Gout is a disease that results in urate deposition due to high blood uric acid levels and/or decreased uric acid excretion caused by disorders of purine metabolism. Uric acid is the end product of purine metabolism in humans, and hyperuricemia is an important biochemical basis for gout. A direct relationship has been demonstrated between blood uric acid levels and both the incidence of subsequent gout and the age of first attack. The diagnosis of acute gouty arthritis is based on the classification criteria established by the American Rheumatism Association in 1977, and the presence of uric acid crystals in the synovial fluid or gout stones is the gold standard for confirming the diagnosis. When the number of crystals in synovial fluid is low, false negative results increase, so some scholars emphasize the importance of clinical evaluation. In recent years, the prevalence of gout has been increasing year by year in both European and American and Eastern peoples, with a prevalence of 0.84% in all age groups. There is no cure for gout, and the aim of current treatment is to control acute attacks of gouty arthritis and reduce blood uric acid levels in time to prevent urate deposition, joint destruction and kidney damage. However, there is still some controversy about gout treatment, so we have reviewed some new understanding of gout treatment in recent years. 1.Non-pharmacological treatment: Research shows that hyperinsulinemia can stimulate renal tubular Na+H+ exchange, which increases uric acid reabsorption while increasing H+ excretion, resulting in hyperuricemia, so improving the body’s sensitivity to insulin is beneficial to uric acid excretion. Therefore, improving the body’s sensitivity to insulin is beneficial to the excretion of uric acid. Reducing body weight and low protein diet can help increase the body’s sensitivity to insulin. Low purine and low protein diets have long been advocated for gout patients, but low purine diets are often high in carbohydrates and saturated fatty acids, which can reduce the body’s sensitivity to insulin and are not conducive to uric acid excretion. Therefore, some scholars suggested that the dietary structure of gout patients should be re-evaluated. They suggested that carbohydrate intake should be restricted and protein and unsaturated fatty acid intake should be increased proportionally to improve the body’s sensitivity to insulin, thus promoting blood uric acid excretion. After 4 months of clinical validation of dietary restructuring, insulin sensitivity increased, blood uric acid levels in gout patients decreased by an average of 18%, and the frequency of gout attacks decreased by an average of 67% per month. Alcohol intake is associated with hyperuricemia and can precipitate acute gouty arthritis. Studies have shown that ethanol metabolism increases blood lactate concentration, and lactate inhibits uric acid secretion from the renal tubules and reduces uric acid excretion. Ethanol also promotes the conversion of adenine nucleotides, which increases the synthesis of uric acid. Therefore, gout patients should strictly avoid alcohol, including the consumption of beer containing large amounts of purines. Many drugs can affect uric acid excretion. Some diuretics, especially thiazides, although their diuretic effect can promote uric acid excretion, they also reduce the secretion of uric acid by the renal tubules, which eventually leads to an increase in blood uric acid. The angiotensin receptor inhibitor cloxacin can promote uric acid excretion and reduce blood uric acid levels, and when combined with dihydrokethionine, it can alleviate the uric acid retention effect of dihydrokethionine. The effect of aspirin on renal uric acid excretion has a dose-related effect, i.e., it inhibits urate secretion from the renal tubules at low doses, which increases blood uric acid levels, and increases uric acid excretion at high doses (>3g/d) by inhibiting uric acid reabsorption from the renal tubules. Studies have shown that in elderly people without kidney disease who take aspirin 75mg/d, there are obvious changes in renal function and uric acid metabolism after 1 week, and uric acid excretion decreases, but when the dose is increased to 150mg/d and 325mg/d, uric acid excretion gradually returns to near the original level. The current use of small doses of aspirin is very common and should be brought to the attention of gout patients. Other drugs that inhibit uric acid excretion include penicillin, vitamin B1, B12, insulin, ethambutol, pyrazinamide, niacin, levodopa and cyclomycin A. In addition, active treatment of gout-related diseases such as hyperlipidemia, hypertension, coronary heart disease and diabetes is important to prevent the recurrence of hyperuricemia. 2, treatment of acute gout: Colchicine is most effective when given within 24h of an acute attack of gout, but its adverse effects are large, with 80% of patients experiencing nausea, vomiting, diarrhea and abdominal pain before complete clinical remission, and this effective dose is similar to the toxic dose, which limits its application. Colchicine has been recommended for the intravenous administration of acute gouty arthritis, but it must be applied with caution because it can produce serious adverse effects such as bone marrow suppression, renal failure, alopecia, diffuse intravascular hemolysis, hepatic necrosis, seizures, and even death. Numerous physicians advocate that the intravenous use of colchicine should be limited or completely banned. Because of the greater adverse effects of colchicine and the reduced efficacy of colchicine after 24 h of acute gout attack, non-steroidal anti-inflammatory drugs (NSAIDs) have become the first line of treatment for acute gouty arthritis. Any one of them can be used, and it is forbidden to take two or more NSAIDs at the same time, otherwise the efficacy will not increase, and the adverse effects will increase. Once the symptoms are reduced, the dosage is gradually reduced and discontinued after 5 to 7 d. Adrenal glucocorticoids may be considered when the above drugs are ineffective or produce adverse reactions. For example, the starting dose of prednisone is 0 5-1 mg?kg-1?d-1, and the dose is rapidly reduced or discontinued after 3-7 d. The course of treatment should not exceed 2 weeks. In patients with acute gouty arthritis involving a single or two joints, intra-articular corticosteroid injections may relieve symptoms. Adjunctive intra-articular corticosteroid injections may also be used in patients with polyarthritis in whom NSAIDs are contraindicated or ineffective. Intra-articular injections of small doses of tretinoin have been used to effectively relieve gout attacks. Intramuscular injections of deferiprone have also been reported for the treatment of acute gout. Not only do uric acid-lowering drugs have no anti-inflammatory and pain-relieving effect on the treatment of acute arthritis, but they can also make the blood uric acid fall too fast due to incorrect use, prompting the dissolution of the gout stone surface in the joint, forming insoluble crystals and aggravating the inflammatory reaction or arthritis migration, so they should not be used in the acute phase of gouty arthritis. 3, treatment of hyperuricemia: when to use uric acid-lowering drugs has been controversial. Some scholars suggest that uric acid-lowering therapy should be considered only when acute gouty arthritis strikes more than four times a year. Others believe that it is worthwhile from the economic point of view to give uric acid-lowering treatment even if there is one attack per year. For patients with gout stones, combined uric acid nephropathy, uric acid kidney stones and renal insufficiency, uric acid-lowering therapy should be given. There are two types of drugs to lower uric acid levels: drugs that promote uric acid excretion (benzbromarone, probenecid, benzosulfone) and drugs that inhibit uric acid production (allopurinol). The principle of selection: if the kidney function is normal or mildly impaired, and if uric acid excretion is reduced or normal, uric acid excretion drugs are available; if the kidney function is moderately impaired or above, and/or if uric acid excretion is excessive, uric acid excretion drugs will cause urate stones and aggravate kidney damage, so uric acid production inhibiting drugs should be used. Whether you choose uric acid-depleting drugs or uric acid-inhibiting drugs, the dosage is gradually increased in small doses to avoid the deposition of large amounts of uric acid in the renal tubules and interstitium, which can cause acute uric acid nephropathy, and to avoid a sharp drop in blood uric acid levels that can trigger the onset of gouty arthritis. The small dose increment method is also beneficial to detect adverse drug reactions. How much lower blood uric acid can reduce arthritis attacks and treat gout stones It has been reported that a decrease in uric acid level of at least 5 9 to 357 mmol/l per month during the first 6 months of uric acid-lowering therapy is necessary to prevent gout attacks. Maintaining blood uric acid level below 357 mmol/l can prevent acute attacks of gout, and if blood uric acid level is maintained below 2975 mmol/l can promote gout stone absorption. Some scholars advocate that for recurrent gouty arthritis, the prophylactic application of colchicine can stop gout attacks and reduce their severity. However, there are many adverse reactions with colchicine, and the actual risk of gout attack in patients treated with uric acid-lowering drugs is 24%, so colchicine is not advocated as preventive treatment. 4. Treatment of asymptomatic hyperuricemia: Evidence shows that the possibility of acute gouty arthritis attack increases with the increase of blood uric acid level, but most patients with hyperuricemia do not develop gout. Therefore, except for chemotherapy and radiation therapy for hematologic malignancies, usually asymptomatic people with hyperuricemia do not require uric acid-lowering therapy. However, some scholars believe that there is no essential difference between hyperuricemia and gout, which can be regarded as an early stage of gout. Simple hyperuricemia without clinical symptoms does not mean that the joint tissues or kidneys are not affected by uric acid deposition, but that the tissue damage caused by this uric acid deposition is relatively mild and has not yet caused significant clinical symptoms. The etiology of hyperuricemia and related factors such as diuretic therapy, weight gain, alcohol consumption, hypertension, and hyperlipidemia should be sought in patients with hyperuricemia.