Since the 1980s, with the continuous improvement of people’s living standard in China, the prevalence of hyperuricemia has been increasing year by year, especially in economically developed cities and coastal areas, the prevalence rate reaches 5% to 23.5%, which is close to the level of western developed countries. At present, the number of patients with hyperuricemia in China is close to 120 million, and hyperuricemia has become the fourth high after the “three highs” – high blood sugar, high blood pressure and high blood lipid – that endanger human health in modern society, and is coming strongly. Uric acid is the end metabolite of purine, the source of purine is divided into endogenous purine 80% from the oxidative decomposition of nucleic acid, exogenous purine mainly from food intake, accounting for 20% of the total purine, uric acid in the human body has no physiological function, under normal circumstances, the body produces uric acid, 2/3 by the kidneys to excrete, the remaining 1/3 from the intestinal tract. The diagnosis of hyperuricemia is defined internationally as a fasting blood uric acid level of >420 μmol/L in men and >360 μmol/L in women on two different days under a normal purine diet. hyperuricemia is divided into primary and secondary hyperuricemia. Secondary hyperuricemia is mostly seen in: 1. renal lesions; 2. pharmacological: thiazide diuretics, other drugs such as aspirin, pyrazinamide, levodopa, ethambutol, ethanol, etc. can also interfere with renal tubular reabsorption of uric acid; 3. increased organic acids in the body such as keto acid and lactic acid can competitively inhibit renal tubular uric acid secretion; 4. excessive generation: mostly seen in bone marrow and lymphoproliferative disorders. Hyperuricemia and gout are inextricably linked. When excessive production of uric acid or reduced uric acid excretion due to kidney disease, and then eat a large amount of purine-containing food, such as more than the body’s ability to remove, it causes an increase in blood uric acid, and then the formation of urate crystals and deposition in body fluids and other tissues in the soft tissue and joint inflammatory reaction is gout. Gout often starts after a drinking party, often in the middle of the night with severe pain, redness, swelling and heat in the toe joints. The first attack involves the bunion in 60% of cases, but can also involve other joints and recurrent attacks. Gout attacks are often accompanied by high blood uric acid, but not 100% of people with high blood uric acid will develop gout. According to statistics, only 5% to 12% of people with high blood uric acid develop gout. Just as the occurrence of lung cancer is related to smoking, it is not necessary for smokers to get lung cancer. In addition to gout, hyperuricemia can also lead to kidney disease and kidney stones, and is an independent risk factor for metabolic diseases (diabetes, metabolic syndrome, hyperlipidemia, etc.), chronic kidney disease, cardiovascular disease, and stroke. Therefore, hyperuricemia needs to be treated regardless of whether it is complicated by gout or not. Hyperuricemia includes general treatment and drug treatment. General treatment includes weight loss, smoking and alcohol cessation, and strict low purine diet. Animal offal, seafood, bone marrow and fish, shrimp, crab, chicken and duck are high in purines, especially pancreas, gravy, anchovies, sardines, animal liver and kidney, brain and soybeans have the highest content and should be strictly limited. As a supplementary source of protein, milk and eggs can be used instead. Green vegetables can be eaten except for spinach and cauliflower, which should be controlled appropriately. Since alcohol reduces the excretion of uric acid, it is necessary to avoid its intake. In particular, beer contains more guanylic acid, which can produce more purines, so it should be strictly controlled. Wine can be consumed in small amounts if special circumstances require. Most of uric acid is excreted through the kidneys, so drinking more water can promote the excretion of uric acid, and it is generally best to drink more than 2000ml (2kg) per day. Alkalinity can increase the solubility of uric acid, so eating food or liquid containing baking soda can promote uric acid excretion; on the contrary, sugar and carbonated drinks can lead to a decrease in uric acid excretion and aggravate hyperuricemia. For patients with urinary pH less than 6.0, baking soda should be applied to alkalize urine to keep the pH level at 6.2-6.8. For patients with combined gout, medication is required if the above treatment fails to achieve the target (uric acid <300umol/L). At present, the drugs to reduce uric acid are divided into those that inhibit uric acid synthesis, promote uric acid excretion and uric acid enzymes. The drugs that inhibit uric acid synthesis are allopurinol and febuxostat. Allopurinol should be applied in small doses and the dose should be adjusted according to the condition; the dose should be reduced or discontinued for those with renal insufficiency. In 2009, the U.S. Food and Drug Administration (FDA) approved a gout drug for the treatment of hyperuricemia - Febuxostat (trade name ULORIC), which has fewer side effects and has been marketed in China. There is also a class of drugs that inhibit the active reabsorption of urate in the renal tubules and increase the excretion of urate, thus reducing the concentration of urate in the blood, slowing or preventing the production of urate crystals, reducing joint damage, and promoting the dissolution of formed urate crystals. Since more than 90% of hyperuricemia is caused by reduced uric acid excretion in the kidneys, pro-uric acid excretion drugs are suitable for a wider range of people. The representative drugs are benzbromarone and probenecid. When using these drugs, it is important to drink more water and use substances that alkalize urine. In addition, urinary uric acid excretion should be measured before using these drugs. If the 24-h urinary acid excretion has increased (>3.54 mmol) or if the patient has urinary stones, these drugs are contraindicated and should be used with caution in ulcer disease and renal insufficiency. Benzbromarone is often used clinically for the treatment of primary and secondary hyperuricemia, intermittent gouty arthritis and gouty nodular swelling, with no significant renal effects with long-term use. Uric acidase drugs catalyze the oxidation of uric acid to the more soluble allantoin and reduce uric acid levels. Since this class of drugs is mostly injectable, it limits the clinical application. In conclusion, high uric acid and gout, with their high incidence and danger, are a matter of health and safety, and require persistent and comprehensive treatment to ensure your health.