Evidence-based medical recommendations of the European League Against Rheumatism (EULAR) on gout treatment and articles written by several rheumatologists in China have mentioned the principles, methods and importance of gout treatment, among which uric acid-lowering therapy, an integral part of gout treatment, has a very important position. In recent years, new ideas and methods of uric acid-lowering treatment have emerged, so it is necessary to discuss and emphasize the uric acid-lowering treatment of gout again to draw the attention of colleagues. The biochemical basis of gout is hyperuricemia. If persistent hyperuricemia is not actively controlled, it can cause acute and recurrent arthritis on the one hand, and urinary stones (the incidence is three times higher than that of normal blood uric acid) and uric acid nephropathy, urinary tract obstruction or renal insufficiency on the other hand. In addition, uric acid can be converted into a pro-oxidant in the body, which not only stimulates the renin-angiotensin system, but also inhibits the release of endothelial nitric oxide, leading to the contraction of renal and other blood vessels, increased blood pressure, atherosclerosis and coronary heart disease and cerebrovascular disease, etc. Hyperuricemia has become an independent risk factor for cardiovascular and cerebrovascular diseases. Therefore, the control of blood uric acid level is related to the prognosis of gout patients and is the cornerstone of treatment for such patients. Second, the strategy and timing of uric acid-lowering treatment should be mastered The “treat-to-target” strategy has been introduced into the treatment concept of gout. Regardless of the patient’s gender, race and age, crystals can be precipitated when the blood uric acid reaches 6.8 mg/dl (405umol/L), so the best target control value for blood uric acid is below 6.0 mg/dl (360umol/L). However, for chronic gout patients with a large number of gout stones, the target control value should be lowered to less than 4 mg/dl in order to accelerate the dissolution of gout stones. During the treatment process, the dose of uric acid-lowering drugs should be adjusted according to the uric acid value monitored regularly, so as to keep the blood uric acid value within the target value at all times, so that new gout stones will not be formed and existing gout stones will be dissolved gradually. This “target treatment” may “cure” gout. The timing of uric acid-lowering treatment should be early rather than late. It is too late to start uric acid-lowering treatment only when there are gout stones visible to the naked eye, chronic gouty nephropathy or joint destruction visible on X-rays, and most scholars now believe that the frequency of acute arthritis episodes as the time to start uric acid-lowering treatment should be changed from ≥3 times/year to ≥2 times/year, and the clinical application of dual-energy CT in recent years has greatly improved the sensitivity and specificity of finding tiny gout stones. The clinical application of dual-energy CT in recent years has greatly improved the sensitivity and specificity of detecting microscopic gout stones, which is conducive to the early timing of uric acid-lowering treatment. Asymptomatic hyperuricemia is not completely free from uric acid-lowering therapy. For patients with a family history of gout, blood uric acid >714μmol/L (12mg/dl) and/or 24h uric acid >1100mg (6.545mmol) despite dietary control, active uric acid-lowering is still required. However, the acute attack of arthritis is not the time to start adding uric acid-lowering drugs, but it should be added after the acute attack is completely controlled (mostly 3-6 weeks after the termination of the attack) to avoid prolonging the attack period, but the uric acid-lowering drug will not be discontinued when another acute attack occurs when a stable dose of uric acid-lowering drug has been used. For chronic gouty stone gout attack without obvious interval, it is necessary to add uric acid-lowering drugs as early as possible while using non-steroidal anti-inflammatory drugs and/or colchicine. The uric acid-lowering drugs can be divided into three major categories, namely uric acid excreting, uric acid synthesizing and uric acid decomposing drugs. Uric acid excretory drugs include benzbromarone, propoxur and benzosulfone, etc. Uric acid synthesis inhibitors include allopurinol and Febuxostat, and uric acid catabolic drugs include rasburicase and pegloticase. For patients under 60 years of age with normal or mildly impaired renal function (Ccr > 50 ml/min), no gout stones or renal calculi, and 24-hour uric acid below 700 mg (4.167 mmol) on a normal diet, uric acid-depleting drugs should be chosen. And for patients with moderate or more renal impairment (Ccr25 ml/min , it is safer to use. When using allopurinol in patients with HLA-B58 positive, chronic kidney disease and thiazide diuretics, one should be alert to the possibility of hypersensitivity syndrome, as the mortality rate is 20%. For those who cannot tolerate allopurinol due to rash alone, desensitization therapy is possible, either by taking oxypurinol, the active metabolite of allopurinol, or by switching to febuxostat. Febuxostat, which was approved by the FDA last February, has no purine-like core structure and is mainly suitable for allopurine allergy, intolerance or treatment failure. Effective. Because the human body lacks uric acid enzyme and cannot degrade uric acid into highly soluble allantoin, the supplementation of this synthetic uric acid enzyme can make up for this defect and has a good application prospect. However, the biggest problem of these drugs is that they are highly antigenic, easy to be allergic and need to be injected intravenously, so they have not been approved for uric acid lowering treatment of gout in Europe and the United States, and are only used for a short period of time for chronic refractory gout with a large number of gout stones to deplete the uric acid pool, and then switched to other uric acid lowering drugs to maintain the efficacy for a long time. For those with renal failure, these drugs may be used instead of allopurinol or in combination with allopurinol. Clinically, it is advisable to choose a “double whammy” of medications according to the disease with which the gout patient is suffering. Gout patients with hypertension can choose crosartan or amlodipine. Domestic and international studies have confirmed that crosartan has both uric acid-lowering and antihypertensive effects, and has a good safety profile, and can increase urinary pH without increasing the formation of urinary crystals. Amlodipine, a third-generation calcium antagonist, also has both uric acid-lowering and antihypertensive effects, and can significantly reduce uric acid levels in cyclosporine A-induced hyperuricemia after renal transplantation. Gout patients with hyperlipidemia can choose Fenofibrate or atorvastatin, both of which can lower blood lipid and uric acid at the same time, the former is suitable for those with mainly increased triglyceride and the latter is suitable for those with mainly increased cholesterol. Fenofibrate 200mg/d for 3 weeks or 160mg/d for 2 months can reduce blood uric acid by 19% and 23% respectively. Fenofibrate also has certain anti-inflammatory properties, and is less likely to induce acute attacks of gout when lowering uric acid. However, these “two birds with one stone” drugs have relatively weak uric acid-lowering effects. For those who have persistent hyperuricemia, if the single medication is not effective, they can be treated with drugs with different mechanisms of action, such as cloxacin and fenofibrate combined with drugs that inhibit uric acid synthesis, or pro-uric acid excretory drugs combined with drugs that inhibit uric acid synthesis, etc. The better the efficacy of uric acid reduction, the more frequent the attacks of gout, especially the risk of inducing attacks within the first year of treatment is significantly higher. (1) Steady uric acid lowering and prevention of dramatic fluctuations of uric acid: uric acid lowering drugs should be gradually increased from small doses, such as the U.S. FDA guidelines suggest that allopurinol starts at 100 mg/d and gradually increases to a maximum of 800 mg/d. Once the uric acid lowering drug is used, if there is another attack, the dose of the uric acid lowering drug should remain unchanged or only be finely adjusted. (2) Concomitant application of NSAIDs or colchicine: continued application for at least 4-6 weeks, or even more than 6 months. However, despite this, about 70% of the patients who use pro-uric acid catabolic drugs may develop gouty arthritis attacks. (3) Optional weak uric acid-lowering drugs such as fenofibrate: Because fenofibrate rarely causes acute attacks of gout when lowering uric acid, it is more appropriate for gout patients with high blood lipids to take fenofibrate to start. When lowering uric acid treatment, non-pharmacological therapy should also be emphasized, including diet control, abstaining from alcohol and drinking more water, and adding alkaline drugs such as sodium bicarbonate or acetazolamide (the latter is suitable for those with cardiac insufficiency), and stopping diuretics that can increase blood uric acid. In particular, those who use uric acid detoxification drugs should drink a lot of water (>2000ml/d) and use alkaline drugs. The dose of alkaline drugs should be increased or decreased according to the urinary pH, so that the urinary pH can be maintained at 6.2~6.8.