Gout is one of the most common inflammatory joint diseases, with a prevalence of 1 to 2 percent in Western men. Gout is caused by the deposition of urate crystals in joints and other tissues and is an important disease that leads to disability and a reduced quality of life for patients. Reducing blood uric acid levels, dissolving urate crystals, reducing acute gout attacks and ultimately curing the disease are important goals of gout treatment. Although there are several versions of guidelines and recommendations for the treatment of gout, they are not perfect. In recent years, the introduction of new drugs for the treatment of gout, the concept of targeted therapy and the application of new technologies have led to significant developments in the diagnosis and treatment of gout. As a result, 474 rheumatologists from 14 countries reached a new consensus on the diagnosis and treatment of gout after a comprehensive no literature review and discussion vote over a 2-year period, summarized in 10 recommendations, which were published in Ann Rheum Dis in July 2013, as follows. (1) Finding urate crystals provides a definitive diagnosis of gout. If urate crystals are not available, the diagnosis can be assisted by typical clinical features (e.g., typical clinical presentation of the foot, gout stones, rapid and effective colchicine treatment) and/or characteristic imaging changes (especially joint ultrasound and dual-energy CT). A definitive diagnosis of gout is important because once diagnosed, lifelong uric acid-lowering therapy is usually recommended. (ii) In patients with gout and/or hyperuricemia, renal function tests should be performed and assessment of cardiovascular risk factors is recommended. ③In patients with acute gouty arthritis, treatment should be based on the patient’s coexisting disease and the risk of adverse drug reactions, including low-dose colchicine (maximum dose of 2 mg per day), NSAIDs and/or glucocorticoids (intra-articular, oral or intramuscular). The strength of evidence for oral and intramuscular hormones was much stronger than for intra-articular injections; the difference in efficacy between selective cyclooxygenase (cox)-2 inhibitors and non-selective non-steroidal anti-inflammatory drugs (NSAIDs) was not statistically significant. ④ Patients were advised to lead a healthy lifestyle, including body mass reduction, regular exercise, smoking cessation, and avoidance of excessive alcohol and sugary drinks. Experts recommend that gout patients avoid beer and spirits as much as possible, and wine may be considered in small amounts. ⑤ Allopurinol should be chosen as the first-line drug for uric acid-lowering therapy, and the next drugs that can be considered include pro-uric acid excretory agents (e.g., benzbromarone, probenecid) or febuxostat. Uric acidase monotherapy should only be used in those cases of severe gouty arthritis where all other treatments have been ineffective or where treatment is contraindicated. The use of uric acid-lowering drugs (except uricase) should be started at a low dose and then gradually increased to bring the blood uric acid down to the target value. (6) When starting uric acid-lowering therapy, patients should be informed of the risk of acute arthritis attacks and how to deal with them. The use of low-dose colchicine (maximum 1.2 mg/d), NSAIDs, or low-dose glucocorticoids may be considered to prevent acute arthritis attacks, with low-dose colchicine having the highest level of evidence (level 1b) and recommendation (level B). The timing of preventive medication should vary from person to person. (vii) Impact of coexisting disease on drug selection. Allopurinol can be used in patients with mild to moderate renal impairment, but should be closely monitored for possible adverse effects. Allopurinol should be started at a lower dose (50-100 mg/d) and gradually increased to achieve target blood uric acid values. Febuxostat and benzbromarone are also available and do not require dose adjustment. (8) The treatment goals are blood uric acid <0.36 mmol/L (60 mg/L), eventual absence of gout attacks, and gout stone dissolution. In patients who have developed gout stones, lower blood uric acid levels facilitate stone dissolution and delay gout recurrence. Clinicians need to monitor the patient's blood uric acid level, frequency of gout attacks, and the size of the gout stones. 9 Treatment of gout stones: Patients should have a consistently low blood uric acid level, preferably <0.30 mmo]]L (50 mg/L). There is no significant difference in the efficacy of various uric acid-lowering drugs. Surgical procedures are used only in certain patients presenting with nerve compression, mechanical injury, or infection. The application of drugs to prevent gouty arthritis, renal disease, and cardiovascular events is not recommended in patients with pure asymptomatic hyperuricemia. However, given the risks associated with hyperuricemia, a healthy lifestyle is recommended. The 10 recommendations for the diagnosis and treatment of gout in 2013 are derived from evidence-based medical evidence and expert consensus, are highly credible and authoritative, provide answers and guidance to common and important questions in clinical work, and are widely accepted by rheumatologists worldwide. Compared with the previous gout guidelines proposed by the American College of Rheumatology, this guideline not only includes the treatment of benzbromarone, but also gives the corresponding level of evidence and strength of recommendation for different drugs, so it is also a more comprehensive and practical recommendation. It is hoped that the latest recommendations on the diagnosis and treatment of gout in 201 3 will serve as a guide to the clinical work of rheumatologists and physicians in related fields in China.