There are many hazards of gout, statistics say that gout patients “gouty nephropathy – clinical 20% – 40%, autopsy 100%” fear. Gout to be visible to the naked eye gout stone, chronic gouty nephropathy or X-ray visible joint destruction before starting uric acid treatment has been late, in order to avoid kidney function damage, joints and other serious damage, regular treatment and diet is still needed. Hyperuricemia is increasing in adults, with a proportion of about 10% in people over 30 years old, and some may be higher. Acute gout attacks Control acute inflammation (treat the symptoms first) NSAIDs: generally very effective (aspirin is prohibited) Colchicine: 0.5mg/tablet, 1/h until relief or gastrointestinal symptoms (nausea, vomiting, diarrhea), max <12 tablets/d. Maintain 1 tablet, tid. Can also be applied intravenously (special effects, but some literature suggests that side effects and efficacy are limited, so choose first) Glucocorticoids: the above are not effective! Intolerable! Heavy symptoms! The rapid fluctuation of uric acid (increase or decrease) can lead to the aggravation of arthritis, and the sudden decrease can lead to the dissolution of gout stone surface and release of crystals, which will be engulfed by white blood cells and release chemokines, which will attract more white blood cells and release lysosomal enzymes and destroy the joints. The more effective the initial uric acid lowering therapy is, the more frequent the gout attacks may be. In order to prevent acute attacks, concomitant application of NSAIDs or colchicine is also considered: continuous application for at least 4-6 weeks, or even more than 6 months (refer to the same above). Promote uric acid excretion drugs Domestic currently mainly uric acid excretion drugs and inhibit inhibit uric acid synthesis drugs, the former propofol ward seems to have no drugs, and instead of safer benzbromarone. The former seems to have been replaced by the safer benzbromarone. It seems that allopurinol is the only drug that inhibits uric acid. The incidence of allopurinol allergic reaction syndrome is about 10%, manifested by fever, rash, eosinophilia, hepatic necrosis and renal abnormalities, and the death rate is as high as 20-25%, so its use has some restrictions and concerns. Benzbromarone 25mg/tablet, 1-2 tablets/d ,1-3w,no decrease,increase 1-2 tablets/d available 2-4 tablets/d Sodium bicarbonate tablets 1.0 TID Drink plenty of water. Indications: normal or mildly impaired renal function (Ccr > 20 ml/min), no renal calculi, urinary uric acid < 600 mg/d (3571 μmol/d) Caution: drink plenty of water/alkaline drugs (solubility increases 100-fold at urinary pH 8), thiazides are contraindicated. 100-fold), thiazide diuretics/aspirin/alcohol are prohibited Third class of drugs for gout; drugs that promote uric acid catabolism including rasburicase and pegloticase are also being studied and progressed. Clinically, the selection of drugs that "kill two birds with one stone" should be advocated according to the diseases that coexist in gout patients. Gout patients with hypertension can choose coxsartan or amlodipine, and domestic and international studies have confirmed that coxsartan has both uric acid-lowering and antihypertensive effects. Gout patients with hyperlipidemia can choose fenofibrate or atorvastatin. The former is suitable for those with mainly increased triglycerides, while the latter is suitable for those with mainly increased cholesterol. Fenofibrate 200 mg/d for 3 weeks or 160 mg/d for 2 months can reduce blood uric acid by 19% and 23% respectively [P2-23]. Fenofibrate also has some anti-inflammatory properties and is less likely to induce acute attacks of gout when lowering uric acid.