Uric acid is the end metabolite of purine compounds in humans. Disturbances in purine metabolism lead to hyperuricemia. A fasting blood uric acid level higher than 420 mmol/L in men and 360 mmol/L in women on two non-same days under a normal purine diet is called hyperuricemia. The prevalence of this disease is influenced by a variety of factors, related to genetics, gender, age, lifestyle, dietary habits, medication and the degree of economic development. According to the reports on the prevalence of hyperuricemia in recent years, there are about 120 million people with hyperuricemia in China, accounting for about 10% of the total population, and the high prevalence age is middle-aged and old men and postmenopausal women, but there is a trend of rejuvenation in recent years.
I. Disease classification
Hyperuricemia can be divided into primary hyperuricemia and secondary hyperuricemia.
(A) Primary hyperuricemia
1, molecular defects of unknown cause.
2. Congenital disorders of purine metabolism.
(ii) Secondary hyperuricemia
Hyperuricemia due to increased blood uric acid production or impaired uric acid excretion caused by various acute and chronic diseases such as hematological diseases or malignant tumors, chronic poisoning, drugs or high purine diet.
Clinical manifestations
Asymptomatic hyperuricemia means that the patient only has hyperuricemia without clinical symptoms such as arthritis, gout stone and uric acid stone. The incidence is 5%-7% in adult males. The patient has never had an attack of gouty arthritis, but only a high uric acid value in the blood is found by chance during physical examination.
1, hyperuricemia and gout: hyperuricemia is the basis for the development of gout, but not enough to cause gout. Gout only occurs when uric acid salt is deposited in the tissues of the body and causes damage; the higher the blood uric acid level, the greater the likelihood of gout occurring in the next five years. The higher the blood uric acid level, the greater the likelihood of gout occurring in the next five years. Blood uric acid levels are not always high during acute gouty arthritis attacks.
2, hyperuricemia and hypertension: Currently, several epidemiological studies have confirmed that blood uric acid is an independent risk factor for the development of hypertension, and for every 59,5 μmol/L increase in blood uric acid level, the relative risk of hypertension increases by 25%. Clinical studies have found that 90% of patients with primary hypertension are combined with hyperuricemia, while only 30% of patients with secondary hypertension are combined with hyperuricemia, suggesting a causal relationship between hyperuricemia and primary hypertension.
3, hyperuricemia and diabetes: long-term hyperuricemia can destroy the function of pancreatic beta cells and induce diabetes, and some studies have confirmed that long-term hyperuricemia has a causal relationship with abnormal glucose tolerance and the development of diabetes.
4. Hyperuricemia and hypertriglyceridemia: Domestic and international epidemiological data consistently show that there is a correlation between blood uric acid and triglycerides. A prospective cohort study on the relationship between uric acid and triglycerides found that basal triglycerides were an independent predictor of future hyperuricemia.
5. Hyperuricemia and metabolic syndrome: The pathophysiological basis of metabolic syndrome is hyperinsulinemia and insulin resistance. Insulin resistance increases the production of blood uric acid during glycolysis and free fatty acid metabolism, and directly leads to hyperuricemia through increased renal reabsorption of uric acid. Metabolic syndrome is combined with hyperuricemia in 70% of patients.
5, hyperuricemia and coronary heart disease: uric acid is an independent risk factor for death from coronary heart disease: some studies have shown that uric acid is an independent risk factor for death from coronary heart disease in the general population, regardless of gender. For every 1 mg/dl increase in blood uric acid, the risk of death increased by 48% in men and 126% in women. Blood uric acid >6mg/dl is an independent risk factor for coronary heart disease; blood uric acid >7mg/dl is an independent risk factor for stroke.
6. Hyperuricemia and kidney damage: uric acid is closely related to kidney disease. In addition to the deposition of uric acid crystals that lead to kidney damage aggravated by small renal arteries and chronic interstitial inflammation, many epidemiological surveys and animal studies show that uric acid can directly cause microangiopathy in the small glomerular arteries, leading to chronic kidney disease.
Three, disease diagnosis
1. Criteria for hyperuricemia: fasting blood uric acid level >7mg/dl for men or >6mg/dl for women on two non-same days under normal purine diet.
2. Typing diagnosis of hyperuricemia: Typing diagnosis helps to detect the cause of hyperuricemia and give targeted treatment. After 5 days of low purine diet in patients with hyperuricemia, 24-hour urine was retained to test urinary uric acid level.
(1) Poor uric acid excretion type: uric acid excretion is less than 0,48mg/(kg,h) and uric acid clearance rate is less than 6,2ml/min.
(2) Excessive uric acid production type: uric acid excretion is greater than 0,51mg/(kg,h) and uric acid clearance rate is greater than or equal to 6,2ml/min.
(3) Mixed type: uric acid excretion is more than 0,51mg/(kg,h) and uric acid clearance rate is less than 6,2ml/min.
Considering the influence of renal function on uric acid excretion, the creatinine clearance is corrected, and hyperuricemia is classified according to the ratio of uric acid clearance/creatinine clearance as follows: >10% is excessive uric acid production type; <5% is poor uric acid excretion type; 5%-10% is mixed type.
Fourth, the danger of disease
Elevated blood uric acid can appear as follows
(1) deposited in joints → gouty arthritis → joint deformation.
(2) Deposited in the kidney → gouty nephropathy, uric acid stones → uremia.
(3) Stimulation of blood vessel walls → atherosclerosis → aggravation of coronary heart disease and hypertension.
(4) Damage to pancreatic B cells → induce or aggravate diabetes.
V. Disease treatment
All patients with asymptomatic hyperuricemia need to undergo therapeutic lifestyle changes and avoid drugs that elevate blood uric acid as much as possible. If asymptomatic hyperuricemia is combined with cardiovascular risk factors or cardiovascular diseases (hypertension, abnormal glucose tolerance or diabetes, hyperlipidemia, coronary heart disease, stroke, heart failure or abnormal renal function), drug treatment should be given for blood uric acid values >8mg/dl; for hyperuricemia without cardiovascular risk factors or cardiovascular diseases, drug treatment should be given for blood uric acid values >9mg/dl. Specific treatment is as follows.
1.Improve lifestyle: including healthy diet, quit smoking, adhere to exercise and weight control.
(1) Healthy diet: for people with gout, hyperuricemia, cardiovascular metabolic risk factors and middle-aged and elderly people, diet should be based on low purine food, strictly control the intake of meat, seafood and animal offal, and moderately reduce the intake of Class B food and eat mainly Class A food.
(2) Drink more water, quit smoking and alcohol: drink water daily to ensure that the urine volume is above 1500ml, quit smoking, ban beer and white wine, red wine in moderation.
(3) adhere to exercise, weight control: daily moderate intensity exercise for more than 30 minutes. Obese people should lose weight, so that the weight control in the normal range.
(2) Alkalize urine: maintain urine pH at 6.2-6.9.
3.Avoid drugs that raise blood uric acid: such as diuretics (especially thiazides), corticosteroids, insulin, cyclosporine, tacrolimus, nicotine, pyrazinamide, niacin, etc. For patients who need diuretics and combined with hyperuricemia, non-thiazide diuretics are preferred, along with alkalinizing urine and drinking more water to keep the daily urine volume above 2000ml. For patients with hypertension combined with hyperuricemia, antihypertensive drugs other than thiazide diuretics are preferred. Patients with hyperuricemia who have conquered with small doses of aspirin are recommended to alkalize urine and drink more water.
4.Uric acid-lowering drugs.
(1) Drugs to increase uric acid excretion: benzbromarone; propofol, sulfopirone.
(2) Adjunctive uric acid-lowering drugs: cloxacin, fenofibrate.
5. Active treatment of metabolic risk factors associated with blood uric acid: Active control of cardiovascular risk factors associated with hyperuricemia such as hyperlipidemia, hypertension, hyperglycemia, obesity and smoking should be an important part of the treatment of hyperuricemia.
VI. Disease prognosis
1, hyperuric acid increases the risk of hypertension in Asian population by 57%, increases the risk of total death by 8%, and increases the risk of cardiovascular death by 21%.
2.High uric acid increases the risk of coronary heart disease by 9%, and increases the risk of death from coronary heart disease by 16%.
3, high uric acid increases the risk of reduced kidney function by 21% and increases the risk of death from chronic kidney disease by 68%.
4. High uric acid increases the risk of stroke by 47%, and increases the risk of death from stroke by 26%.
VII. Disease prevention
1. Avoid strenuous exercise or injury.
2. Limit high purine (offal, seafood), soft drinks and fructose; not all seafood is high purine diet: sea cucumber, jellyfish skin and seaweed are low purine; not all vegetables are low purine diet: soybeans, lentils, shiitake mushrooms and nori are high purine, but do not increase the risk of gout.
3, no alcohol: especially beer and white wine, can be appropriate to drink red wine.
4.Control your weight.
5, drink more water: >2000ml/d drink tap water and mineral water (PH value 6.5-8.5); do not drink pure water (PH value 6.0), drink before bedtime can prevent urinary stones).
6, long-term alkalinization of urine: commonly used sodium bicarbonate.