones occur in the joints, they can cause erosion and destruction of joint cartilage and bone, reactive hyperplasia, fibrosis of periarticular tissue, and persistent joint pain, swelling, ankylosis, deformity, and even fracture, called chronic gouty stone arthritis. Primary gout lacks etiological treatment and therefore cannot be cured. The objectives of treatment are: (1) to rapidly control acute attacks of gouty arthritis; (2) to prevent recurrence of acute arthritis; (3) to correct hyperuricemia in order to prevent joint destruction and kidney damage caused by urate deposition; (4) to surgically remove gouty stones and perform orthopedic surgery on damaged joints in order to improve the quality of life. Treatment of gout: (1) General treatment: ① Diet control: low calorie diet, maintain ideal body weight, and avoid high purine foods. Foods with high purine content mainly include animal offal, sardines, clams, oysters and other seafood and thick meat soup, followed by fish and shrimp, meat, peas, etc., while various cereal products, fruits, vegetables, milk, dairy products, eggs, etc. contain the least purine. In addition, strictly control alcohol, especially beer. Drink more than 2000ml of water daily. ② Avoid causative factors: avoid overeating and alcoholism, cold and damp, excessive fatigue and mental tension; wear comfortable shoes to avoid joint injury; use drugs affecting uric acid excretion, such as thiazide diuretics, with caution. (3) Prevention and control of concomitant diseases: treat concomitant hyperlipidemia, diabetes mellitus, hypertension, coronary heart disease, cerebrovascular disease, etc. at the same time. (2) Treatment of acute gouty arthritis: bed rest, elevation of the affected limb, avoid weight bearing. Withhold the use of uric acid-lowering drugs to avoid fluctuations in blood uric acid, prolonging attacks or causing metastatic gout. It is recommended to use ① Colchicine: it can inhibit inflammatory cell chemistry and has anti-inflammatory effect. It should be used early, and most patients can have significant pain relief within 24h after medication; ②Non-steroidal anti-inflammatory drugs: NSAIDs are used more often than colchicine for acute attacks, usually starting with a full dose and reducing the dose after the symptoms are relieved. Common side effects are gastrointestinal symptoms, which can also aggravate renal insufficiency and affect platelet function. (3) Glucocorticoids: usually used for those who are ineffective or intolerant to colchicine and NSAID, and can be administered systemically for a short period of time or by local injection. (3) Treatment of intermittent and chronic phase: The goal is to control blood uric acid below 357umol/L. There are two major categories of uric acid-lowering drugs, ① Pro-uric acid excretory drugs: including benzbromarone, propoxur and sulfopyrone, which promote uric acid excretion by inhibiting the reabsorption of uric acid in the proximal renal tubules and are suitable for patients with normal renal function or mild abnormalities without urinary tract stones and uric acid nephropathy. ②Inhibitors of uric acid production: Allopurinol blocks the conversion of xanthine into uric acid and reduces urea production by inhibiting xanthine oxidase, and is the most commonly used drug to lower uric acid. The main side effects include gastrointestinal reactions, skin rash, drug fever, bone marrow suppression, liver and kidney function impairment, etc. Allopurinol allergy syndrome may occur in severe cases. (4) Treatment of asymptomatic hyperuricemia: For people with blood uric acid level below 525umol/L and no family history of gout, drug treatment is generally not necessary, but diet should be controlled, causative factors should be avoided, and close follow-up should be performed. On the contrary, uric acid-lowering drugs should be used. In case of concomitant hypertension, diabetes mellitus, hyperlipidemia, cardiovascular disease, etc., blood uric acid should be lowered appropriately while treating the concomitant disease.