This year, January caught up with two holidays, and the holiday season took up almost half of the month. After the Spring Festival, many of the patients who came to the pain center had similar symptoms. For example, sudden onset of severe pain in a single joint at night, with redness, swelling, heat and dysfunction. It is mostly seen in the thumb and first metatarsophalangeal joint, but resolves on its own after a few days. Most of these patients are middle-aged men with a long history of alcohol consumption or obesity. Which disease do they have? A simple blood test was done to find out – blood uric acid measurement. All of their blood uric acid was significantly higher than normal (>420 μmol/L for men and >350 μmol/L for women), so the cause of their joint pain was gout. Gout is a heterogeneous group of diseases with increased blood uric acid due to disorders of purine metabolism and/or impaired uric acid excretion. Its clinical features are hyperuricemia, recurrent episodes of gouty acute arthritis, gout stone deposition, characteristic chronic arthritis and joint deformity, often involving the kidney causing chronic interstitial nephritis and kidney uric acid stone formation. Primary gout cannot be cured at present. The prevention and treatment aims at controlling hyperuricemia and preventing urate deposition; rapidly terminating acute arthritis attacks; and preventing uric acid stone formation and renal function damage. First of all, we should regulate the diet, control the total calorie intake, restrict high purine food (such as heart, liver, kidney, brain, fish, shrimp, sea crab and other sea food, meat, soybean products, yeast, etc.), strictly prohibit the consumption of alcohol (including beer containing a lot of purine); appropriate exercise; drink more water, above 2000ml per day, to increase the excretion of uric acid; do not use drugs that inhibit uric acid excretion. For acute gouty arthritis, absolute bed rest, elevation of the affected limbs, rapid administration of colchicine and non-steroidal anti-inflammatory drugs. The common mechanism of action of NSAIDs is to inhibit the cyclooxygenase activity in the metabolism of arachidonic acid, which in turn inhibits the synthesis of prostaglandins and achieves anti-inflammatory and analgesic effects. Contraindications such as active peptic ulcer and gastrointestinal bleeding should be noted during application. The most widely used drug is indomethacin, with an initial dose of 75-100 mg, followed by 50 mg once every 6-8 hours. Compared to indomethacin, COX-2 inhibitors (e.g., etoricoxib, rofecoxib, etc.) have fewer side effects on the GI tract. In the case of etoricoxib, not only does it have fewer GI side effects, its half-life is 22 hours, and it can be taken orally once a day, which is convenient compared to indomethacin. In recent years, a large number of clinical trials at home and abroad have proved that etoricoxib has the same efficacy as indomethacin in the treatment of gout pain. For patients in the inter-episode and chronic phases, the aim of treatment is to maintain uric acid at normal levels. Uric acid-removing drugs (benzbromarone, propoxur, sulfopiridone) are suitable for patients with still good renal function, mainly to inhibit the reabsorption of urate in the proximal renal tubules and increase the excretion of uric acid, thus reducing uric acid levels. The main drugs that inhibit uric acid production include allopurinol, whose mechanism of action is to reduce uric acid production by inhibiting xanthine oxidase, and is suitable for those who have excessive uric acid production or those who are not suitable for uric acid excreting drugs. Physiotherapy and physical therapy are available for those with impaired joint movement. If the gout stone is large or broken through the skin, it can be removed surgically. Gout is a lifelong disease, and those without renal impairment or joint deformity can maintain a normal life and work with effective treatment.