Detail 1: Don’t waste diet control and medication There are two wrong tendencies in treating this issue of gout treatment: one is to rely unilaterally on diet control and refuse medication; the other is to rely completely on medication and ignore diet treatment. Diet control is an effective measure to reduce blood uric acid, but not all hyperuricemia can be completely solved by diet control alone. This is because 70%-80% of uric acid in the body is produced by the patient’s own body, and only 20%-30% comes from external factors such as diet. Strictly limiting the intake of high purine foods can only reduce blood uric acid by 60 μmol/L (1 mg/dL). Therefore, in patients with significantly elevated blood uric acid levels, dietary control often needs to be accompanied by medication. Although any medication has side effects, the safety of uric acid-lowering drugs is guaranteed as long as they are applied properly. Likewise, dietary treatment should not be relaxed for patients taking uric acid-lowering drugs. Good lifestyle habits are essential for gout patients. Patients should adhere to a low purine diet, drink 2000-3000mL of water daily, and avoid overeating. Detail 2: Combined with other diseases, gout is a metabolic syndrome, many patients are combined with hypertension, hyperuricemia and obesity. Coxsartan (Coxua) is an antihypertensive drug that has been proven to have both renal protection and uric acid-lowering effects, and is the first choice for patients with gout combined with hypertension. In addition, angiotensin-converting enzyme inhibitors (such as Lodinexin and Yashida), which have renal protection, are also good choices for antihypertensive drugs. Gout patients should not use antihypertensive drugs are thiazide diuretics and compound preparations containing thiazide diuretics, because the latter can inhibit uric acid excretion, increase blood uric acid levels and induce gout attacks. Fenofibrate (Lipingzhi) has both uric acid and lipid-lowering effects, and is a good choice for patients with gout combined with hyperlipidemia. Details 3: Avoid factors that can trigger gout There are many triggers for gout attack, including overeating, trauma and surgery, certain drugs, cold and damp, excessive fatigue, mental stress, infection and so on. The main drugs that can cause an increase in blood uric acid are: potassium-depleting diuretics (e.g. thiazide diuretics, tachyphylaxis); anti-TB drugs (e.g. pyrazinamide, ethambutol); anti-tumor drugs (e.g. methotrexate, cyclosporine); low-dose aspirin (<2g/d); β-blockers; levodopa, etc. Patients with hyperuricemia and gout should try to avoid the above-mentioned triggers, and try not to take those drugs that can raise blood uric acid when choosing drugs. Detail 4: How much blood uric acid control is appropriate Gout attacks and blood uric acid levels are positively correlated. Some domestic scholars found that when blood uric acid <357μmol/L, gout rarely occurs even when there are strong triggers; arthritis, gout stones, kidney stones and renal insufficiency mostly occur when blood uric acid is ≥477μmol/L. Therefore, the blood uric acid of gout patients should be controlled at the level of 477μmol/L. Therefore, the ideal level of blood uric acid in gout patients should be controlled below 357μmol/L. In patients with chronic gouty arthritis who have gout stones, blood uric acid should ideally be controlled below 300 μmol/L to facilitate the dissolution of uric acid stones. Patients are reminded that in the process of lowering uric acid, the blood uric acid level should be monitored regularly and the dose of uric acid-lowering drugs should be adjusted according to the blood uric acid value so that the blood uric acid level can be consistently achieved in the long term. Details 5: Pay attention to the identification of gout and these diseases 1. Acute gouty arthritis should be distinguished from septic arthritis, traumatic arthritis, dermatitis and pseudogout. Pseudogout is caused by the deposition of calcium pyrophosphate in the cartilage of the joints, and the performance is similar to that of gout during acute attacks. But there are the following characteristics: ① older people are more common, slightly more women than men; ② lesions mainly invade the knee, shoulder, hip and other large joints; ③ X-ray film can be seen in the joint space narrowing and cartilage calcification foci in the form of dense dots or lines, no bone destruction changes; ④ serum uric acid content is often normal; ⑤ synovial fluid can be found in the calcium pyrophosphate monoclinic or triclinic crystals; ⑥ colchicine treatment is less effective. 2, the chronic phase of identification The chronic phase must be distinguished from rheumatoid arthritis, osteoarthritis and psoriatic arthritis. Among them, psoriatic arthritis is also common in men, often asymmetrically invading the distal finger and toe joints, and 1/5 patients have elevated blood uric acid content. (3) X-ray shows severe joint destruction, widening of joint space, and shortening of bone resorption at the end of the finger and toe in the form of cutting; (4) joint symptoms are reduced with improvement of skin lesions or aggravated with deterioration of skin lesions.