Gout is a disease caused by abnormal purine metabolism, characterized by the development of recurrent dysregulation of uric acid metabolism with severe localized arthritis, known as acute attacks of gouty arthritis, which eventually results in the deposition of sodium urate crystals in human tissues, causing complications such as joint deformity, stiffness, gouty surfaces and urinary tract stones, and renal hypofunction. Gout is often associated with manifestations of abdominal obesity, hyperlipidemia, hypertension, type 2 diabetes mellitus and cardiovascular disease.
Gout disease can occur at any age, most commonly in 40?50 years old, 90% of men; brain workers are mostly; the incidence rate in Europe and the United States is about 0.3%, China used to be relatively rare, but with the improvement of people’s standard of living, lifestyle changes, changes in diet structure, the incidence of hyperuricemia and gout is increasing, especially in middle-aged and elderly men, obesity, alcoholism, high purine diet, and It is more likely to develop in patients with chronic cardiovascular disease and diabetes mellitus. The disease has a tendency to increase year by year, and the age of first onset is progressively earlier. Since most of the gout disease can be controlled by diet, it is important to consider the following
1.The source of uric acid in the body
The main cause of the disease is high blood uric acid caused by the malfunction of uric acid metabolism. Uric acid is a metabolic product of the breakdown of purines and nucleic acids.
Purines are widely present in the nucleic acids of plant and animal tissues, and can be produced by the breakdown of nucleoproteins in the food consumed (mainly animal food).
Excessive uric acid can also be secondary to kidney disease or decreased uric acid excretion due to certain drugs, myeloproliferative disorders, and increased uric acid production due to chemotherapy for tumors.
The most important biochemical basis of gout is hyperuricemia. Normal adults produce about 750mg of uric acid daily, 80% of which is endogenous and 20% is exogenous, which enters the uric acid metabolic pool (about 1200mg). Problems in any of these links can lead to hyperuricemia.
2. Acute gouty arthritis is caused by high blood uric acid concentration in a supersaturated state, which leads to the deposition of sodium urate microcrystals in joint cartilage, periosteum and surrounding tissues, activating local mononuclear macrophages, inducing inflammatory cell infiltration such as neutrophils, secreting inflammatory factors and other series of inflammatory reactions, causing the onset of acute gouty arthritis. High purine diet, full meals, obesity, starvation, overexertion, trauma and surgery induce acute inflammation; gouty arthritis can often resolve on its own after an acute attack.
3, gout stone and chronic arthritis gout stone formation is a characteristic change of gout. When the blood uric acid level continues to exceed its saturation level, it can lead to the deposition of uric acid salt in the form of crystals in joint cartilage, bone, synovium, tendons and subcutaneous tissue, causing a chronic inflammatory response, surrounded by a large number of mononuclear phagocytes, forming epithelial granulomas. Repeated attacks of acute gouty arthritis may develop into multi-joint involvement and develop from localized swelling of joints in the acute phase to localized bone defects and joint deformities caused by gouty stones in the bone in the chronic phase.
4, the nephropathy of gout is clinically divided into three types.
(1) urate nephropathy: urate crystals deposited in the renal medulla and renal papillary interstitium, which are surrounded by encapsulated mononuclear phagocytes, is common clinically and generally manifests as interstitial renal-tubular inflammation, which is mild and progresses slowly.
(2) Urinary tract stones: uric acid crystals are deposited in the distal convoluted tubules and collecting ducts, leading to dilatation and atrophy of the proximal convoluted tubules and formation of renal stones.
(3) Acute obstructive nephropathy: A large amount of uric acid crystals are deposited in the renal interstitium and renal tubules, and the renal tubules are blocked causing oliguric renal failure.
5.Auxiliary examination
(1) Blood uric acid measurement.
(2) uric acid measurement: after 5 days of low purine diet, 24-hour uric acid excretion >600mg is the type of excessive uric acid production (about 10%); <300mg indicates the type of reduced uric acid excretion (about 90%). Under normal diet, 24-hour urinary uric acid excretion is differentiated by 800mg, and exceeding the above level is considered as increased uric acid production.
(3) Uric acid salt examination: polarized light microscopy shows needle-like or rod-like monosodium urate crystals.
(4) Imaging and ultrasonography.
6.The principles of dietary treatment of gout can be seen from the etiology, the dietary treatment of gout disease is nothing but to reduce the formation of exogenous uric acid and at the same time promote the excretion of uric acid in the body.
(1) Limit purine intake to less than 150 mg per day (600-1000 mg in normal diet), so foods containing very high purine, such as liver, kidney, pancreas, brain and other animal offal, gravy, meat loaf, sardines, etc. are completely prohibited.
(2) limit the total caloric energy in general gout patients are more obese, so weight control, the total daily caloric energy should be reduced by 10%-15% than normal, but the caloric energy should be gradually reduced to avoid the acute attack of gout disease due to fat burning caused by excessive weight loss of ketoacidosis
(3) Limit fat because it has the effect of hindering the excretion of uric acid by the kidneys, so it should be limited.
(4) Rational choice of protein Generally speaking, foods with high protein content also have higher purine content, therefore, special attention should be paid when choosing protein. Plant proteins should be the mainstay when the disease is severe. Milk and eggs do not have a complex cell structure and do not contain nucleoproteins, so they are not a source of purines and can be chosen at will by those without other contraindications.
(5) Increase the intake of vitamin B and C. A large amount of vitamin B and C can promote the dissolution of uric acid salts accumulated in tissues. In addition, uric acid is easy to precipitate crystals in an acidic environment, but easy to dissolve in an alkaline environment, so you should eat more alkaline foods, such as vegetables and fruits, and should increase the amount of water drunk daily, preferably pure water containing less inorganic salts, in order to reduce the possibility of uric acid salt crystals.
(6) Prohibit foods that excite the nervous system, such as wine, strong tea, coffee and all spicy condiments.
7. Dietary arrangements for the acute attack of gout disease
(1) During the 2-3 days of the acute period, the patient often loses appetite and has abdominal discomfort. Recipes should be arranged according to the condition and appetite, using foods with little or no purine content, and prohibiting foods with very high purine content.
(3) Give sufficient milk and eggs to provide the required protein and use fine foods such as refined rice and refined bread.
(3) Limit fat so as not to interfere with the elimination of uric acid.
(4) Try to encourage patients to drink more than 3,000 ml of water daily to facilitate the elimination of uric acid.
(5) Alcohol and other stimulating drinks and condiments are prohibited. Sodium carbonate drinks can be consumed between meals to relieve gastrointestinal discomfort and create an alkaline environment to facilitate the elimination of uric acid and reduce the formation of stones.
(6) Vegetables can be consumed 1-1.5 kg or fruits 4-5 times a day. Adopt a cyclical raw plant diet, such as “cucumber day”, “watermelon day”, “apple day”, “salad day “etc. This is done 2 times a week at 3 days intervals.
8.Classification of purine content in common foods
(1) Foods with little or basically no purine content
Eggs, all kinds of fats and oils, all kinds of fruits, all kinds of dried fruits, sugar and candy and many kinds of vegetables.
(2) Foods with less purine content, with purine content not exceeding 75 mg per 100 g of edible portion
Lobster, cauliflower, beans, spinach, mushroom, cereal, eel, tuna, peas, chicken, crab, ham, lobster, lamb, oyster, tripe, beef soup.
(3) Foods with high purine content, not exceeding 75-150 mg per 100 g of edible portion
Carp, cod, halibut, trout, shellfish, beef, beef tongue, pork, lamb, turkey, duck, goose, pigeon, mallard, quail, chicken soup, broth, liver soup, lentils.
(4) Purine content is extremely high, the purine content per 100 grams of edible parts does not exceed 150-1000 mg of food anchovies 363 mg, beef loin 200 mg, brain flower 195 mg, roe and crab yolk are more than 500 mg. Pancreatic 825 mg, anchovy 363 mg, beef loin 200 mg, brain flower 195 mg, fish roe and crabmeat all exceed 500 mg.