Gout is a very old and widespread disease, recorded in the history of medicine in BC, but it was not until more than 100 years ago that its pathogenesis was confirmed to be related to an increase in blood uric acid, a group of diseases caused by disorders of purine metabolism that result in excessive production and/or decreased excretion of uric acid. Primary gout is caused by a congenital disorder of purine metabolism and has a tendency to run in families. Secondary gout is caused by various causes such as blood disorders, kidney disease or drugs, etc. National Health Survey data from 1983 to 1985 showed that the incidence of gout was 13.6 per 1000 men and 6.4 per 1000 women. These figures have increased even more rapidly in recent years. Clinical gout often develops through four stages: asymptomatic hyperuricemia, acute gouty arthritis, intermittent phase, and gout stone formation. Asymptomatic hyperuricemia is defined as a serum uric acid concentration of more than 416 μmol/l, reaching a state of supersaturation, without gouty arthritis or kidney stones. Although gouty arthritis occurs during hyperuricemia, it does not mean that hyperuricemia is equivalent to clinical gout. Patients with hyperuricemia are more prone to gout and kidney stones, but clinical treatment is mostly not advocated, and its importance is prompted to look for the cause of hyperuricemia. An acute attack of gout is characterized by sudden onset of joint pain, redness, swelling and limitation of movement. Thomas Sydenham, a 17th century English physician, described an acute attack of gout from his own experience: “…… awakened at 2 a.m. by a violent pain in the big toe …… as violent as a broken bone …… next, felt chills, low fever, the pain became more and more intense …… feet have been unable to bear the weight of the quilt, the floor caused by people walking around the house trembling also makes the pain more unbearable ……”. The joints involved are, in order of frequency, the metatarsophalangeal joint, dorsum of the foot, ankle, knee, wrist and fingers, with single joints predominating. In women, it often occurs after menopause. After an acute attack, the disease enters an asymptomatic interval, which becomes more frequent, with shorter asymptomatic intervals and more joints involved. Gout stones are chalky deposits of uric acid salts. The most common sites are the joints of the hands and feet, with the auricular, elbow, and Achilles tendons being slightly less common but more classic sites. It is more likely to occur in: those with multiple joint involvement, blood uric acid concentrations >535 μmol/l, and early onset. In 1985, the American Holmes diagnostic criteria, the diagnosis of gout can be confirmed by having one of the following: 1. Leukocytes in the bursal fluid have phagocytosis of urate crystals; 2. Gout nodules and synovial biopsies have urate crystals; 3. There are recurrent acute arthritis, asymptomatic intervals, hyperuricemia and those who are effective on colchicine treatment. It should be differentiated from dengue, cellulitis, other arthritis and pseudogout. The goals of gout treatment are termination of acute attacks, uric acid-lowering therapy, prevention of recurrence, and treatment of comorbidities. NSAIDs, colchicine and glucocorticoids are the first treatment for patients without complications. Indomethacin, diclofenac, etoricoxib, and piroxicam are quite effective and treatment should be started as early as possible. Contraindicated in patients with peptic ulcer, renal failure, liver disease, decompensated heart failure, and those taking anticoagulants. Note that elderly patients are more likely to experience side effects. Colchicine was one of the first drugs used in the treatment of gout. Despite its obvious efficacy, the therapeutic-poisoning dose of this drug is close, and 80% of patients will experience gastrointestinal side effects such as nausea, vomiting and diarrhea, and the therapeutic effect may be less than ideal for patients who have been suffering from the disease for a long time. At present, it is advocated to apply small doses. Intra-articular injection of glucocorticoids can minimize the chance of side effects. Oral prednisone can be given to patients who have multiple joint involvement or who have been affected for a long time and cannot tolerate other drugs, often for one week. At the same time, attention should be paid to alkalinizing the urine so that the urine PH reaches 6.0-6.6. Uric acid-lowering drugs are mostly used two weeks after the acute attack of gout has completely disappeared, and early application can aggravate the condition of metastatic gout. There are mainly two types of drugs that inhibit uric acid synthesis and promote uric acid excretion. Allopurinol is a potent inhibitor of xanthine oxidase dehydrogenase, which rapidly reduces uric acid synthesis. The most serious allergic reactions are rash, fever, bone marrow suppression, hepatotoxicity, renal failure and systemic vasculitis. The most serious allergic reactions are rash, fever, myelosuppression, hepatotoxicity, renal failure and systemic vasculitis. Drugs that promote uric acid excretion include benzbromarone and probenecid, which can be used in most patients with gout, as most patients have inadequate uric acid excretion. Patients with renal failure, a history of previous kidney stones, and those taking small doses of aspirin are not candidates for uric acid excretory drugs. Gout arthritis prevention with low-dose colchicine is administered during the interval from the start of uric acid-lowering drugs until the blood uric acid falls to the target level (<360umol/l) and remains stable for 3-6 months. If colchicine is not tolerated, an NSAID can be chosen instead. For gout patients with concomitant hypertension, hyperlipidemia, diabetes mellitus, coronary artery disease, and cerebrovascular disease, treatment should be given for these diseases at the same time. In addition to diet control, non-pharmacological treatment, exercise, weight reduction, lifestyle changes, moderate intake of VitC foods, avoiding strain and trauma, drinking more water, and alkalinizing urine are also very important.