Gout is a disease caused by a disorder of purine metabolism and persistent elevation of blood uric acid due to an inherited or acquired cause. It is a group of diseases in which long-term disorders of purine metabolism and elevated blood uric acid lead to tissue damage. Clinical features include hyperuricemia, recurrent episodes of gouty acute arthritis, gout stone formation and deposition, gouty nodular chronic arthritis, and gouty nephropathy. According to Chinese medicine, the etiology of gout includes wind, phlegm, dampness, and stasis, and is similar to the painful paralysis or walking paralysis in paralysis. The prevalence of gout in Europe and the United States is 0.3 to 0.5%. The prevalence of gout in China is increasing year by year, and the incidence is younger. Two large-scale epidemiological surveys of gout in the community showed that the prevalence rate was 0.2% in the first survey in 1992, while the second survey 5 years later showed that the prevalence rate had increased to 0.34% and the prevalence of hyperuricemia was 10.1%. According to the survey, there are about 4 million gout patients in China, and about 100 million people with high blood uric acid values. More than 90% of gout patients are men, and women rarely suffer from gout before menopause because estrogen can promote uric acid excretion and inhibit arthritis attacks. Purines in the body undergo a series of metabolic changes and the end product is called uric acid, a waste product of human metabolism. Under normal circumstances, 2/3 of uric acid is excreted by the kidneys through urine and 1/3 is excreted by the intestines. The body constantly produces and excretes uric acid, maintaining a dynamic balance. When abnormal purine metabolism causes excessive uric acid production or when uric acid excretion by the kidneys decreases, it can lead to hyperuricemia. When the concentration of uric acid in the blood exceeds its solubility in the blood, just as overly concentrated salt water precipitates white salt crystals on the walls of a container, urate or uric acid crystals are deposited from the blood into the joints, causing arthritis, and deposited into the soft tissues to form stones (gout stones, kidney stones). Acute gouty arthritis is characterized by: 1. rapid onset and development, with a peak of 24 to 48 hours; 2. marked redness, swelling, heat, pain, and severe pain, causing the patient to toss and turn, unbearable, and may also lead to fever; 3. 70% of the first attack is in the first metatarsophalangeal joint of the foot; 4. single joint involvement; 5. after the initial attack, the milder cases resolve themselves within a few hours or one to two days, while the more severe cases last for several days After the inflammation subsides, the local skin is dark red and lavender, accompanied by desquamation and mild itching, and no discomfort remains during the remission period. The diagnosis is usually made in the early stages based on the above characteristics combined with elevated blood uric acid, but after the formation of gouty nodular chronic arthritis, the above characteristics are not obvious, and the diagnosis should be made only after excluding other diseases that cause arthritis, and if necessary, joint aspiration is required to find uric acid crystals to confirm the diagnosis. Gout nephropathy includes: 1. chronic hyperuricemic nephropathy: early proteinuria and microscopic hematuria, gradually increased nocturia, decreased urine specific gravity, and finally from azotemia to uremia; 2. acute hyperuricemic nephropathy: rapid increase in blood uric acid concentration within a short period of time, crystals in the urine, hematuria, leukocyturia, and finally oliguria, anuria, acute renal failure and death; 3. uric acid kidney stones: 20 % to 25% are complicated by uric acid urinary stones, and most patients may have renal colic, hematuria and urinary tract infection symptoms. Obesity, aggressiveness, and type A personality with a strong attachment to set goals are prone to gout. Overexertion, emotional stimulation, and exposure to cold and moisture also cause gout attacks, but walking can reduce gout attacks by lowering uric acid values. The incidence of primary gout is closely related to the amount of protein intake in the diet. Constant feasting, frequent intake of high purine foods (e.g., animal offal, seafood) and alcohol abuse can all increase blood uric acid levels significantly and trigger gout. Drinking a bottle of beer can double the blood uric acid level, and eating a hot pot can be up to ten times more purine intake than an ordinary meal. So many gout patients will develop as soon as they go to a banquet. Summer is coming, the city has a lot of people like to drink beer to eat hot pot, the doctor here advises: drinking alcohol in moderation, to prevent the development of gout.