Gout is a crystal-associated arthropathy caused by monosodium urate deposition and is directly related to hyperuricemia due to disorders of purine metabolism and/or decreased uric acid excretion. Gout refers specifically to acute gouty arthritis and chronic gouty stone disease, which can be complicated by renal lesions, joint destruction and renal impairment in severe cases, often accompanied by hyperlipidemia, hypertension, diabetes, atherosclerosis and coronary artery disease. Its incidence is increasing year by year. In October 2012, the American College of Rheumatology (ACR) officially released the 2012 ACR Gout Treatment Guidelines, and the following is a brief explanation of the guidelines. 1. Non-pharmacologic and pharmacologic treatment of hyperuricemia 1.1 The first part of the non-pharmacologic treatment guidelines begins with a detailed description of non-pharmacologic uric acid-lowering treatment of gout, including patient education, diet and lifestyle. Lifestyle and dietary modifications are designed to reduce the risk and frequency of gout attacks and lower blood uric acid levels. Obese individuals are advised to reduce body mass, quit smoking, exercise, and drink more water. The diet of gout patients is divided into three categories: Avoid: animal offal, high fructose beverages, high calorie beverages, excessive alcohol consumption (2 servings per day for men and 1 serving per day for women) in any patient, and alcohol consumption is prohibited in patients with acute attacks or poorly controlled gout; Limit: beef, lamb, pork, seafood with high purines (sardines, shellfish), sweet juices, desserts, sweet drinks, alcohol, especially beer; Encouraged: low-fat or fat-free dairy products, vegetables. The guidelines also state that dietary control and lifestyle changes alone have a limited role in lowering uric acid and preventing gout attacks. Small doses of aspirin can inhibit uric acid excretion by the renal tubules and are considered an important trigger for hyperuricemia, but the guidelines suggest that the negative effects of aspirin are negligible in patients who already have gout, so there is no need to discontinue or switch medications. Before determining the diagnosis of gout, improve the relevant tests to exclude various causes of elevated uric acid. 1.2 Choice of uric acid-lowering drugs In the choice of drugs for uric acid-lowering therapy, xanthine oxidase inhibitor (XOI) allopurinol and febuxostat are both recommended as first-line drugs, but it is noted that there is a lack of safety data for febuxostat in patients with chronic kidney disease (CKD) stage 4 and above. Dosage of allopurinol: The guidelines recommend that in order to reduce gout flares after initiation of uric acid-lowering therapy and to reduce the occurrence of severe hypersensitivity syndrome (AHS) with allopurinol, the initial dose must not exceed 100 mg/d, and if there is moderate to severe CKD, the initial dose should be less than 50 mg/d, then the dose should be gradually increased to reach the appropriate therapeutic dose in 2 to 5 weeks, with the dose for each patient based on individual The principle is determined. The guidelines state that allopurinol monotherapy at doses ≤300 mg/d fails to reduce blood uric acid to target values (<6 mg/dl or <5 mg/dl) in more than half of patients, therefore, maintenance doses of allopurinol can exceed 300 mg/d, even in patients with CKD, with adequate patient education and close monitoring for various adverse effects, of course. AHS is the main cause of allopurinol dosing, with an incidence of about 1:1000 in the United States, with severe AHS in 20-25%. Concomitant use of thiazide diuretics and renal involvement are risk factors for the occurrence of AHS, which often occurs in the first few months of starting treatment and can be reduced by starting at low doses. Because patients with a positive HLA-B*5801 gene are at significantly higher risk of developing severe AHS, the guidelines recommend rapid PCR screening for the HLA-B*5801 gene in high-risk groups (Han Chinese, Thai, and Koreans with CKD stage 3 or higher) before starting allopurinol therapy. The guidelines recommend propofol as a first-line agent for uric acid-lowering therapy if the patient is contraindicated or intolerant to xanthine oxidase inhibitors, but propofol is not recommended for uric acid-lowering therapy alone if the patient has a creatinine clearance <50 ml/min. First-line uric acid excretory agents are contraindicated with a history of urinary tract stones (because the associated risk of urinary tract stones from propofol or benzbromarone administration is 9% to 11%). To reduce the risk of urinary stones, the guidelines recommend that the amount of uric acid should be monitored before starting treatment and that pro-uric acid excretory drugs should be contraindicated if uric acid is elevated, suggesting increased uric acid production. Fluid intake should be increased and urine alkalinized (potassium citrate) during uric acid-lowering therapy. The guidelines recommend that uric acid-lowering therapy can be initiated during an acute gout attack once effective anti-inflammatory therapy has been initiated. This differs from previous guidelines that recommended starting uric acid-lowering therapy 2 weeks after the symptoms of acute arthritis have resolved. For patients with prolonged unremitting gouty arthritis symptoms or gout stones, blood uric acid is required to be lowered, usually to <5 mg/dl. For patients whose blood uric acid does not reach the target after treatment or whose gout signs and symptoms are not controlled, the guidelines recommend increasing the dose of xanthine oxidase inhibitor, which can be found in the drug instructions The guidelines recommend increasing the dose of xanthine oxidase inhibitors to the maximum dose tolerated by the patient. If one xanthine oxidase inhibitor is ineffective or not tolerated, another xanthine oxidase inhibitor or a combination of the uric acid excretory drugs propofol, fenofibrate, or cloxacin can be used. In this guideline, fenofibrate and coxsartan are used in the treatment of refractory gout as drugs with uric acid excretory effects. Patients with severe gout, who do not respond to or cannot tolerate oral uric acid-lowering drugs, can use polyethylene glycolized recombinant uric acid oxidase. 2. Treatment of acute gouty arthritis and prevention of recurrence The second part of the guideline is about the treatment and prevention of acute gout. The guidelines recommend that acute gouty arthritis requires medication and that treatment should ideally be started within 24h of onset, the earlier the treatment, the better the outcome, and that the uric acid-lowering therapy already started should be continued during an acute gout attack. Patient education includes not only diet and avoidance of any triggers, but also instruction in the timely management of acute gout attacks, so that patients know that gout is caused by high blood uric acid and that only by lowering blood uric acid can they be "cured" of gout. The choice of medication for acute gouty arthritis is determined by the degree of joint pain and the number of joints involved. For mild or moderate pain, involving one or a few small joints and one or two large joints, non-steroidal anti-inflammatory drugs (NSAIDs), systemic glucocorticoids, and oral colchicine alone are recommended; for severe pain, involving ≥4 joints and one to two large joints, combination therapy is recommended. For the 3 classes of drugs, there is no priority recommendation in the guidelines, and physicians are advised to consider the choice of drugs based on patient preference, response to previous treatment, and comorbidities. nSAIDs treatment emphasizes adequate dosage, adequate duration (until complete remission of acute gouty arthritis), and reduced dosage for patients with comorbidities and hepatic and renal impairment. Colchicine therapy may be chosen if the patient is not on colchicine prophylaxis at the time of the gout attack, or if, although on colchicine prophylaxis, a loading dose of colchicine is not used for acute gouty arthritis within 14 d. The loading dose is 1.2 mg (0.6 mg per tablet) or 1.0 mg (0.5 mg per tablet), followed by 0.6 mg (or 0.5 mg) after 1 h. After 12 h, follow 0.6 mg, taken l to 2 times a day, or 0.5 mg, maintained 3 times a day until complete remission of gout. If a patient is treated prophylactically with colchicine and a loading dose of colchicine is used within 14 d, colchicine is no longer an option for this episode and NSAIDs or glucocorticoids are chosen. Colchicine should be used within 36h of onset of the attack, with attention to drug interactions during its use, and for special cases of use it is recommended to refer to the drug instructions. Regarding the systemic and local use of glucocorticosteroids, the guidelines recommend first assessing the number of joints involved and administering oral prednisone at a dose of 0.5 mg/kg/day/kg for 5-10 d with direct discontinuation, or 0.5 mg/kg/day/kg for 2-5 d, followed by gradual dose reduction and discontinuation for 7-10 d. Methylprednisolone can also be chosen. If 1 or 2 large joints are involved, glucocorticoid intra-articular injections can be chosen at a dose determined by the size of the involved joint, in combination with oral glucocorticoids or NSAIDs or colchicine. Guidelines recommend a single intramuscular injection of tretinoin 60 mg followed by oral prednisone or prednisolone as an option. Subcutaneous injection of adrenocorticotropic hormone (ACTH) alone intramuscularly for the treatment of gouty arthritis and in patients able to take oral medications was not unanimously agreed upon by the guidelines. In patients with severe acute gout attacks, the guidelines recommend combination therapy with combination regimens including NSAIDs + colchicine, oral glucocorticoids + colchicine, intra-articular glucocorticoids + colchicine or NSAIDs or oral glucocorticoids. Patients with acute gout attacks (defined as <20% improvement in VAS score within 24h of drug therapy or <50% improvement in VAS score ≥24h of therapy) who do not respond adequately to initial therapy need to be reconsidered for a gout diagnosis and treatment considered with a switch to another drug therapy or an IL-1 inhibitor (anakinra 100mg subcutaneously once daily for 3 d),. or canakinumab 150 mg, subcutaneously. There are currently no indications for the 2 biologics for gout. The guidelines recommend that fasting patients with 1 or 2 joints involved choose intra-articular glucocorticoid injections at a dose determined by the size of the joint. The guidelines recommend also intramuscular or intravenous methylprednisolone at a starting dose of 0.5 to 2 mg/kg or subcutaneous ACTH 25 to 40 IU. After initiation of uric acid-lowering therapy and increased frequency of acute gout attacks, the preferred drug for relapse prevention is colchicine at a dose of 0.5 or 0.6 mg once or twice daily, in case of moderate to severe renal impairment or drug interactions. The dose was further reduced. Low-dose NSAIDs in combination with proton pump inhibitors or other peptic ulcer suppressants may also be used as a first-line option. For patients who are intolerant to colchicine and NSAIDs, have contraindications, or are ineffective, the guidelines recommend low-dose prednisone or prednisolone (10 mg/d) to prevent gout flares. Duration of therapy: The guidelines recommend, (1) at least 6 months; (2) 3 months after achieving uric acid target values in patients without gout stones on physical examination; and (3) 6 months after the disappearance of gout stones on physical examination and achieving uric acid target values in patients with previous gout stones.