Gout attack, careful drug selection

Gout is a crystal-associated joint disease caused by deposition of monosodium urate, which is directly related to hyperuricemia caused by a decrease in sputum metabolism and/or uric acid excretion, but only a small part (about 10%) Patients with hyperuricemia develop gout. Kidney disease can be complicated, and severe joint damage and renal dysfunction can occur.

4 factors affect the degree of pain during gout attack
Some people think that the higher the blood uric acid level, the more severe the pain when the gout attacks. Clinically, many patients with acute gout attacks have elevated blood uric acid levels, but acute causes of normal blood uric acid levels are not uncommon. Therefore, the severity of gout attacks has little to do with uric acid levels, which are mainly related to the following factors:


Acute episodes of gout can be manifested as red, swollen, hot, painful and other inflammatory reactions, which are mediated by the immune system in the receptor and produce inflammatory factors. It has been reported that the levels of inflammatory factors IL-1β and NALP3 have a greater impact on the acute episode of gout. The higher the level, the more severe the inflammatory response and the more severe the symptoms.

Patient tolerance

Each patient has a different sensitivity to painful stimuli. The more sensitive the patient feels the more severe the pain during the onset of gout, the more likely it is to be considered severe.

Destruction of joints by tophi

The tophi is the urate crystal. The clinical features of gout are recurrent acute and chronic arthritis and soft tissue damage caused by urate deposition. Severe gout is often accompanied by extensive destruction or even ulceration of bone, cartilage and soft tissue, the larger the scope, the more serious.

Tophidis dissolution

Acute episodes of gout can also be caused by the dissolution of tophi. In the acute episode, the more frequent the tophidis dissolves, the more obvious the symptoms of red, swollen, hot and painful patients.

Acute attacks can’t “reducing uric acid”
The first thing to be reminded is that during the acute episode of gout, regardless of the level of blood uric acid, urate-lowering therapy is not recommended. Because uric acid can induce the dissolution of tophi, aggravating pain symptoms. Multiple gout guidelines recommend the use of non-steroidal anti-inflammatory drugs (such as acetaminophen, indomethacin) to relieve symptoms during acute attacks. For patients with contraindications to non-steroidal anti-inflammatory drugs, low-dose colchicine (1.5 to 1.8 mg/day) is recommended. The colchicine tablets have more adverse reactions and are recommended to be taken under the guidance of a doctor or pharmacist. If it is not tolerant to non-steroidal anti-inflammatory drugs and colchicine, short-term glucocorticoids (such as prednisone 30 mg / day for 3 days) can be used in the same town as non-steroidal anti-inflammatory drugs. Painful effect.

For patients with frequent episodes of acute gout (>2 times/year), patients with chronic gouty arthritis or tophi, or after 2 weeks of acute gout relief, urate-lowering therapy is recommended. The goal of urate-lowering therapy is to prevent the acute recurrence of gout arthritis and the formation of tophi, and to help toxin dissolve. The patient’s blood uric acid level is stably controlled below 360 μmol/L (micromol/L), which helps to relieve symptoms and control the disease. Optional uric acid-lowering drugs have inhibitors of uric acid-producing drugs allopurinol, febuxostat, and uric acid excretion drugs include probenecid and benzbromarone. It is recommended to use it under the guidance of medical staff.

Correct high uric acid, start from the details of life
According to epidemiological surveys, the prevalence of gout in China is about 1% to 3%, and it is increasing year by year. The main cause of gout patients is joint pain, followed by fatigue and fever. To prevent acute gout attacks, attention should be paid to controlling uric acid levels and life conditioning.

Lifestyle conditioning

Adjusting lifestyle helps to prevent and treat gout. Drinking alcohol, eating a lot of meat, seafood, animal offal, drinking fructose-rich beverages, strenuous exercise, sudden cold, obesity, fatigue, diet, irregular work and smoking, smoking are all risk factors for gout. Regular work and proper exercise, eating fresh vegetables is a protective factor for gout.

(1) Limited wine

Studies have shown that drinking alcohol increases the risk of gout attacks, and alcohol intake is dose-dependent with the risk of gout. When alcohol intake ≥ 50 g / day, the risk of gout is 153% higher than that of non-drinkers.

(2) reduce sorghum food intake

Studies have shown that eating a large amount of meat, seafood, animal viscera and other sorghum foods than the consumption of a small amount of uric acid levels average 28.8μmol / L, and the risk of acute gout attacks.

(3) Prevent strenuous exercise or sudden cold

According to the National Center for Rheumatology Data Center’s “Multi-Center Network Registration and Follow-up Study for Patients with Gout Hyperuricemia”, strenuous exercise is the third cause of gout. Sudden cold is the second cause of female gout, the fifth cause of men.

(4) Reduce the intake of fructose-rich beverages

Studies have shown that fructose-rich or sugar-containing soft drinks can increase the risk of gout attacks.

(5) Drink plenty of water (more than 2000 ml per day)

Too little drinking water is a risk factor for hyperuricemia and gout. Studies have shown that drinking plenty of water can reduce the time of gout attack and shorten the average length of hospital stay.

(6) Control weight

Obesity is an independent risk factor for gout. Studies have shown that the greater the body weight BMI index (weight kg / height square), the higher the relative risk of gout.

(7) Increase the intake of fresh vegetables

Regular consumption of fresh vegetables is a protective factor for the onset of gout, which can reduce the risk of gout attacks.

(8) regular diet and work and rest

Diet, irregular work and frequent fatigue, the risk of gout and hyperuricemia is 1.6 times higher.

(9) Regular movement

Regular exercise in gout patients, in addition to reducing the number of gout attacks, also helps to lower the BMI index, shorten the waist circumference, reduce triglycerides, blood sugar and blood uric acid levels.

(10) Non-smoking

Smokers have a 50% higher risk of gout/hyperuricemia than non-smokers, and people who smoke more often have a 35% higher risk of gout/hyperuricemia than those who occasionally smoke.

2. Uric acid reduction

High uric acid is the pathological basis of gout. In addition to causing gout, high uric acid is closely related to metabolic syndrome, type 2 diabetes, hypertension, cardiovascular disease, chronic kidney disease, kidney stones, etc., and is an independent risk factor for these diseases. . Therefore, under the guidance of a doctor, standardizing drug treatment and controlling uric acid levels become crucial.

The goal of urate-lowering therapy is to prevent the acute recurrence of gout arthritis and the formation of tophi, and to help toxin dissolve. Stabilizing the patient’s blood uric acid level below 360 μmol/L helps relieve symptoms and control the disease. Therefore, gout treatment guidelines recommend frequent episodes of acute gout arthritis (> 2 times / year), patients with chronic gout arthritis or tophi, should be treated with uric acid lowering.

Gout has the characteristics of recurrent attacks. The continuous deposition of urate will destroy joints and damage kidney function, resulting in limited or even disabling activities. Therefore, patients with gout should pay attention to self-conditioning, prevent recurrent gout and improve the quality of life.