With changes in lifestyle and diet, hyperuricemia in China is growing as rapidly as the diabetic population. From the epidemiological survey data, there may be a surge in the population of hyperuricemia in China. As a result, the incidence of gout has also increased significantly. Therefore, we call hyperuricemia the “fourth high”, which is the fourth high after hypertension, hyperglycemia and hyperlipidemia. It is important to enhance our understanding of the “fourth high”. The effect of lifestyle on uric acid Lifestyle can certainly reduce uric acid, but the percentage of reduction is not high. This is because hyperuricemia is not mainly caused by “eating”, but by two mechanisms: excessive endogenous production and the inability to excrete uric acid. Therefore, about 80% of patients with hyperuricemia do not have dietary factors as the cause of their disease. Although dietary control needs to be managed well, it is not the primary means of lowering uric acid. Many patients with hyperuricemia require pharmacological treatment to obtain good intervention results. Asymptomatic hyperuricemia is not the same as harmless Hyperuricemia may cause diabetic nephropathy as well as other vascular damage, and in addition, current research suggests that hyperuricemia also causes an increased incidence of stroke. Therefore, hyperuricemia with particularly high uric acid levels should be treated with medication despite the absence of gout symptoms. The treatment strategy for asymptomatic hyperuricemia should be stratified with reference to the patient’s risk factors: if the patient has no risk factors for cardiovascular disease, a uric acid level above 540 umol/L requires pharmacological intervention; if the patient has risk factors for cardiovascular disease, a uric acid level above 480 umol/L requires pharmacological intervention. Intervention for asymptomatic hyperuricemia For patients with asymptomatic hyperuricemia, most of them need to start with lifestyle intervention, exercise therapy, and weight loss therapy. If the uric acidemia does not decrease after six months of weight loss treatment, pharmacological intervention should be considered. At this point medications should be applied from the smallest dose and better results can be obtained when uric acid levels are reduced to below 360 umol/L. Treatment Inhibitors of uric acid synthesis: first-line recommendation Drugs for hyperuricemia include drugs that inhibit uric acid synthesis and drugs that promote uric acid excretion, each of which has its own relative focus. Drugs that inhibit uric acid synthesis tend to be more effective in cases of tumors or increased endogenous synthesis of uric acid. Pro-uric acid excretory drugs are more effective in treating patients with impaired uric acid excretion. For most people, both mechanisms of excessive uric acid synthesis and impaired uric acid excretion coexist. Therefore, patients with severe hyperuricemia often require a combination of drugs for both mechanisms to achieve a better outcome. The 2012 American College of Rheumatology gout treatment guidelines include uric acid synthesis inhibitors (XOI) as the first-line recommended uric acid-lowering drugs. XOI is represented by febuxostat, and this class of uric acid synthesis inhibitors has many important advantages, including: 1. very strong therapeutic effect, which is very important; 2. good or bad renal function of the patient does not affect the drug treatment plan; 3. side effects in terms of The incidence of allergic reactions and exfoliative dermatitis is relatively low; 4. Taking once a day can improve compliance. In conclusion, this class of drugs has strong uric acid-lowering, precise efficacy and low side effects, so it can be designated as the first-line uric acid-lowering drugs by the American College of Rheumatology. In recent years, more new uric acid-lowering drugs have been researched and marketed, and the efficacy of new uric acid-lowering drugs is very good in the main body, but there are still some patients with poor efficacy, so there is a need for treatment plans with stronger uric acid-lowering effects. Secondly, mechanistically, we need to further demonstrate whether uric acid-lowering can reduce the occurrence of endpoint events, especially cardiovascular events. If uric acid-lowering drugs can be shown to significantly reduce cardiovascular events, the evidence for the use of uric acid-lowering drugs will be greatly enhanced.