Gout (gout) is a heterogeneous group of metabolic diseases caused by disorders of purine metabolism. Its clinical features are hyperuricemia and the resulting recurrent acute arthritis, chronic arthritis, joint deformities, gout stones, uric acid urinary tract stones and interstitial nephritis, which can cause acute renal failure in severe cases. Clinically, gout is generally referred to as gout only when arthritis occurs, and patients are more often associated with obesity, diabetes, hyperlipidemia, hypertension, atherosclerosis and coronary heart disease. The natural course of gout is divided into an asymptomatic hyperuricemic phase, an acute and intermittent arthritic phase, and a chronic gouty arthritic phase. Asymptomatic hyperuricemia can last for about 20 years before a gout attack or kidney stone occurs. The first attack of gout is most often seen in men aged 40-60 years or women over 60 years. A variety of medications can raise blood uric acid levels and make gout more likely to flare up, especially diuretics. Most attacks of gout occur as monoarthritis, especially early in the course of the disease. It occurs in the first toe joint (foot gout) and is often acute and painful. It is often differentiated from infectious arthritis and other crystalline arthritis, especially pseudogout. X-rays, ultrasound, CT and MRI of the affected joints are useful diagnostic aids. The pathogenesis of gout is clear and the treatment is effective, but clinically refractory gout is increasing year by year and is known as “the most intractable curable joint disease”. To add insult to injury, one of our studies found that only 70.6% of patients were confident that gout, an easily diagnosed and well-treated disease, was manageable. It is generally accepted that inappropriate medication and poor patient compliance are the two main factors for poor gout control. In addition to strengthening patient education, clinicians have been asked to improve the level of gout diagnosis and treatment and standardize treatment. Standardized gout treatment. Patient education and appropriate lifestyle and dietary modifications are the basis for long-term gout treatment, while complex medication requirements (different types of medications at different times) lead to poor compliance. An analogy can better explain to gout patients the different effects of medications at different stages. The NSAIDs or colchicine can be used to put out the fire, but the match is still there and to avoid rekindling, prophylactic colchicine is used to wet the match and make it difficult to rekindle it, while allopurinol and other uric acid-lowering therapies actually remove the match from the body. Early control during acute attacks of gout: monotherapy or combination of NSAIDs, colchicine and steroid hormones. The principle of treatment during an acute attack of arthritis is early administration of medication to relieve symptoms. In addition, proper management of precipitating factors such as acute infection, surgical procedures, and mental overstimulation. NSAIDs should be administered in adequate dosage and duration (until the acute gouty arthritis is completely relieved), and the dosage should be reduced in patients with hepatic or renal impairment. Colchicine loading dose is 1.2mg or 1.0mg, 0.6mg or 0.5mg after 1 hour, and 0.6mg or 0.5mg after 12 hours, taken 1-2 times daily until complete remission of gout. Regarding systemic and topical glucocorticoids, the guidelines recommend first assessing the number of joints involved and administering prednisone 0.5mg/kg*d orally for 5-10 days with direct discontinuation; or 0.5mg/kg*d for 2-5 days, followed by gradual reduction and discontinuation for 7-10 days; methylprednisolone is also an option; few joints involved (1-2) can be injected directly into the joint cavity. If the initial single drug is ineffective (i.e., pain improvement <20% within 24 hours of treatment or <50% after 24 hours of treatment), another drug may be switched or a combination therapy may be taken. Common regimens include NSAIDs + colchicine, oral glucocorticoids + colchicine, intra-articular glucocorticoids + colchicine/NSAIDs/oral glucocorticoids. Combination medication is recommended for severe acute gout flare-ups. Second-line IL-1 antagonists may be considered in those who remain ineffective. Local application of ice packs may help control pain during acute attacks. In some cases, analgesics, including narcotics, may also be added. Relapse prevention: for gout control. A small daily dose of colchicine is used to prevent acute attacks with an efficiency of up to 85%. Colchicine 0.6 mg or 0.5 mg, taken once or twice daily, is usually well tolerated. Patients who also use statins (HMG-CoA reductase inhibitors) or cyclosporine in combination should be alerted to the development of rhabdomyolysis. Low-dose NSAIDs in combination with proton pump inhibitors or other peptic ulcer suppressants may also be a first-line option for patients who cannot tolerate one colchicine tablet per day. Low-dose prednisone (no more than 10 mg/d) may be considered in those who are intolerant to both colchicine and NSAIDs or have contraindications or are ineffective. Treatment guidelines recommend a minimum of 6 months, maintained for 3 months after uric acid lowering for patients without gout stones on physical examination, and 6 months after uric acid attainment for patients with previous gout stones, after the disappearance of gout stones. It should be noted that the prophylactic use of colchicine or some kind of NSAID can block the acute inflammatory response, but does not change the deposition of crystals in the tissues, gout stones and cartilage and bone destruction will still progress, and uric acid-lowering drugs should be used at the same time. Gout "root cause": uric acid-lowering treatment to meet the standard. Any patient with a clear diagnosis of gouty arthritis and the following clinical conditions should be treated with uric acid-lowering therapy: 1) clinical or imaging findings of gouty stones; 2) frequent episodes of acute gouty arthritis (at least 2 episodes per year); 3) combined chronic kidney disease stage 2 and above; 4) urinary stones. Reduction of blood uric acid level to below 360umol/L (6mg/dl) is the minimum goal of treatment. For gout patients with existing gout stones, the blood uric acid level should be reduced to below 300umol/L (5mg/dl) for better long-term improvement of the patient's clinical signs and symptoms. In recent years, guidelines have suggested that uric acid-lowering therapy can be initiated at the time of an acute gout attack if effective anti-inflammatory management is planned. Uric acid-lowering drugs include those that inhibit uric acid production (xanthine oxidase inhibitors), those that promote uric acid excretion, and those that promote uric acid catabolism. Xanthine oxidase inhibitors (XOI) allopurinol and febuxostat are recommended as first-line agents. About 20% of patients using allopurinol experience side effects and 5% discontinue the drug. Common side effects include gastrointestinal reactions and skin rash. The most serious is allopurinol hypersensitivity syndrome (AHS), a spectrum of disease that includes not only Stevens-Johnson syndrome and toxic epidermolysis bullosa, but also systemic diseases with various clinical features, such as eosinophilia, vasculitis, erythema and end-organ disease. The condition is most common in patients with renal insufficiency and those taking thiazide diuretics. The highest risk of severe AHS is seen in the first months of treatment, therefore it is emphasized that the starting dose of allopurinol should not exceed 100 mg per day, and in CKD stage 4 or worse, the starting dose is even lower (50 mg per day). The dose is gradually increased during treatment, reaching the appropriate therapeutic amount in 2-5 weeks, with the dose for each patient determined according to individual principles. Rapid PCR screening for the HLA-B5801 gene is recommended prior to the use of allopurinol in high-risk populations (Han Chinese, Thai and Koreans with CKD stage 3 or higher). Febuxostat is a more potent xanthine oxidase inhibitor different from allopurinol, which is metabolized mainly by the liver and can be excreted through the kidney and gastrointestinal tract. It is safe and effective in mild to moderate renal insufficiency and is the best choice for patients who are intolerant or allergic to allopurinol. If the patient is contraindicated or intolerant to xanthine oxidase inhibitors, the pro-uric acid excretion drug benzbromarone may be used. Pro-uric acid excretory drugs are contraindicated in patients with a history of urinary tract stones and increased uric acid production. For those who do not meet the uric acid standard after treatment, it is recommended to increase the dose of xanthine oxidase inhibitor to the maximum dose that the patient can tolerate. If this is still not effective or tolerated, the patient may be switched to another xanthine oxidase inhibitor or to a combination of uric acid excretory drugs. Fenofibrate and coxsartan are used as drugs with uric acid excretory effects for the treatment of refractory gout or related comorbidities. In patients with severe gout, who do not respond to oral uric acid-lowering drugs or cannot tolerate them, polyglycolylated recombinant uric acid oxidase (pegloticase) can be used. In conclusion, the current status of gout treatment in China needs to be further improved. While patient education should be strengthened to improve compliance, clinicians' mastery of the standardized diagnosis and treatment of the disease, especially primary care hospitals and community doctors, should be enhanced to effectively control gout, which is the "king of diseases", at an early stage.