Author: Gcplive
Source: Center for Drug Evaluation< /p>
The overall prevalence of hyperuricemia in China is 13.2%, and gout is 1.1%. It has become another common metabolic disease after diabetes.
Question 1: What is gout?
1. Whether male or female, the blood uric acid level exceeds 420μmol/L twice on different days , called hyperuricemia.
2.Urate crystal deposition in patients with hyperuricemia causing arthritis (gouty arthritis), uric acid nephropathy, and kidney stones called gout.
3.Estrogen not only promotes uric acid excretion, but also Inhibit the formation of uric acid crystals in the joints, and the ratio of male to female patients with gout is as high as 20:1.
Question 2:What is asymptomatic hyperuricemia?
A considerable number of patients with hyperuricemia will not develop obvious symptoms such as arthritis for life. It is called asymptomatic hyperuricemia.
It is worth reminding that:In patients with asymptomatic hyperuricemia, joint Subclinical gout can be diagnosed by ultrasound,dual-energy CT or X-ray findings of sodium urate crystal deposition and/or gouty bone erosion.
Question 3: Are hyperuricemia and gout hereditary?
1. blood uric acid level heritability is 27%~41%.
2.Gout has a 30% heritability, and 20% of gout patients have a family history.
3.incidence of goutand environmental factors (drinking, overeating, catching a cold) more closely related.
gout The good time is midnight or early morning, etc.
Poor blood supply to the foot, low skin temperature, and low pH of tissue fluid , Under high pressure, most of the joints that cause gout are the first metatarsophalangeal joints.
Question 4: What is the relationship between hyperuricemia and hypertension?
1. For every 60μmol/L increase in serum uric acid, the relative risk of hypertension increased by 1.4 times.
2. Hypertension can cause damage to blood vessels and kidneys, affect uric acid excretion, and lead to elevated blood uric acid levels.
3. Uric acid-lowering drugs (allopurinol, febuxostat, etc.) can slightly reduce blood pressure in patients with hyperuricemia.
Question 5: What effects do antihypertensive and lipid-lowering drugs have on blood uric acid?
1.Thiazide diuretics (eg, hydrochlorothiazide, indapamide) can increase serum uric acid.
2. Beta-blockers (eg, metoprolol) can increase serum uric acid.
3.ACEI (pril) and ARB (sartan, except losartan) can increase serum uric acid.
4. Losartan can slightly lower uric acid (about 50μmol/L).
5. Amlodipine, cilnidipine and nifedipine had no adverse effect on serum uric acid.
6.Atorvastatin can promote renal uric acid excretion.
7.Fenofibrate can inhibit uric acid reabsorption.
Question 6: Are hyperuricemia patients prone to diabetes?
1. For every 60μmol/L increase in blood uric acid level, the risk of new-onset diabetes increased by 17%.
2. Uric acid-lowering therapy can reduce the incidence of diabetes mellitus in people with hyperuricemia, and reduce the incidence of renal, cardiovascular and other complications.
3. Insulin can lead to increased blood uric acid levels.
4.SGLT-2 inhibitors (empagliflozin, etc.) slightly lower uric acid effect.
5. Metformin, α-glucosidase inhibitors, thiazolidinediones and other drugs had no adverse effect on blood uric acid.
Question 7: Do I need uric acid-lowering therapy for asymptomatic hyperuricemia?
1. Preferred non-drug treatment, such as diet adjustment, weight control, etc.
2. Use medication with caution. The urate-lowering drug allopurinol can cause fatal allergic reactions, febuxostat can increase the risk of cardiovascular events, and benzbromarone can cause severe liver damage.
3. The clinical diagnosis and treatment guidelines of China and Japan recommend that patients with asymptomatic hyperuricemia should start uric acid-lowering drug therapy when the blood uric acid level is ≥540 μmol/L .
4. Clinical diagnosis and treatment guidelines in Europe and the United States suggest that patients with asymptomatic hyperuricemia should only be treated in patients with CKD andUric acid-lowering drug therapy is required only when cardiovascular risk factors are present.
Question 8: For gout patients, what is the target blood uric acid control level?
1. Long-term control of blood uric acid at <360 μmol/L can not only dissolve urate crystals, reduce the number and volume of crystals, but also Avoid the formation of new crystals.
2. The serum uric acid level should be controlled to <360 μmol/L in all gout patients, and <300 μmol/L in severe gout patients. Long-term control of serum uric acid to <180 μmol/L is not recommended.
Question 9: Which uric acid lowering drugs can be used for gout patients?
1. Gout patients can choose drugs that inhibit uric acid synthesis (allopurinol, non-Buxostat) and uricosuric drugs (benbromarone).
2. Asymptomatic hyperuricemia patients can choose allopurinol or benzbromarone.
3.The fatality rate of allopurinol hypersensitivity reaction is as high as 30%, and there is a significant correlation with HLA-B*5801. The frequency of the Han population carrying this genotype HLA-B*5801 gene detection should be performed before using allopurinol.
4. Febux should be used with caution in elderly patients with cardiovascular and cerebrovascular diseases He and pay close attention to cardiovascular events.
5. For patients whose blood uric acid is still not up to the standard after a single drug with sufficient dose and a full course of treatment, two uric acid-lowering drugs with different mechanisms of action can be considered in combination.
Question 10: Which uric acid-lowering drug should be preferred for patients with chronic kidney disease complicated with gout?
1. Uric acid-lowering therapy helps to delay the progression of chronic kidney disease (CKD).
2. For gout patients with chronic kidney disease stage 3 or above (glomerular filtration rate <60ml/min), uric acid synthesis inhibitors (allopurinol, febuprofen are preferred) Secretary).
3.FebuxostatEspecially suitable forpatients with chronic renal insufficiency.
Question 11: Do patients who take benzbromarone need to take baking soda at the same time?
1. Oral sodium bicarbonate has a certain effect on reducing uric acid, but the effect of reducing uric acid is very limited, about 50μmol/ L.
2. Long-term use of sodium bicarbonate can cause water and sodium retention, which can not only cause and aggravate hypertension, but also induce heart failure.
3.When the pH value of urine is <6.0, it is recommended to take sodium bicarbonate to alkalize the urine to maintain the pH value of morning urine at 6.2 ~6.9 to reduce the risk of uric acid nephrolithiasis and facilitate the dissolution of uric acid nephrolithiasis.
Question 12: How to properly use colchicine?
1. Compared with high-dose drugs, low-dose colchicine is equally effective in the treatment of gout, and the adverse reactions are significantly reduced.
2. During acute gout attack, the first dose of colchicine is 1 mg, followed by 0.5 mg 1 hour later, and 0.5 mg qd after 12 hours or bid.
3. When starting uric acid-lowering drug treatment, because the fluctuation of blood uric acid level can easily induce acute gout attack, prophylactic use of colchicine for at least 3～ 6 months can reduce the acute attack of gout, the dosage is 0.5~1.0mg/day.
Question 13: Why are obese people prone to gout attacks?
1. Gout is a metabolic disease, and patients are often accompanied by obesity.
2. Obese patients consume more calories than they consume. Due to the increased energy intake, the synthesis of purines is increased, and the production of uric acid is increased.
3.Obesity (especially abdominal obesity) can lead to insulin resistance, and insulin resistance can lead to elevated blood uric acid levels.
4. Most gout treatment guidelines recommend weight control for gout patients.
Question 14: Why is it easy to have gout attacks after drinking alcohol?
1. Beer and hard alcohol increase the risk of gout attacks, and there is little evidence that red wine increases the risk of gout attacks.
2. Drinking alcohol increases uric acid levels because:
The metabolism of alcohol increases the consumption of adenosine triphosphate, which leads to an increase in the production of uric acid;
Alcohol leads to an increase in serum lactate, thereby reducing uric acid excretion ;
The presence of purines in wine leads to increased uric acid production.
Question 15: How to choose fruits and vegetables for gout patients?
1.Do not eat too many sugar-sweetened beverages and fruits high in sugar (especially fructose), such as apples, oranges , longan, lychee, grapefruit, persimmon and pomegranate.
2. It is not advisable to eat more plant foods with high purine content such as mushrooms, straw mushrooms, asparagus, seaweed, kelp and grain germ.
3. Watermelon, coconut, grapes, strawberries, plums and peaches can be eaten in moderation.
4. Relatively speaking, lemon, cherries and olives are beneficial to gout patients.
5. The vast majority of melons, tubers, roots and most leafy vegetables are low-purine foods and are recommended for consumption.
Question 16: How to choose animal food for gout patients?
1. Red meat (mammals, including cattle, sheep, pigs, etc.) has higher purine content than white meat (non-mammalian animals, including chickens, ducks, geese, etc.).
2. The purine content of animal offal such as liver, kidney and heart is generally higher than that of ordinary meat.
3. The daily meat intake of gout patients should not exceed 100g. When cooking, it is recommended to discard the soup after boiling.
4. Cured, cured or smoked meat has high purine and salt content, which interferes with uric acid metabolism and should not be eaten by gout patients.
5. Eggs, milk, sea cucumber and other purine content are low.
Question 17: How to drink water for gout patients?
1. In the absence of kidney disease, heart failure and other contraindications, the total amount of drinking water per day is 2~3L, and the daily urine output is about 2L as far as possible , uric acidity (pH value) is 6.3~6.8.
2.Drinking water in different times, it is recommended to drink about 500ml of water three times in the morning, noon and evening.
3. Drinklemonade (such as 1~2 fresh lemon slices into 2~3L of water) span>Helps lower uric acid.
Question 18: How to exercise for gout patients?
1. Strong exercise can increase sweating, decrease blood volume, renal blood flow, decrease uric acid excretion, and even > Can induce gout attacks.
2. Low-intensity aerobic exercise (jogging, Tai Chi, etc.) can reduce the incidence of gout, and the frequency of exercise should be 4 to 5 times a week , every 0.5~1h.
3. Because low temperature can easily induce acute gout attacks, avoid cold baths and air conditioners after exercise.
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