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Gout is an ancient disease. In the past, gout occurred mostly in the wealthy, well-fed, and sorrowful, and it was given a nice name – “Imperial Disease.” In modern society, with the improvement of living standards, the food on the table is becoming more and more abundant, and it has to be noted that the incidence of gout has increased rapidly in recent years.

When we talk about gout, we will naturally think of high uric acid. Because only 10% of hyperuricemia develops into gout, most people will not have a “painful death” phenomenon, and they do not know that they have hyperuricemia. These diseases that do not have symptoms of gout for life are called asymptomatic hyperuricemia.


Asymptomatic does not mean no harm. Elevated blood uric acid can not only cause gouty arthritis, but also gouty nephropathy, uric acid stones and even uremia; aggravate atherosclerosis, hypertension, coronary heart disease; induce or aggravate diabetes. Following the “three highs” of high blood sugar, high blood pressure and high blood fat, the “fourth high” – high uric acid is one of the most common diseases that endanger health. Some people even know that their blood uric acid is high, but they will be ignored because they have no symptoms. Therefore, asymptomatic hyperuricemia lurks in the body as a “bane.”



What is hyperuricemia?

Hyperuricemia is a uric acid value >420 μmol/L (male) or >360 μmol/L (female) in the blood. Blood uric acid exceeding 420 μmol/L can cause urate crystals to precipitate and deposit in the joint cavity and other tissues to cause high uric acid-related diseases such as gout.

Do patients with hyperuricemia have to undergo lifestyle interventions?

Once hyperuricemia/gout is diagnosed, lifestyle intervention should be performed immediately. Including alcohol, diet control, drinking more water, weight loss and so on.

When do you start medication?

For blood uric acid levels above 540μmol/L, no matter how “healthy”, urate-lowering drugs should be used immediately; if combined with cardiovascular and cerebrovascular diseases or abnormal glycolipid metabolism, 420μmol/L is the starting point for starting drug treatment.

What is the ideal level of blood uric acid?

It is generally recommended to control the blood uric acid level in patients with hyperuricemia to within 360 μmol/L, and continue to take the drug for 6 months after reaching the standard.

For patients with obvious symptoms of gout, the uric acid level should be stable within 300μmol/L. After reaching the standard for 1 year, the gout attack can be significantly reduced.

What are the uric acid-lowering drugs?

The two main causes of hyperuricemia are: excessive production of uric acid and poor uric acid output. The causes are different and the treatment strategies are different.


1. Inhibition of uric acid synthesis drugs

Representative drugs: allopurinol, febuxostat

(1) Allopurinol – a classic drug that prevents the synthesis of uric acid, has a long history and a definite curative effect, and is currently the drug of choice for the treatment of hyperuricemia.

However, allopurinol has adverse drug reactions that induce severe hypersensitivity reactions, and the proportion is higher in Asian populations including Han Chinese. The study found that this is associated with a significantly higher proportion of Caucasians carrying a susceptibility gene called “HLA-B*5801” than Caucasians.

In order to reduce the risk of adverse reactions, the use of allopurinol should start from a small dose, gradually increase, adult initial dose of 50mg each time, 2 to 3 times a day, if the target is not up to 50-100mg, the maximum daily dose of 600mg. If the conditions permit, it is recommended to carry out the susceptibility gene test before the drug is used, and the positive result is forbidden.

(2) Febuxostat – a new type of drug that inhibits uric acid synthesis. Studies have shown that the rate of blood uric acid compliance is higher than allopurinol, and the safety is better than allopurinol, especially in patients with impaired renal function. However, its price is expensive, which limits the popularization of drugs. The initial dose of the drug is 40mg/day, once a day, after 2~5 weeks, the blood uric acid does not meet the standard, and the maximum dose is 80mg/day.


2. Urtic acid excretion

Representative drug: benzbromarone

In the pathogenesis of hyperuricemia, the proportion of “excessive uric acid production” is not high, and more than 90% of patients have a “light or severe uric acid discharge”, so “uric acid excretion” The drug has a wider range of people, and the representative drug is benzbromarone. It has short onset time, stable and long-lasting effect, small burden of liver and kidney metabolism, and high drug safety. It is the first-line drug for urate-lowering treatment.

Rather, the mechanism of action of benzbromarone is not a direct “promoting”, but rather inhibits the kidney from recovering uric acid from the urine, thus not burdening the kidney filtration.

The initial dose of benzbromarone is 50mg/day, once a day, after breakfast. After taking the medicine, the uric acid in the blood will be discharged through the urine in a large amount, and the concentration of uric acid in the urine is significantly increased. In order to prevent uric acid from forming calculus in the urinary tract, it is necessary to ensure daily drinking water during the course of medication, not less than 1.5 to 2 liters throughout the day. The sodium bicarbonate or citric acid mixture may be combined as appropriate in the first 2 weeks of the start of administration to control the pH of the urine between 6.2 and 6.9, and it is preferred to periodically measure the pH of the urine.

Possible problems in the treatment of uric acid

1. Sometimes during the treatment, joint pain is more obvious. Is the drug dose insufficient?

For patients who have not been treated with uric acid, taking uric acid-lowering drugs during the onset of gouty arthritis sometimes increases the severity and duration of pain. This is because when uric acid is lowered, the urate crystals deposited in the joints are first broken down into smaller crystals, which leads to an increase in local inflammation. At this time, the patient should not adjust the dosage of the drug by himself. Instead, he should consult a doctor or a pharmacist. Generally, he should start uric acid lowering treatment after the acute symptoms are relieved, and at the same time take drugs that control the onset of gout, such as colchicine.

2. If uric acid is normal, can you stop using uric acid-lowering drugs?

Even if the blood uric acid is normal, uric acid lowering therapy is still needed, because it takes time for the uric acid deposited in the tissue to dissolve into the blood. Therefore, normal blood uric acid does not mean that the total amount of uric acid in the whole body has been reduced to the normal range.

3. Do some drugs have an effect on uric acid?

Older patients are often accompanied by heart and brain diseases. Some diuretics, aspirin and other drugs can affect the excretion of uric acid, but whether to stop, it is necessary to combine the patient’s overall condition, the doctor or pharmacist to give treatment decisions.

4. Is blood uric acid lower as possible?

Although hyperuricemia can cause systemic diseases such as gout, kidney, endocrine metabolism, cardiovascular and cerebrovascular diseases, it has protective effects on diseases such as Alzheimer’s disease and Parkinson’s disease, so it is not recommended to reduce uric acid to 180 μmol. /L below.

5. How long does it take to review uric acid after taking uric acid?

When the initial uric acid is lowered, it is recommended to test the blood uric acid 2 to 4 weeks, and adjust the drug according to the blood uric acid value. After the blood uric acid control is stable, the monitoring time can be prolonged.

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