Gout is a crystal-associated arthropathy caused by uric acid deposition. The acute phase is characterized by painful swollen joints, which can recur, especially in patients with poorly controlled blood uric acid and a long history of the disease. Hyperuricemia is the basis for the development of gout. If the blood uric acid level is elevated for a long time, the concentration of uric acid salts will increase and crystals will be deposited in the joints, leading to acute attacks of gout. At this time, the timely use of non-steroidal anti-inflammatory painkillers, colchicine, glucocorticoids and other drugs can quickly relieve joint symptoms, but do not reduce uric acid levels. During the interval and remission period without joint symptoms, if uric acid-lowering treatment is not continued and drugs that inhibit uric acid production or promote uric acid excretion are used, the concentration of uric acid salts will rise again and crystals will be deposited in the joints repeatedly, resulting in recurrent attacks of acute gout. With the increase in the number of attacks, the patient will form obvious gout stones in the joints. At this time, the disease has turned into a chronic stage, joint swelling and pain persist, and gradually erode the joint bone surface, resulting in joint deformity and affecting normal function, and the effect of conventional treatment drugs is not satisfactory. Therefore, for patients with poorly controlled blood uric acid, gout attacks will be frequent, eventually forming gout stones and turning into the chronic arthritis stage.