1. Typical cases As endocrinologists, we often encounter such patients in our clinical work: Case 1: the first toe joint of the foot was suddenly red, swollen, and painful, and the walking was impaired, and the patient was seen in orthopedics or rheumatology clinic. Blood uric acid level was higher than 420 umol/L in men and 357 umol/L in women, and it still met this criterion after review, diagnosis: asymptomatic hyperuricemia. Case 3: Type 2 diabetic patient with concomitant hypertension, hyperlipidemia, obesity, coronary artery disease, cerebral infarction, biochemical examination often reveals increased blood uric acid levels as well, additional diagnosis: hyperuricemia. All 3 cases above involved 2 key words: blood uric acid hyperuricemia. The serum uric acid (UA) test is usually one of the blood biochemical renal function tests and is an indicator of the degree of impaired renal function.UA is a product of purine metabolism in the body. There are two sources of purine in the human body: endogenous by self-synthesis or nucleic acid degradation (about 600mg/d), which accounts for about 80% of the total uric acid in the body; exogenous by intake of purine diet (about 100mg/d), which accounts for about 20% of the total. The uric acid pool in the body under normal conditions is 1200mg, producing about 750mg of UA per day and excreting about 800-1000mg, with 30% excreted from the intestine and biliary tract and 70% excreted by the kidneys. Under normal circumstances, the human body basically maintains a dynamic balance between the production and excretion of UA every day. Any factors that affect the production and/or excretion of blood UA can lead to an increase in the level of blood UA and become HUA, such as acute and chronic nephritis, kidney disease, kidney stones, gout, as well as leukemia, multiple myeloma, true erythrocytosis, etc. 2, the epidemiology of hyperuricemia In recent years, with the development of economy and improvement of dietary structure, the prevalence of HUA in our population has increased steeply, and the survey after the mid-1990s showed that the prevalence of men was 8.2%-19.8% and women 5.1%-7.6% [1]. The prevalence of HUA has increased 10 times on average in 10 years, and the prevalence in coastal areas has even reached 30%. According to reports from all over the world, it is conservatively estimated that the number of HUA patients in China can reach 120 million, with the high prevalence of middle-aged and elderly men and postmenopausal women, but the prevalence is gradually becoming younger, with about 2.4-5.7% of people under 20 years old. 3.Risk factors of hyperuricemia HUA is related to age, gender, regional distribution, race, genetics and social status. Eating high purine food such as meat, seafood, animal offal, thick broth, etc., drinking alcohol (beer, liquor) and strenuous physical exercise all raise the blood UA level. The prolonged application of certain drugs can lead to the increase of blood UA, such as thiazide diuretics, compound antihypertensive tablets, nifedipine, and pranalol, etc. all prevent UA excretion. 4.Diagnostic criteria of hyperuricemia Under normal purine diet, the fasting blood UA level on two non-same days is >420 umol/L (7mg/dl) for men and >357 umol/L (6mg/dl) for women. It was previously thought that HUA is a biochemical characteristic of gout, and its main risk is to cause joint swelling, pain, kidney stones and interstitial nephritis. In 1634 Antonj Van Leeuwenhock found gout stone urate crystals by microscopy and uric acid stones were also found in Egyptian mummies. Case 1 is very typical of gouty arthritis caused by HUA. The incidence of gout in foreign countries is reported to be about 0.6% in men and 0.1% in women. Because of its external manifestations of redness and swelling of the joints of the feet, severe pain, and obvious walking impairment, the first department is mostly orthopedics, rheumatology or surgery. However, due to the limitations of various medical conditions, grass-roots community hospitals inevitably fall into the misunderstanding of “treating the head when the head aches and treating the foot when the foot hurts”, resulting in medical disputes due to misdiagnosis and mistreatment. Therefore, to identify and correctly deal with gouty arthritis, we should start from recognizing HUA, especially for young, obese men with no previous history of arthralgia and sudden onset of red, swollen and hot foot and joint pain after drinking alcohol, blood UA should be a routine test. HUA without gout attack is called asymptomatic HUA, or case 2. In the past, it was believed that simple HUA mostly had no obvious specific symptoms and was long mistaken as a simple metabolic disease and not given enough attention. However, there is increasing evidence that HUA is closely related to the occurrence, development, and morbidity and mortality of cardiovascular and cerebrovascular diseases in conjunction with the classically defined metabolic syndrome (MS) components such as disorders of glucose and lipid metabolism, hypertension, obesity, insulin resistance, and other risk factors. More than 10 studies enrolling more than 100,000 patients in the past 20 years have further confirmed that HUA is an independent risk factor for cardiovascular disease, and patients with cardiovascular disease combined with HUA are more likely to induce heart attack and stroke, which is the case we often encounter in our clinic3. 5, hyperuricemia and metabolic syndrome In fact, it can enhance HUA and diabetes, hypertension, hyperlipidemia, obesity and other infamous The pathophysiological basis of MS is hyperinsulinemia and insulin resistance. The pathophysiological basis of MS is hyperinsulinemia and insulin resistance, which increase the production of UA during glycolysis and free fatty acid metabolism, and directly lead to HUA by increasing the reabsorption of uric acid in the kidneys. 70% of MS patients also have HUA. In a report published in Diabetologia in April this year, the WHO Expert Advisory Group pointed out that MS has many limitations as a diagnostic tool. The American Academy of Diabetes (ADA) and the European Academy of Diabetes (EASD) even believe that MS should be left undiagnosed and untreated. However, a large body of evidence has been accumulated that MS is objective, and that combating common risk factors for the metabolic syndrome is important for reducing the risk of diabetes and cardiovascular events in high-risk populations, while saving health resources and maximizing benefits. The two university associations also believe in targeting individual risk factors for prevention and treatment. Therefore the close relationship between HUA as a member of the extended MS component and risk factors such as hypertension, abnormal glucose metabolism, hyperlipidemia and obesity deserves further attention. (1) HUA and hypertension 90% of patients with primary hypertension are combined with HUA, while only 30% of patients with secondary hypertension are combined with HUA, suggesting a causal relationship between HUA and primary hypertension. Data from the famous American Framingham Heart Study showed that 3329 adult subjects were free of hypertension, myocardial infarction, heart failure, renal failure and gout at baseline, and 36.1% of them were prehypertensive and 13.8% were hypertensive after 4 years of follow-up. The prevalence of hypertension increased with increasing UA levels, and multivariate analysis showed that for every 1 standard deviation increase in UA, the risk of hypertension and hypertension increased by 17% and 11%, respectively. Further analysis of patients who were not on antihypertensive medication during the follow-up period showed that UA levels were associated with systolic and diastolic blood pressure at 4 years, suggesting that elevated UA is an independent predictor of hypertension in adults. The Losartan Hypertension Patient Survival Study (LIFE) compared the incidence of endpoint events (stroke, myocardial infarction, and death) between the losartan and atenolol-treated groups. In patients with hypertension and left ventricular hypertrophy, lowering blood uric acid levels reduced the risk of cardiovascular events, and the 29% reduction in risk in the losartan-treated group was attributed to the different blood uric acid levels in the two groups. (2) HUA and obesity and dyslipidemia Obesity, hypertriglyceridemia, hypertension and alcohol consumption are the main risk factors for HUA in middle-aged people. Framingham et al. found that a 30% increase in body weight was associated with a 0.1 mg/dl increase in UA levels in men and a 50% increase in body weight was associated with a 0.8 mg/dl increase in UA levels in women. When comparing the prevalence of obesity in the normal population with the HUA population with UA levels below 7.0 mg/dl and above 7.0 mg/dl, it was found that 31.3% of the normal population were overweight, suggesting that the frequency of obesity in the HUA population was significantly higher. The prevalence of obesity in the HUA population was found to be 31.3% in the normal population, suggesting that the frequency of obesity in the HUA population is significantly higher. In addition, it was reported that the incidence of HUA in abdominal obesity was significantly higher than that in obesity with increased subcutaneous fat, and abdominal obesity was closely related to the increased generation of UA. It shows that HUA is closely related to obesity, and weight control, especially central obesity, may play a role in preventing HUA. It is suggested that HUA is a manifestation of dyslipidemia, as 75-80% of gout patients have hypertriglyceridemia and 82% of hypertriglyceridemia patients have HUA, and even in healthy people, UA is positively correlated with high triglyceride levels. There is only one prospective cohort study on the relationship between uric acid and triglycerides, which was followed up for 8 years and found that basal triglycerides were an independent predictor of future HUA. (3) HUA and abnormal glucose metabolism Long-term HUA can disrupt pancreatic β-cell function and induce diabetes. Two studies suggest a causal relationship between long-term HUA and abnormal glucose tolerance and the development of diabetes. In two prospective clinical studies from Korea and Japan, a total of 2951 middle-aged HUA patients were enrolled and followed up for 6-7 years, and it was found that those with baseline blood uric acid levels >398umo/l had a 78% increased risk of developing long-term abnormal glucose tolerance and type 2 diabetes compared to those with <280umo/l. The reason why type 2 diabetes is prone to HUA is related to hyperinsulinemia, and insulin can promote renal reabsorption of The finding that insulin promotes the reabsorption of UA by the kidneys, resulting in a decrease in renal excretion of UA and an increase in blood UA provides a possible way to reduce UA. No matter from the etiology and pathological mechanism of HUA, basic research, or clinical practice and evidence-based medical research, we can definitely conclude that HUA is closely related to MS, is in line with various risk factors of cardiovascular lesions, and has a clear causal relationship with the outcome of cardiovascular diseases, and HUA is both an accurate predictor and capable of reducing cardiovascular and cerebrovascular events after intervention. Therefore, in 2009, an expert group consisting of dozens of well-known experts in China, led by Professor Hu Dayi of the Cardiovascular Physicians Branch of the Chinese Medical Association, completed the first "Expert Consensus on Recommendations for the Diagnosis and Treatment of Asymptomatic Hyperuricemia Combined with Cardiovascular Diseases" in China, which provides positive and powerful guidance for the majority of clinicians in China. In our work, we should make full use of blood UA, the simplest and economical biochemical index, as a screening item for MS and cardiovascular disease prevention and treatment, to make early diagnosis, early intervention and standardized treatment, and to reduce health care costs.