I. Some basic concepts of gout.
With the change of lifestyle and diet structure, the prevalence of hyperuricemia and gout in China is increasing year by year and has reached 10% and 0.84% respectively. The number of patients with gout leading to renal insufficiency and uremia is also increasing year by year, posing a serious threat to patients’ health and life.
As clinicians or patients, we should first clearly distinguish hyperuricemia and gout as two different concepts, and change the concept that “gout is an acute arthritic attack and pain control is sufficient”. We should fully understand that the natural course of gout includes three stages, namely asymptomatic hyperuricemia, acute gouty arthritis and chronic gout, in order to develop reasonable individualized treatment plans for patients in different stages.
Second, the current status of gout treatment.
(1) Non-pharmacological treatment: Non-pharmacological treatment includes weight loss for obese people, restoring normal weight as much as possible, promoting healthy diet, proper exercise, quitting smoking, and ensuring adequate water intake; avoiding the following diets as much as possible: 1. High purine animal offal: such as pancreas, liver, kidney, etc.; 2. High sugar, soda, drinks, soy products, etc.; 3. Excessive alcohol consumption; 4. Seafood, etc.
(2) Treatment of acute gout.
Drugs: Colchicine, glucocorticoids, and non-steroidal anti-inflammatory drugs (NSAIDS) are the first-line treatment drugs for acute arthritis attacks.
Colchicine should be started within 36 hours of a gout attack. The first loading dose is 1 mg, followed by 0.5 mg orally 1 hour later, and up to 0.5 mg three times a day after 12 hours.
The recommended dose of glucocorticoids is prednisone 0.5mg/kg, with discontinuation for 5-10 days; or 0.5mg/kg to start, with 2-5 days of dosing and gradual reduction and discontinuation over 7-10 days.
In the selection of NSAIDs, selective cyclooxygenase inhibitors are preferred and etoricoxib is recommended, followed by non-selective cyclooxygenase inhibitors, such as diclofenac sodium and nimesulide.
(3) Treatment of intermittent and chronic phase.
1.Promote uric acid excretion drugs: including benzbromarone, propofol, etc.
They are suitable for those with reduced uric acid excretion and low uric acid level, but they are not suitable for those with significantly higher uric acid.
At the early stage of medication, drink more water and take sodium bicarbonate or potassium citrate to alkalize uric acid to prevent high uric acid crystals from aggravating kidney damage or forming stones.
2.Inhibit uric acid synthesis drugs: xanthine oxidase inhibitors that inhibit uric acid production, including allopurinol and febuxostat.
Febuxostat is a new type of xanthine oxidase inhibitor, and the obvious difference between it and allopurinol is that its molecular structure is completely different. The former has significantly lower severe allergy and hepatic and renal toxicity and is indicated for patients with allopurinol and mild to moderate renal insufficiency, with the disadvantage that it is expensive.
III. Precautions.
1. Drug therapy should be given within 24 hours after acute gout attack;
2.Uric acid-lowering drugs already used during acute gout attack can continue to be used;
3.The uric acid should be measured to determine the type of hyperuricemia, to identify the nature of uric acid stones and to select uric acid-lowering drugs;
4.Usually, the treatment of acute attack of gout should be controlled by treatment for at least 4 weeks before starting additional uric acid-lowering treatment to control the blood uric acid at normal level and prevent and protect the damaged organ function;
5.The maintenance target of blood uric acid: below 327umol/L;
6.The faster and greater the decrease of blood uric acid concentration, the greater the possibility of gout;
7.Febuxostat is preferred for patients with mild to moderate hepatic and renal insufficiency and allopurinol allergy.