How does the UK with high incidence of gout reduce uric acid?

It is no doubt that the association between uric acid crystals and gout is an epoch-making breakthrough. The research was done by a famous British doctor.

In 1848, the British doctor invented a chemical method to detect uric acid in the blood and urine, found that the concentration of uric acid in the blood of patients with gout increased abnormally, and deduced that uric acid is the cause of gout, which people associate with gout.

Britain’s Tudor Dynasty was afflicted with gout, and Henry VII and Henry VIII were both victims. The following comic strip of gout, familiar to gout sufferers, was created by British painters in the 18th century.

According to the modern epidemiological survey, the incidence rate of gout in Britain is the highest in Europe, about 2.5%. As early as 2007, the British Rheumatology Association published guidelines for the management of gout, and 10 years later, the guidelines have been updated with new drugs and evidence for the treatment of gout.

Next, we will list 10 recommendations for the treatment of gout in the UK Gout Management Guidelines.

1. The choice of hyaluronic therapy should be explained to the patient who has been diagnosed with gout, and relevant information should be given to the patient: Gout patients should be fully involved in deciding when to start hyaluronic therapy. The importance of regular and continuous reduction of uric acid therapy to prevent gout recurrence is indicated. Patients should be reminded before the implementation of hyaluronic acid therapy during this period because of the sharp decline in uric acid may lead to an increase in acute gout attacks.

2. Patients diagnosed with gout should be discussed and recommended hyaluronic acid treatment. The following patients should be specially recommended for hyaluronic acid treatment: gout recurrence (more than twice within one year); gout stone; chronic gouty arthritis; joint injury; kidney injury (glomerular filtration rate less than 60); a history of urolithiasis; Other diseases need to be treated with diuretics, and primary gout is younger.

3. The onset time of hyaluronic acid therapy should be delayed until the acute inflammation of gout disappears completely, so patients without pain can better discuss hyaluronic acid treatment.

4. The initial aim of hyaluronic acid is to reduce and maintain the uric acid below 300 micromoles per liter to prevent further formation of uric acid crystals and to eliminate existing crystals: the lower the uric acid in the blood, the faster the crystallization of uric acid is eliminated. After several years of successful treatment, when the gout stone has been removed and the patient has no symptoms of gout, the dosage of urate-lowering drugs can be adjusted to maintain blood uric acid below 360 micromoles per liter to avoid possible adverse reactions caused by crystallization and hypouric acid levels.

5. Consider recommending allopurinol as a first-line uric acid-lowering drug: starting at a low dose (50-100 mg daily) and increasing the dose by about 100 mg every four weeks until blood uric acid reaches the standard (maximum dose is 900 mg daily). For patients with renal impairment, a small increment (50 mg) should be used, and the maximum dose should be reduced accordingly, but the target serum uric acid level is the same.

3. The onset time of hyaluronic acid therapy should be delayed until the acute inflammation of gout disappears completely, so patients without pain can better discuss hyaluronic acid treatment.

4. The initial aim of hyaluronic acid is to reduce and maintain the uric acid below 300 micromoles per liter to prevent further formation of uric acid crystals and to eliminate existing crystals: the lower the uric acid in the blood, the faster the crystallization of uric acid is eliminated. After several years of successful treatment, when the gout stone has been removed and the patient has no symptoms of gout, the dosage of urate-lowering drugs can be adjusted to maintain blood uric acid below 360 micromoles per liter to avoid possible adverse reactions caused by crystallization and hypouric acid levels.

5. Consider recommending allopurinol as a first-line uric acid-lowering drug: starting at a low dose (50-100 mg daily) and increasing the dose by about 100 mg every four weeks until blood uric acid reaches the standard (maximum dose is 900 mg daily). For patients with renal impairment, a small increment (50 mg) should be used, and the maximum dose should be reduced accordingly, but the target serum uric acid level is the same.

6. For patients who can’t tolerate allopurinol, or whose renal function impairment prevents allopurinol doses from increasing enough to achieve therapeutic goals, allopurinol can be replaced with non-budastatin as a second-line xanthine oxidase inhibitor: the initial dose is 80 mg per day, and if necessary, it can be increased to 120 mg per week after 4 weeks. Days to achieve treatment goals.

7. Patients who are resistant to or intolerant of xanthine oxidase inhibitors may use drugs that promote uric acid excretion: for patients with normal or mild renal function, the preferred drug is probenecid (500-2000 mg daily); for patients with mild to moderate renal insufficiency, benzbromarone (50-100 mg daily) may be selected. ).

8. Losartan (antihypertensive) and fenofibrate (lipid-lowering) should not be used as the main drugs to reduce uric acid, but when hypertension and dyslipidemia need to be treated, the two drugs should be considered separately because of their weak uric acid excretion-promoting effect. Vitamin C (500 to 1500 mg daily) also has a weak effect on promoting uric acid excretion.

9. With the best dose of monotherapy, patients whose blood uric acid is not up to standard can be treated with combination of uric acid-stimulating drugs and xanthine oxidase inhibitors (inhibition of uric acid production), but the side effects of the drugs need to be monitored more closely.

10. In order to prevent the onset of acute gout, low-dose colchicine (0.5 mg once daily) may be considered as a preventive drug for 6 months in any patient whose uric acid-lowering therapy is initiated or whose uric acid-lowering dosage is raised. For patients who cannot tolerate colchicine, consider replacing low doses of NSAIDs with gastric protective agents.

The recommended doses are set for Westerners, some of which may not be suitable for Easterners because of differences in genes, weight and body size, so specific doses need to be determined under the guidance of a doctor.

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