1.Why does gout occur?
Gout is caused by a metabolic disorder in the body, resulting in the production of a large amount of a metabolite called purine. Purine can be converted into uric acid and excreted in the urine. However, hyperuricemia occurs when uric acid increases beyond the body’s ability to excrete it or when the kidneys’ ability to excrete uric acid decreases. Long-term hyperuricemia mainly causes damage to the joints and kidneys, producing gout stones in the joints, kidneys, and skin, etc. Long-term hyperuricemia is also associated with hyperlipidemia, hyperglycemia, and coronary heart disease. The damage of high uric acid to the body is a long process, and many people just find high blood uric acid in the examination, but don’t feel any discomfort. However, as more and more uric acid salts accumulate in the body, coupled with a lack of attention to diet, they will show swollen and painful joints. Therefore, if a gout patient only stops the pain when the joints hurt, but does not thoroughly discharge the uric acid that has accumulated over the years, it will certainly lead to recurrent gout attacks.
2, gout patients which food can not eat or to eat less?
① legumes and vegetables: soybeans, lentils, purple cabbage, shiitake mushrooms, spinach, cabbage, wolfberries, string beans, peas, mushrooms, bamboo shoots, kelp, silver fungus, peanuts, cashew nuts, chestnuts, lotus seeds.
② meat: liver (pig liver, beef liver, chicken liver, duck liver, goose liver), intestine (pig intestine, beef intestine, chicken intestine, duck intestine, goose intestine), heart (pig heart, beef heart, chicken heart, duck heart, goose heart), belly and stomach (pig liver, beef liver, chicken stomach, duck stomach, goose stomach), kidney (pig kidney, beef kidney), lung brain, pancreas, dried meat, thick gravy, minced meat, etc.
③Aquatic seafood: fish (fish skin, fish eggs, dried fish, sardines, anchovies, mackerel, silver carp, eel, shark, striped bass, kissing fish, sea eel, dried bream, pomfret), shellfish (clams, oysters, clams, oysters, tamari, dried shellfish), shrimp (grass shrimp, golden hook shrimp, small shrimp, shrimp rice), sea cucumber.
④Other: yeast powder, various kinds of alcohol (especially beer).
3.How should gout be treated?
The treatment of gout is divided into two stages: the first stage is pain relief and anti-inflammation during acute attacks, and the second stage is uric acid reduction treatment during intermittent and chronic periods. Many patients only stay in the first stage of treatment, but in fact, the second stage of uric acid reduction is the most critical, but the most difficult to adhere to. Because this stage requires the use of uric acid-lowering drugs to control the uric acid level below 360μmol/L, the treatment time is longer, during which the dosage should be adjusted under the guidance of doctors, and the blood routine, liver and kidney function and other indicators should be reviewed regularly. Many patients are just afraid of trouble and can’t stick to it. Some of them think that they don’t need to take medicine if they don’t have pain, while some are worried about the side effects of long-term medicine.
4.What are the commonly used drugs to reduce uric acid?
Drugs that inhibit uric acid synthesis: Allopurinol tablets, commonly used dose is 0.1 3/day, serious side effect is hypersensitivity reaction leading to exfoliative dermatitis. Febuxostat tablets, commonly used in doses of 40-80 mg/day, can be used without dose adjustment in patients with mild to moderate hepatic or renal impairment.
Drugs to promote uric acid excretion: benzbromarone, commonly used in doses of 25-100 mg/day, is contraindicated in patients with moderate to severe renal impairment (glomerular filtration rate less than 20 ml/min) and in patients with kidney stones. Drink more water, more than 2000ml per day, to increase the urine volume to facilitate the excretion of uric acid. Also co-administer sodium bicarbonate tablets 3g/day to alkalize the urine (urine pH should be adjusted at 6.2~6.8) to promote uric acid dissolution and prevent urate crystals from depositing in the renal tubules. A small number of patients may develop severe liver function damage.
5.How to treat acute attack of gout?
Generally, colchicine, hormones and non-steroidal anti-inflammatory and analgesic drugs such as ibuprofen, Fotarine and Cilpro are used in acute attacks. Uric acid-lowering drugs are generally not used in the acute phase because they can trigger an acute attack of gout. If you are already using uric acid-lowering drugs when you have a gout attack, you do not need to stop using them, but only need to use them for acute gout attacks.
6.Does it mean that gout patients do not need treatment after their pain is relieved?
For gout patients, gout is only a superficial phenomenon, and high uric acid in the body is the root cause of the disease, and if uric acid is not high, naturally there will be no uric acid crystals, and there will be no clinical symptoms of gout. Therefore, when treating patients, clinicians must consider two aspects: the first is pain relief, and the second is uric acid reduction. Pain relief is certainly important, otherwise the patient is tormented by pain and cannot tolerate it. However, at the same time, we cannot ignore the fundamental problem, that is, the treatment of lowering uric acid. Only when the uric acid is lowered to normal, will the gout be treated well from the root.
7.Why did uric acid drop after we used uric acid-lowering drugs, but gout got worse instead?
Because for patients with long-term hyperuricemia, a large amount of uric acid is deposited in their muscles, skin, blood vessels, organs and bones, and when the uric acid in the blood is lowered, the uric acid in the tissues is bound to transfer to the blood, which then easily breaks the balance of uric acid concentration in the joints, and makes it easy to produce crystals in the joints and other tissues, thus inducing an acute gout attack. In addition, one aspect, as the concentration of uric acid in the blood and in the joints decreases, it makes the gout stones in the joints melt, and the large gout stones become small gout stones, and the small gout stones are more likely to fall off the cartilage of the joints, thus inducing joint inflammation and triggering gout. If this happens, we can appropriately combine small doses of colchicine or non-steroidal anti-inflammatory drugs in the process of long-term uric acid-lowering drugs.
8.Why is the blood uric acid not high during gout attack?
①The difference between central body temperature and peripheral joint temperature gradient is large, and there is a difference in the solubility of uric acid.
②The body is in a state of stress and secretes more adrenocorticotropic hormones to promote the excretion of serum uric acid, while the content of sodium urate in the distal joints is still relatively high.
(iii) The effect of having been treated with uric acid excreting drugs or corticosteroids. Some patients also have poor appetite in the state of pain, and as the amount of food eaten decreases, i.e., less raw uric acid is produced, and thus blood uric acid does not increase.