Gout is a disease caused by abnormal purine metabolism, about 2/3 of uric acid is derived from endogenous cellular metabolism and 1/3 from dietary purine intake. Gout is a chronic disease and can be divided into asymptomatic hyperuricemia, acute phase, intermittent phase and chronic phase. Acute attacks of gout are characterized by: typical clinical manifestations: rapid onset (6-12 hours) of severe pain, often at night, with joint swelling, pressure pain and skin redness. Systemic symptoms: malaise, fever/chills. 90% of first attacks are monoarthritic (in men), but can also be oligoarthritic (especially in women). The most commonly affected joints are the first metatarsophalangeal joint (MTP), the ankle and the knee. The next most commonly affected areas are the hand, wrist, elbow, and hawkbone bursa. When acute attacks of gout or other unexplained inflammatory arthritis are suspected, the efficacy of local icing should be part of the history taking and physical examination. Serum uric acid levels are of limited diagnostic value. Most hyperuricemia does not flare up with gout. Serum uric acid levels may be elevated or decreased during acute attacks of gout. 39% – 49% of patients have normal serum uric acid levels during acute attacks of gout. Gout is diagnosed by the presence of monosodium urate crystals in the joint fluid. Initial classification criteria for primary acute gouty arthritis: >1 episode of acute arthritis; <1 day progression of inflammation to peak; monoarthritis; redness of joints; pain/swelling of the first metatarsophalangeal joint; unilateral first metatarsophalangeal joint involvement; unilateral tarsal joint involvement; gout stones; monosodium urate crystals found in joint fluid during acute episode; hyperuricemia; negative joint fluid culture during acute episode; x-ray suggestive of asymptomatic joint swelling; X-ray confirmed subcortical cysts without bone erosion. Diagnosis is made with 6 of 11; or 1 major criterion is met: MSU crystals or gout stones found in the joint fluid. The goal of gout treatment is to control inflammation/pain in the acute phase and to control blood uric acid levels in the chronic phase. Non-pharmacologic treatment of gout in the acute phase includes pain section rest (1-2 days), and local ice therapy. Pharmacological treatment includes NSAIDs, oral colchicine, glucocorticoids and IL-1 antagonists (trial phase). How should NSAIDs be applied? Any type of NSAIDs can be used: selective and non-selective COX2 inhibitors are effective; apply as soon as possible; use adequate doses and courses; monitor for toxic effects; FDA approved for acute gout attacks: indomethacin, naproxen, sulindac; studies have not found which NSAID is superior. Short courses of systemic glucocorticoids are as effective as NSAIDs in controlling acute gout attacks within 5-7 days, with fewer adverse effects than NSAIDs. Other drugs for the treatment and prevention of acute gout attacks: Linacipran; IL-1 trap; kanamab; ACZ885; IL-1 receptor-associated kinase 4 (IRAK-4): a signaling molecule located downstream of the IL-1 receptor; activated CD4+ T cells expressing the CD40 ligand (CD154) have a regulatory role in inflammation. Canakinumab is superior to tretinoin for pain relief. Summary of gout acute attack treatment: The available therapeutic drugs for acute gout attacks include NSAIDs, colchicine, glucocorticoids (oral, intravenous, intramuscular, joint cavity injection); combination therapy is often required, and specific methods still need to be further explored; there are no RCT studies comparing the efficacy of colchicine with NSAIDs for acute gout attacks; trials related to Il-1 inhibitors have provided new approaches for the treatment of acute gout The trials related to Il-1 inhibitors provide new hope for the treatment of acute attacks of gout. Uric acid-lowering drugs include the following: inhibitors of uric acid synthesis: xanthine oxidase inhibitors, which inhibit uric acid synthesis, including allopurinol and febuxostat. Uric acid catabolic drugs, such as allantoin, which promote the conversion of uric acid to allantoin (Prescriptive). Uric acid excretory agents that inhibit the reabsorption of uric acid from the distal renal tubules include propofol, benzbromarone (withdrawn from market in Europe and the US), cloxacin, fenofibrate. Treatment goals Blood uric acid level ≤ 6.0 mg/dL; reduction or avoidance of acute gout attacks; reduction of crystals in the joint cavity; reduction in the volume of gout stones; no new gout stone formation; disappearance of the double track sign on ultrasonography. Uric acid treatment should be started with small doses of uric acid-lowering drugs, and the dose should be increased slowly and gradually. If blood uric acid > 6 mg/dL allopurinol is upped at a rate of 100 mg/d or febuxostat to 80 mg/d. If blood uric acid does not reach the target, a xanthine oxidase inhibitor may be combined with another or an additional uric acid excretory agent (level of evidence C). Monitor uric acid every 2-5 weeks after initial uric acid-lowering therapy until uric acid. Summary of uric acid-lowering therapy: Blood uric acid should be monitored regularly to ensure compliance with <6.0 mg/dL (every 2-5 weeks before compliance and every 6-12 months after compliance). Allopurinol and febuxostat are the main uric acid-lowering drugs. Prescripta, may be the first choice for induction therapy (lowering the uric acid pool), followed by maintenance with chronic oral uric acid-lowering drugs. Newer uric acid-lowering drugs such as Lesinurad, Arhalofenate and BCX4208 may be new options for patients with suboptimal serum uric acid values.