What is Hyperuricemia?
Hyperuricemia (HUA) means that under normal purine diet, the fasting blood uric acid level is twice higher than 420 mol / L in men and higher than 360 mol / L in women, which is called hyperuricemia.
Basic Information
- English name
- hyperuricemia
- Visiting department
- Division of Rheumatology
- Common causes
- Related to reduced uric acid excretion or excessive uric acid production
- Common symptoms
- May be asymptomatic or show signs of arthritis, gout, hypertension, etc.
Classification of hyperuricemia
- Hyperuricemia can be divided into primary hyperuricemia and secondary hyperuricemia.
- Primary hyperuricemia
- (1) Unexplained molecular defects.
- (2) Congenital disorders of purine metabolism.
- 1) The increase in the activity of 5-phosphate nucleotide-1-pyrophosphate synthetase (PRPPS), resulting in excessive synthesis of 5-phosphate nucleotide-1-pyrophosphate synthetase, excessive production of uric acid, and a genetic characteristic of X-linkage.
- 2) Hypoxanthine-guanine phosphorotransferase (HPRT) is partially missing, which causes the concentration of 5-phosphate nucleotide-1-pyrophosphate synthetase, excessive uric acid production, and X-linked genetic characteristics.
- 3) Hypoxanthine-guanine phosphorotransferase is completely lacking, and uric acid production is increased due to increased purine synthesis. It is found in Lesch-Nyhan syndrome and is genetically characterized as X-linked.
- 4) Glucose-6-phosphatase deficiency, excessive uric acid production and decreased renal clearance of uric acid caused by increased purine synthesis, are found in glycogen accumulation disease type I, and the genetic feature is an autosomal recessive inheritance.
- 2. Secondary hyperuricemia
- A variety of acute and chronic diseases such as hematological or malignant tumors, chronic poisoning, hyperuricemia due to increased blood uric acid production due to drugs or a high purine diet, or hyperuricemia due to uric acid excretion disorders.
Causes of hyperuricemia
- Hyperuricemia is caused by excessive uric acid production and / or insufficient excretion in the body, which can be divided into two categories: primary and secondary.
- Primary hyperuricemia
- (1) 90% reduction in uric acid excretion The cause of hyperuricemia in patients with primary gout is related to decreased uric acid excretion. The possible mechanisms are: decreased glomerular filtration; increased renal tubular reabsorption; decreased renal tubular secretion .
- (2) Excessive uric acid production is defined as excessive endogenous uric acid production: in a low-purine diet (<17.9 mol / d), the uric acid excretion in urine is still greater than 3.58 mmol after more than 5 days. The cause of hyperuricemia in 10% of patients with primary gout is related to excessive uric acid production. The mechanism may be excessive endogenous uric acid production. It is related to the increase in the number and activity of some enzymes in the process of uric acid production and / or the decrease in the number and activity of some enzymes that inhibit uric acid production. Defects of enzymes are related to genetic mutations, which can be multiple genes or single genes. The inheritance methods can be divided into autosomal recessive, autochromic dominant inheritance and sex-linked inheritance.
- 2. Secondary hyperuricemia
- (1) Decreased renal uric acid excretion Nephropathy, such as glomerular lesions, results in reduced uric acid filtration and renal tubule lesions, resulting in decreased uric acid secretion; Diuretics, especially thiazide diuretics, other drugs such as aspirin, pyrazinamide, levodopa Dopa, ethambutol, and ethanol can also interfere with the reabsorption of uric acid by renal tubules. Increased organic acids in the body such as keto acid and lactic acid can competitively inhibit renal uric acid secretion.
- (2) Excessive uric acid production is more common in bone marrow and lymphoproliferative diseases. During the chemotherapy and radiotherapy of leukemia and lymphoma, due to the destruction of a large number of cells, nucleic acid metabolism can be accelerated, resulting in secondary hyperuricemia.
Clinical manifestations of hyperuricemia
- Asymptomatic hyperuricemia means that the patient has only hyperuricemia (male and female blood uric acid are> 420 mol / L and 360 mol / L, respectively) and no clinical symptoms such as arthritis, gout stone, uric acid stone. The incidence is 5% to 7% in adult men. The patient had never had an attack of gouty arthritis, but when he was examined, he accidentally found that the blood uric acid value was too high.
- 1. Hyperuricemia and gout
- Hyperuricemia is the basis of the onset of gout, but it is not enough to cause gout. Gout only occurs when urate is deposited in the tissues of the body to cause damage. The higher the blood uric acid level, the greater the possibility of gout in the next 5 years. Blood uric acid levels are not necessarily high during the onset of acute gouty arthritis.
- 2. Hyperuricemia and hypertension
- At present, multiple epidemiological studies have confirmed that blood uric acid is an independent risk factor for the development of hypertension. For every 59.5 mol / L increase in blood uric acid level, the relative risk of hypertension is increased by 25%. Clinical studies have found that 90% of patients with primary hypertension have hyperuricemia, while only 30% of patients with secondary hypertension have hyperuricemia, suggesting a causal relationship between hyperuricemia and primary hypertension.
- 3. Hyperuricemia and diabetes
- Long-term hyperuricemia can destroy pancreatic -cell function and induce diabetes, and studies have confirmed that long-term hyperuricemia is causally related to impaired glucose tolerance and the onset of diabetes.
- 4. Hyperuricemia and hypertriglyceridemia
- Epidemiological data at home and abroad consistently show a correlation between blood uric acid and triglycerides. A prospective cohort study on the relationship between uric acid and triglycerides found that basic triglycerides are independent predictors of future hyperuricemia.
- 5. Hyperuricemia and metabolic syndrome
- The pathophysiology of the metabolic syndrome is hyperinsulinemia and insulin resistance. Insulin resistance increases blood uric acid production during glycolysis and free fatty acid metabolism. At the same time, it increases hyperuricemia directly by increasing reabsorption of uric acid by the kidneys. 70% of patients with metabolic syndrome are concurrently hyperuricemia.
- 6. Hyperuricemia and coronary heart disease
- Uric acid is an independent risk factor for coronary heart disease death: Studies have shown that, regardless of gender, uric acid is an independent risk factor for coronary heart disease death in the general population. For every 1 mg / dl increase in serum uric acid, the risk of death increases by 48% in men and 126% in women. Blood uric acid> 357 mol / L is an independent risk factor for coronary heart disease; blood uric acid> 416.5 mol / L is an independent risk factor for stroke.
- 7. Hyperuricemia and Kidney Damage
- Uric acid is closely related to kidney disease. In addition to uric acid crystal deposition leading to renal arterioles and chronic interstitial inflammation exacerbating renal damage, many epidemiological investigations and animal studies have shown that uric acid can directly cause glomerular arterioles to undergo microvascular disease, leading to chronic kidney disease [3 ] .
Hyperuricemia diagnosis
- 1. Criteria for hyperuricemia
- Under the normal purine diet, the fasting blood uric acid level in two times on the same day was> 416.5 mol / L for males or> 357 mol / L for females.
- 2. Typing diagnosis of hyperuricemia
- Typing diagnosis can help find the cause of hyperuricemia and give targeted treatment. After 5 days of low-purine diet in patients with hyperuricemia, 24 hours of urine was taken for uric acid levels.
- (1) Poor uric acid excretion The uric acid excretion is less than 2.86 mol / (kg · h), and the uric acid clearance rate is less than 6.2 ml / min.
- (2) Excessive uric acid production Excretion of uric acid is greater than 3 mol / (kg · h), and uric acid clearance is greater than or equal to 6.2 ml / min.
- (3) The excretion of mixed uric acid exceeds 3 mol / (kg · kh), and the clearance rate of uric acid is less than 6.2 ml / min.
- Considering the effect of renal function on uric acid excretion, the creatinine clearance rate was corrected, and the classification of hyperuricemia according to the uric acid clearance / creatinine clearance ratio is as follows:> 10% is the type of uric acid overproduction; <5% is uric acid excretion Bad type; 5% to 10% are mixed.
Hyperuricemia complications
- Elevated blood uric acid can occur:
- (1) Deposit on joints gouty arthritis joint deformation.
- (2) Deposited in kidney gout nephropathy, uric acid stones uremia.
- (3) Stimulate the blood vessel wall atherosclerosis aggravate coronary heart disease and hypertension.
- (4) Damage to pancreatic B cells induce or exacerbate diabetes [4] .
Hyperuricemia Treatment
- All patients with asymptomatic hyperuricemia need to undergo therapeutic lifestyle changes and avoid medications that raise blood uric acid as much as possible. Asymptomatic hyperuricemia with cardiovascular risk factors or cardiovascular disease (hypertension, impaired glucose tolerance or diabetes, hyperlipidemia, coronary heart disease, stroke, heart failure or abnormal renal function), blood uric acid value> 476 mol / L was given medication; hyperuricemia without cardiovascular risk factors or cardiovascular disease, blood uric acid value> 535.5 mol / L was given medication. The specific treatment is as follows:
- 1. Improve lifestyle
- This includes healthy eating, smoking cessation, exercise and weight control.
- (1) Healthy diet has gout, hyperuricemia, cardiovascular metabolic risk factors, and the middle-aged and elderly population. The diet should be based on low purine foods. Strict control of food intake such as meat, seafood and animal offal, moderate Reduce the intake of type B foods, and eat mainly type A foods (see table).
- (2) Drink plenty of water. Quit smoking and drinking. Drink a daily urine volume of 1500ml or more. Quit smoking, ban beer and liquor, and moderate amount of red wine.
- (3) Persist in exercise and control your weight for more than 30 minutes every day. Obese people should lose weight to keep their weight in the normal range.
- Table 100g of purine in food
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- 2. Alkaline urine
- The urine pH was maintained at 6.2 to 6.9.
- 3. Avoid using drugs that raise blood uric acid
- Such as diuretics (especially thiazines), corticosteroids, insulin, cyclosporine, tacrolimus, pyrazinamide, niacin and so on. For patients who need to take diuretics and who are complicated by hyperuricemia, non-thiazide diuretics are the first choice. At the same time, the urine should be alkalized and drink plenty of water to keep the daily urine volume above 2000ml. For patients with hypertension and hyperuricemia, antihypertensive drugs other than thiazide diuretics are preferred. Patients with hyperuricemia who have been instructed to take small doses of aspirin are advised to alkaline urine and drink more water.
- 4. Uric acid lowering drugs
- (1) Drugs that increase uric acid excretion Brombromolone can be used in patients with hyperuricemia with mild to moderate renal insufficiency. Adults with a creatinine clearance of 45-60ml / min are 50mg daily; adults with a creatinine clearance of> 60ml / min are 50-100mg daily. Side effects: uric acid stones, liver and kidney stones. Probenecid and Sulpyridone can only be used in patients with normal renal function, and liver damage is more common.
- (2) Assisted uric acid lowering agents losartan and fenofibrate.
- 5. Active treatment of metabolic risk factors related to serum uric acid
- Active control of cardiovascular risk factors related to hyperuricemia such as hyperlipidemia, hypertension, hyperglycemia, obesity and smoking should be an important part of the treatment of hyperuricemia.
Prognosis of hyperuricemia
- 1. Hyperuric acid increases the risk of hypertension in Asian population by 57%, increases the overall risk of death by 8%, and increases the risk of death from cardiovascular disease by 21%.
- 2. High uric acid increases the risk of coronary heart disease by 9%, and increases the risk of coronary heart disease death by 16%.
- 3. High uric acid increases the risk of renal function by 21%, and increases the risk of death by chronic kidney disease by 68%.
- 4. High uric acid increased the risk of stroke by 47%, and increased the risk of stroke death by 26%.
Hyperuricemia prevention
- 1. Avoid strenuous exercise or injury.
- 2. Limit high purine (viscera, 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: soy beans, lentils, mushrooms and Laver is high purine but does not increase the risk of gout.
- 3. Prohibit alcohol, especially beer and liquor, and drink red wine appropriately.
- 4. Control your weight.
- 5. Drink plenty of water,> 2000ml / d, drink tap water and mineral water (pH 6.5 ~ 8.5); do not drink pure water (pH 6.0), drink before going to bed to prevent urinary stones).
- 6. Long-term alkaline urine, commonly used sodium bicarbonate.
- References:
- [1]. Chinese Medical Doctors Association Cardiovascular Physician Branch. Chinese Expert Consensus on Asymptomatic Hyperuricemia Complicated with Cardiovascular Diseases. Chinese Journal of Frontiers of Medicine, 2010, 2 (3): 49-55.
- [2] Guo Lixin et al. Gout, Internal Medicine. Peking University Medical Press, 2012, 856-864.
- [3] Zhang Xuewu. The latest progress of gouty arthritis. In November 2012, the Beijing Medical Association Rheumatology Branch Academic Annual Meeting.
- [4] Liu Xiangyuan, Xiao Yulan, Ren Suqin, Tang Lijun, Zhang Liyun. Investigation and analysis of influencing factors of hyperuricemia in the elderly. Chinese Journal of Rheumatology, 2005, 9 (5): 280-283.