Rheumatic and immune diseases often require long-term drug therapy. In recent years, the development of related drugs has been in full swing, and some of the best ones have gradually entered the clinic. The seemingly uneventful rheumatology department has started to see a lot of new trends. Gout is a disease caused by an impairment of purine metabolism in the human body. Its diagnosis requires a focus on two gold standards, namely, the detection of specific urate crystals in synovial fluid and the presence of sodium urate crystals in proven gout stones. It is important to note that about 40% of patients with acute attacks of gouty arthritis have normal blood uric acid, so a single hyperuricemia is not a basis for the diagnosis or exclusion of gout. Gout should be differentiated from rheumatic fever, dengue, cellulitis, septic arthritis, traumatic arthritis, and pseudogout. Non-pharmacological treatment of gout, such as weight loss and diet restriction, should be used throughout the treatment of gout. Research in recent years has made the importance of non-pharmacological treatment increasingly recognized by physicians. Acute attacks: colchicine is no longer used in high doses The latest European League Against Rheumatism treatment guidelines recommend that acute attacks of gout should be treated with oral NSAIDs or colchicine, and that NSAIDs should be used as much as possible in the absence of contraindications. Studies have shown that the effective control of acute attacks of gout depends on the timing and dose of NSAIDs, and the earlier they are used and the more adequate the dose (doubling the dose in the first two days), the more effective they are. When colchicine is chosen, the current small dose therapy (0.5mg per time, 3 times a day) with less adverse effects and no reduction in efficacy is advocated, while the previous large dose therapy (0.5mg per time, 1 time per hour) is abandoned. For persistent gout attacks limited to 1 or 2 joints, intra-articular injections of long-acting steroid hormones can be given for rapid and effective symptom relief. For refractory gout attacks or when the above drugs are contraindicated, oral prednisone in moderate doses or biological agents such as anti-interleukin-1 or anti-tumor necrosis factor alpha agents may be used. For the treatment of uric acid reduction in the interictal and chronic phases, it is not considered necessary to reduce uric acid as soon as the blood uric acid is increased. There are indications for uric acid-lowering therapy, including frequent arthritic episodes (≥2/year), persistent, severe or refractory gouty arthritis with gout stones, urinary stones and chronic gouty nephropathy, blood uric acid >536 mol/L despite dietary control, and destruction of affected joints on X-ray. Early and middle stage treatment of gout is based on pro-uric acid excretory drugs, while middle and late stage is based on drugs to inhibit uric acid synthesis. The first start of uric acid-lowering therapy should be started 1 to 6 weeks after the gout attack has subsided. The blood uric acid level should be monitored regularly during the process of uric acid lowering, and the dose of uric acid-lowering drugs should be adjusted according to the blood uric acid value to make the blood uric acid level reach the standard consistently in the long term. Blood uric acid is generally targeted at <360 mol/L, while for patients with chronic gouty arthritis who have a large number of gout stones, blood uric acid <300 mol/L may be more appropriate. In addition, to avoid acute attacks induced by excessive fluctuations in blood uric acid during uric acid lowering, the dose of uric acid-lowering drugs should be started from small doses and gradually increased, and small doses of colchicine or non-steroidal anti-inflammatory drugs should be used to prevent acute attacks of gout. Refractory gout: new uric acid-lowering drugs bring new hope Many patients with chronic gouty stone gout are allergic, ineffective or intolerant to the above traditional uric acid-lowering drugs and can only seek treatment with other new uric acid-lowering drugs. In recent years, a variety of new uric acid-lowering drugs have been marketed one after another. New drugs that inhibit uric acid synthesis, such as febuxostat, are a new non-purine type of highly efficient selective xanthine oxidase inhibitor, which is an effective alternative for patients with allopurinol allergy or intolerance to gout, especially for gout patients with renal insufficiency. It has a high rate of dissolution of gout stones and is rarely associated with lethal allergy syndrome. A second-generation uric acid excretory agent is the uric acid transporter protein 1 inhibitor RDEA-594, which is characterized by the absence of hepatotoxicity. Phase II clinics have shown that its efficacy is comparable to that of allopurinol, it is effective in mild to moderate renal insufficiency, has a very low risk of inducing kidney stones, and has no serious adverse events. New drugs that promote uric acid catabolism such as Precahi. It is well known that during the evolution of humans and higher primates, the expression of uricase, which directly breaks down uric acid, was lost, and it is the role of uricase that is exerted by Prescriptives. It is used only in adult refractory gout patients for whom conventional uric acid-lowering therapy has not been effective, and is contraindicated in people with 6-phosphoglucose dehydrogenase deficiency and used with caution in people with congestive heart failure. Its rapid dissolution of gout stones effectively improves the quality of life, but the main problems are infusion reactions, frequent gout attacks at the beginning of treatment and expensive.