Uric acid in the blood above 420 μmol/L is called hyperuricemia. Uric acid is mainly produced by the breakdown of nucleic acids and purine analogues from cellular metabolism and the breakdown of purines in food. In hyperuricemia, crystals formed from uric acid salts are deposited in a variety of tissues, including the kidneys and synovial joints, causing tissue and organ damage. Gout is a condition in which serum uric acid is elevated and urate is deposited in the synovial membrane of joints, leading to recurrent acute arthritis, gout stones and deformed joint lesions. Hyperuricemia and gout are often associated with obesity, hyperlipidemia, hypertension, elevated blood sugar or type 2 diabetes, and are risk factors for atherosclerosis, coronary heart disease and cerebrovascular disease. Most patients with hyperuricemia have no clinical symptoms in the early stages, only fluctuating or persistent hyperuricemia, and the time from increased blood uric acid to the onset of symptoms can be years to decades, but the prevalence of gout increases with age and is associated with the level and duration of hyperuricemia. Hyperuricemia can cause gouty arthritis, which is more common in young and middle-aged men, often starting in the first toe joint of the toe or in joints such as the ankle and knee. The onset of the disease is rapid, with a peak within 24 hours. The initial attack often involves a single joint and lasts for several days to weeks, while repeated attacks gradually increase the number of joints involved, prolong the duration of symptoms and shorten the interval between arthritic attacks. Hyperuricemia can also cause kidney lesions, which can lead to gouty nephropathy and uric acid nephrolithiasis. The onset of the disease is insidious, with only intermittent proteinuria in the early stage and persistent proteinuria as the disease progresses; in the late stage, renal insufficiency may occur, manifested as edema, hypertension, elevated blood urea nitrogen and creatinine, and in a few patients, acute renal failure with oliguria or anuria. Prevention and treatment of hyperuricemia and gout I. Prevention and treatment objectives: 1. control hyperuricemia and prevent uric acid deposition; 2. rapidly terminate the attack of acute arthritis; 3. prevent the formation of uric acid stones and renal function damage. The principles of prevention and treatment: 1. Limit the intake of high purine food; drink a lot of water, more than 2000ml per day; use drugs that inhibit uric acid excretion, such as thiazide diuretics, and avoid triggering factors, such as drinking alcohol and consuming large amounts of seafood in a short period of time. 2.Uric acid lowering treatment: mainly should take drugs that excrete uric acid, such as benzbromarone; also can take drugs that inhibit uric acid production, such as allopurinol, febuxostat, etc. It should be combined with alkalizing urine treatment, such as oral sodium bicarbonate tablets. Limiting the intake of high purine foods is very important for hyperuricemia or gout. In the acute attack period of gout, it is appropriate to choose foods containing less purine, mainly milk and its products, eggs, vegetables, fruits and fine grains. During the remission period, it is appropriate to choose foods containing medium amount of purines, such as meat use not more than 120g per day, especially do not eat too much in one meal. Foods with high purine content, such as animal liver, sardines, thick chicken soup and fish soup, should be avoided in both the acute and remission periods. According to the amount of purine contained in 100 grams of food, food is divided into the following three categories: High purine food: 150-1000 mg of purine per 100 grams of food; restricted for patients with high uric acid and gout disease. Medium purine food: 25-150 mg of purine per 100 grams of food; suitable for patients with high uric acid and gout. Low purine food: less than 25 mg of purine per 100 grams of food; can be eaten safely by patients with high uric acid and gout disease.