Gout is the deposition of monosodium urate from supersaturated extracellular fluid in tissues or organs, which can trigger recurrent acute arthritis, urinary stones and gouty nephropathy. It can be divided into 4 stages: asymptomatic hyperuricemia, acute gouty arthritis, intermittent and chronic gouty arthritis. Hyperuricemia (HUA) is a chemical variant of extracellular fluid supersaturation. a UA value > 2 SD above the normal mean value, > 7.0 mg/dl in men and > 6.0 mg/dl in women, is called hyperuricemia. Acute gouty arthritis attacks are characterized by sudden onset at night or in the morning, initial monoarticular (85%), initial toe > 50%, toe involvement > 90%, redness, swelling, heat and severe pain, peripheral joint redness and swelling, spontaneous remission in 3-10 days, no sequelae, and recurrence. Laboratory tests may reveal: synovial fluid urate crystals (+), synovial fluid leukocytes ↑, negative culture, normal or elevated blood uric acid, elevated ESR, WBC, PIT. In imaging, ultrasound shows the double track sign, which means that MSU crystals cover the articular cartilage, with a specificity of 95-100% and sensitivity of 21-92% for the diagnosis of gout, also seen in asymptomatic HUA. dual energy CT (DECT) has high sensitivity and specificity for detecting uric acid deposits, but false positives have also been reported. The effective options for the treatment of acute gouty arthritis (AGA) include non-steroidal anti-inflammatory drugs (NSAIDs), colchicine (CC ), glucocorticoids, ACTH, long-acting hormones in the joint cavity, and biologics. master the contraindications to NSAIDs. Chronic gouty arthritis presents with multiple symmetrical arthritis, extensive gouty stones, high blood uric acid, x-r joint destruction lesions, kidney stones or chronic kidney disease. Gout stones are commonly found in the periarticular soft tissue, subcutaneous tissue, synovium, subchondral bone, hawk C, forearm extensor, fingers, toes, Achilles tendon, auricle, kidney, and other sites (heart valves, spinal cord, eyes). Patients with gout are prone to a variety of co-morbidities, such as hypertension, hyperlipidemia, diabetes and cardiovascular disease. So how to lower blood uric acid treatment? Indications for uric acid-lowering treatment are ≥2 arthritic episodes per year, HUA (>6.8mg/dl), visible gout stones, X-R changes in bones and joints, history of urinary stones, and chronic kidney disease. Indications for not using uric acid-lowering drugs include asymptomatic HUA, acute gout attacks, and intermittent periods of non-gouty stone gout. The aim of uric acid-lowering therapy is to bring blood uric acid to the standard (6-4 mg/dl), promote gout stone dissolution, prevent reversal of crystal deposition disease, and control gout signs and symptoms. Adjunctive treatment includes: low purine diet, avoid alcohol, drink more water, urinate >2000ml/d, maintain urine pH 6.5~6.8, alkaline drugs. New uric acid-lowering drugs include: febuxostat, felofibrate, uricase, cloxacin, lesinurad, amlodipine. Allopurinol has a slow hypouric acid-lowering effect, inhibits new synthesis of uric acid, has no effect on pre-existing hyperuric acid, maximum effect occurs within 14 days, can be complicated by nephropathy, more than half of patients with blood uric acid failing to meet the standard when using doses <300 mg/d. Febuxostat (febuxostat) is a new class of selective xanthine oxidase inhibitor, with specific strong inhibition of xo, does not affect other purine and Pyrimidine metabolizing enzymes, hepatic metabolism does not depend on renal excretion, and is safe for the treatment of hyperuricemia and gout. Side effects of febuxostat include: abnormal liver function, diarrhea, headache, off, muscle and bone symptoms. The ACR guidelines for the management of gout and HUA emphasize patient education, list allopurinol or febuxostat as first-line agents, and blood uric acid should be reduced to lasting improvement of signs and symptoms. It is recommended that the HLA-B5801 gene should be tested before using allopurinol, and a combination of a pro-uric acid excretory agent can be used for those whose blood uric acid does not reach the standard with allopurinol or febuxostat. Uric acidase is an option for those with severe gout and resistant to treatment or intolerant to oral uric acid-lowering drugs. The recommendations for the diagnosis and management of gout are: 1. detection of uric acid crystals; 2. renal and CV testing for gout or HUA; 3. treatment of acute arthritis with low-dose colchicine (max 2 mg/d), NSAID, and or glucocorticoids (intrathecal, oral, or intramuscular), depending on the condition; 4. healthy lifestyle; 5. allopurinol should be the first-line uric acid-lowering agent, and its alternative is a pro-uric acid excretory agent (phenylephrine) if it is not available. Allopurinol should be the first-line uric acid-lowering agent, but if not available, its alternative is a uric acid excretory agent (benzbromarone or probenecid) or febuxostat; uricase may be used in severe gout or in cases where other treatments have failed or are contraindicated. The target of treatment is blood uric acid < 6 mg/dl, absence of gout attacks and dissolution of gout stones.9 Surgical treatment is available only in selected cases.10. No pharmacological treatment is recommended for asymptomatic HUA. The recommended treatment for refractory gout is up-regulation of allopurinol to the maximum appropriate dose, with febuxostat substitution for intolerance or adverse reactions to allopurinol. Effective options include the addition of uric acid-removing drugs (propofol, felofibrate, cloxacin), and uricase can be used for those for whom other treatments have failed but are not first-line agents. Gout has endangered adolescents and should be taken seriously. Do not use uric acid-lowering drugs for acute arthritis, keep your mouth shut during intermittent follow-up, properly carry out uric acid-lowering treatment until the standard is reached, and maintain the drug for a long time if the blood uric acid is reduced to 6-4 mg/dl, replace it with febuxostat if allopurinol is not tolerated or is ineffective, and use both types of uric acid-lowering drugs in special cases, and use uricase for those with anti-traditional treatment. In addition, attention should be paid to the diagnosis and treatment of gout patients with co-morbidities, and doctors at all levels should be good at the diagnosis and treatment of gout and strengthen the education of patients and their compliance. Acute attack: rapid fire extinguishing, anti-inflammatory and pain relief - short course - treating the symptoms; chronic gout: eliminating stones and clearing pollution, lowering blood uric acid - long-term - treating the root cause; reaching consensus between doctors and patients: long-term uric acid lowering cures gout.