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. It can be complicated by renal lesions, and in severe cases, joint destruction and impaired renal function can occur. It belongs to the category of metabolic rheumatism. Hyperuricemia is the most important biochemical basis of gout, and urate crystallization is the result of hyperuricemia, and the incidence of gout is significantly and positively correlated with blood uric acid level. The key to gout prevention and treatment is to control the blood uric acid level. Myth 1: Treatment only during acute attacks During acute attacks, patients often go to the hospital because of unbearable joint pain, and once the joint pain improves, patients think they are “well” and do not need to see a doctor or treatment again. In fact, gout treatment is divided into acute attack treatment and chronic maintenance treatment, and the key to prevention and treatment is chronic maintenance treatment, including a reasonable diet, appropriate exercise, joint protection, and the use of uric acid-lowering drugs when necessary, so that the blood uric acid is controlled at a certain level to avoid another attack of gouty arthritis. Therefore, even if the joint pain improves, gout patients still need to visit the hospital regularly for follow-up. Myth 2: Unauthorized adjustment of drug doses Elevated blood uric acid is a key factor in gout attacks, which leads many patients to believe that a rapid reduction in blood uric acid levels will prevent gout attacks. For this reason, some patients increase the dose of medication without authorization, expecting that the blood uric acid can be reduced to a lower level in a short period of time. In fact, this is often counterproductive. This is because when the high level of blood uric acid is reduced rapidly, on the one hand, the insoluble uric acid crystals already deposited in the joints and surrounding tissues can be dislodged, and on the other hand, the blood uric acid can be deposited in the joint cavity, which can lead to acute gouty arthritis attacks. Patients are advised to slowly lower their blood uric acid levels. If necessary, patients can use a combination of uric acid-lowering drugs and colchicine or non-steroidal anti-inflammatory drugs under the guidance of a doctor to prevent triggering acute gouty arthritis. Myth 3: Ignore the importance of non-pharmacological treatment Many gout patients believe that they have been using uric acid-lowering drugs and their blood uric acid is under control, so they neither control their diet nor exercise while taking the drugs. Many patients do not know that non-pharmacological treatment is crucial in the treatment of gout. Patients should avoid eating large amounts of high purine foods in a short period of time to prevent a sharp increase in blood uric acid levels, which can cause an acute attack of gout. And proper exercise can promote local blood circulation in joints and avoid local blood uric acid dissolution saturation in joints, which can avoid gout attack again to a certain extent. In clinical practice, we can often see some patients whose blood uric acid level is not very high, but due to the lack of exercise, once the joint area is cold or injured, it can trigger gout. In this regard, it is recommended that gout patients should pay attention to diet, exercise and lifestyle changes in addition to drug treatment. Therefore, to prevent gout, you must first control your mouth. Eat more fruits, vegetables and other low purine alkaline food, less meat, fish and other acidic food, a light diet, low fat, low sugar, drink more water, to facilitate the excretion of uric acid in the body. Reasonable cooking methods can reduce the amount of purine contained in food, such as cooking meat first and discarding the soup before cooking. Spicy, stimulating food, spices can excite the plant nerves, inducing gout, and should not eat more. Next, exercise in moderation. Because gout is a metabolic disease, all the ways that can increase metabolism and promote excretion are good, such as walking, tennis, fitness and other aerobic exercises that consume a lot of oxygen. But pay attention to the intensity of exercise, because strenuous exercise can trigger an acute attack of gout. In addition, strong mental factors such as excessive fatigue and anxiety may also trigger gout. Again, it is important to identify the gout manifestations. The acute attack of gouty arthritis is the most common form of gout patients, its sudden onset, most of the attacks in the middle of the night, single or multiple joints with significant redness and severe pain, if not timely control, not only the patient suffering, affecting normal life and work, once the chronic will lead to joint destruction and kidney damage and other serious consequences. Therefore, it is important to stop the acute attack of gouty arthritis in time. During an acute attack of gouty arthritis, the patient must rest in bed, slightly elevating the affected limb and minimizing limb movement. The painful joint should be placed naturally in the most comfortable position, and rest is generally required until the joint pain is relieved for 72 hours before starting to resume activities. Once an acute attack of gout occurs, the patient must go to a hospital specialist in a timely manner and be given non-steroidal anti-inflammatory drugs, colchicine, glucocorticoids and other medications, and the patient should drink more water, more than 2,000 ml of water daily to maintain urine output. Limit high purine food, avoid alcohol, mental tension and cold and humidity. Drugs that affect uric acid excretion, such as diuretics, penicillin, cephalexin and small doses of aspirin, should also be avoided. During intermittent episodes and chronic periods after acute inflammation is controlled, uric acid-lowering drugs (such as allopurinol and propoxur) must be used under the guidance of a physician to prevent recurrence of acute arthritis, joint destruction, and kidney damage from the root.