With the improvement of people’s living standard and the change of diet structure, the number of people with increased blood uric acid level found in health checkups is increasing year by year, especially the middle-aged and elderly people have a higher incidence, and men are significantly higher than women. Since patients have no clinical symptoms, they often do not attract their attention and neglect treatment. Studies have proven that hyperuricemia is associated with a variety of diseases and is as dangerous to the health of middle-aged and elderly people as hypertension and diabetes, and is a problem that cannot be ignored. The following is an introduction to the formation of hyperuricemia, its hazards and treatment strategies. I. Formation of hyperuricemia Uric acid is a purine metabolite in the body, 80% of which comes from the body’s internal source, also known as endogenous uric acid, and 20% from food intake, also known as exogenous uric acid. Uric acid is eliminated from the body through the kidneys and digestive tract without being broken down. Under normal circumstances, there are about 1000~1200mg of uric acid in the body, about 600mg of uric acid is formed and 600mg of uric acid is excreted every day, so that uric acid in the body is in a dynamic balance. When the serum uric acid value is greater than 416 umol/L (7. 0 mg/dl), it is called hyperuricemia. A transient rise in serum uric acid values can be produced by the consumption of high purine foods, alcohol consumption, and strenuous exercise. Therefore, a diagnosis of hyperuricemia is made by repeating the measurement 2 to 3 times in 1 to 2 weeks under the usual diet if it consistently exceeds 416 umol/L (7. 0 mg/dl). The normal reference values may vary slightly due to the different testing methods used by each hospital laboratory. There are many causes of hyperuricemia, but the causes are excessive production and decreased excretion of uric acid. Factors that cause excessive production of uric acid include excessive intake of high purine foods, obesity, myeloproliferative disorders such as multiple myeloma, lymphoproliferative disorders, infectious mononucleosis, hemolytic anemia, tumors, psoriasis, hepatic glycogen accumulation disease, fructose intake, hereditary fructose intolerance, hypoxemia, intense muscle exercise, acute and chronic ethanol poisoning, etc.; factors that affect decreased uric acid excretion include Renal insufficiency, ketoacidosis, lactic acidosis, increased tubular urate uptake, hyperparathyroidism, hypoparathyroidism, hypothyroidism, hypertension, lead poisoning, post-chemo-radiotherapy for tumor patients, hyperaldosteronism, nephrogenic uremia, starvation, and medications such as ethambutol, pyrazinamide, niacin, acetylsalicylic acid, diuretics, etc. In addition, the blood uric acid concentration in human body is also affected by gender and age, for example, the value of uric acid in women is lower than that in men before menopause, but it will increase slowly after menopause; the concentration of uric acid in blood is low before puberty, but it will gradually increase after puberty and approach that in adults. In general, patients with hyperuricemia are often asymptomatic, but persistent hyperuricemia can cause or accompany a variety of diseases that endanger the health of middle-aged and elderly people. 1. Gout: Gouty arthritis must be preceded by a period of hyperuricemia, but hyperuricemia does not necessarily develop into gout, which generally accounts for 5% to 12% of cases. It takes 5 to 10 years to go from asymptomatic hyperuricemia to the first attack of gouty arthritis. The first symptom is often a sudden onset of pain in the first toe and metatarsal joint at night, with localized redness and swelling and increased skin temperature. Gout is prone to recurrence, and after repeated attacks, it can involve several joints and lead to joint deformity. In a few patients, the disease starts with kidney stones, which may cause back pain, hematuria and other symptoms, and in severe cases, it may also cause renal failure, focal segmental sclerosis of the glomerulus and interstitial fibrosis. There is increasing evidence that hyperuricemia accelerates the rate of renal failure, but the exact mechanism is unclear. In a recent clinical study of 6403 patients, blood uric acid levels were found to be an independent risk factor for abnormal renal function. It has been reported that many patients with kidney disease have a significant increase in blood uric acid at an early stage. In the survey statistics of patients with IgA nephritis, it was found that hyperuricemia seems to be more common in this group. 2. Other diseases: In addition to gout, hyperuricemia is also closely related to hypertension, coronary heart disease, hyperlipidemia and diabetes. Some data show that the incidence of hypertension in patients with hyperuricemia is 8.1%~13.6%, diabetes is 5.1%~15.7%, hyperlipidemia is 32%~66.5%, coronary heart disease is 3.2%~6.3%, and cerebral infarction is 0.46%. In recent years, a large-scale clinical investigation on the relationship between hyperuricemia and cardiovascular system has been done overseas, and now it is basically confirmed that hyperuricemia is an independent risk factor for cardiovascular system diseases. There is evidence that elevated blood uric acid levels promote the oxidation of LDL cholesterol and lipid peroxidation; are accompanied by increased production of oxygen radicals and participate in the inflammatory response, which plays a key role in the formation of atherosclerosis; and also promote platelet aggregation and the formation of intracoronary thrombi in patients with acute coronary syndromes. In addition, a study by medical experts from the University of Kuopio, Finland, published in a new issue of the prestigious medical journal Archives of Internal Medicine, concluded that hyperuricemia is an independent and significant risk factor for cardiovascular and other causes of death in middle-aged healthy men. They suggest that blood uric acid levels may serve as a simple, feasible, and inexpensive marker of risk for cardiovascular death. It is generally believed that asymptomatic hyperuricemia does not require drug treatment, but only diet adjustment, avoidance of obesity, overwork, alcohol abuse and mental stimulation to reduce blood uric acid level, but drug treatment is required when combined with gout, hypertension, diabetes, hyperlipidemia and coronary heart disease. 1. Diet: drink more than 2000ml of water daily, coffee, milk, cocoa, tea, eggs, noodles, rice, fruits, cabbage, tomatoes, cucumbers, cauliflower, etc. are low purine foods, which should be the main food on weekdays; eat moderate amount of medium purine foods: beef, pork, lamb, spinach, peas, mushrooms, dry beans, lentils, asparagus, peanuts, etc. For meat foods, you can cook soup and discard soup before cooking The purine content can be reduced. Forbidden foods with high purine content: animal offal – heart, liver, kidney, pancreas, minced meat, broth, carp, mackerel, fish eggs, shrimp, sardines, goose, quail, yeast. Investigation proves that: a hot pot is 10 times more purine than a regular meal; spicy and other stimulating foods should not be eaten; also resolve to quit drinking, because 1 bottle of beer can raise blood uric acid 1 times; avoid overeating or hunger; carbohydrates can promote uric acid excretion, each meal should be based on steamed buns, noodles, corn. You should actively participate in physical exercise, gradually increase the amount of exercise, do not overdo it, prohibit strenuous sports such as soccer, fast running, ice skating, swimming, mountain climbing, etc. Maintain the ideal weight, overweight or obese people should actively control their weight, but reduce weight should also be gradual, 1 kg per month, otherwise it is easy to lead to acute attacks of gout. 2, drugs: oral baking soda, neutralize uric acid, prevent the formation of kidney stones. This kind of drug is mainly used to promote the excretion of uric acid, and this kind of drug has fewer side effects and is more commonly used than the neutral Galician (benzbromarone). 3, hyperuricemia combined with hypertension: Coxsartan is the only antihypertensive drug that can lower blood pressure and promote uric acid excretion. Dosage: 50mg~100 mg per day, taken orally once in the morning. Aspirin, diuretics will inhibit the excretion of uric acid and should be prohibited.