As people's life pace accelerates and their dietary habits change, gout is very common in diagnosis and treatment. Let's take a look at the causes, pathogenesis, clinical manifestations of gout, diagnosis and treatment, and dietary precautions.
01 Concept
02 uric acid production process
uric acid is the terminal product of purine metabolism in the human body. The synthesis of uric acid is jointly participated by the human body's amino acid , carbon dioxide , ribose phosphate and adenosine triphosphate (ATP), and adenine is formed through the action of certain enzymes in the human body, which then produces uric acid under the action of xanthine oxidase or hypoxanthine converting enzyme.
03 The relationship between gout and hyperuricemia
Hyperuricemia does not equal gout! Hyperuricemia is the basis of gout. When the uric acid level in the blood is relatively high, urate crystals will be produced. Urate crystals are deposited in the joints, which can cause local inflammatory reactions, destroy local tissues, and induce gout.
, but Not every patient with hyperuricemia will have gout , and some patients will never show up in their lifetime. The onset of gout is closely related to uric acid levels. The higher the uric acid and the longer the duration, the greater the risk of gout.
So when you are detected to have hyperuricemia, you need to pay more attention to your daily diet and life, and don’t let hyperuricemia continue to worsen, which will turn into gout.
04 Clinical stage of gout
Gout manifests as an intermittent onset of severe painful arthritis (gout attacks), which is caused by the innate immune response to deposited monosodium urate crystals.
▸ Features: Pain, swelling, burning, beating, etc.
One or more joints suddenly have severe pain, swelling, redness and tenderness, which can occur in joints or tissues around the joints (for example, burses, tendons and tendons). Pain includes tingling, gnawing, burning or thrusting. One or more of the affected joints become swollen, tender, warm and red. Over time, it may cause bone and soft tissue damage and joint deformities.
Gout is most common to affect the big toe, but other joints in may also be affected, including:
Other joints on the feet, ankles, knees, elbows, wrists, fingers, and kidneys.
gout attacks are mainly divided into five stages, namely asymptomatic hyperuricemia, acute gout arthritis, gout intermittent period, chronic arthritis, and gout kidney disease period.
Asymptomatic hyperuricemia phase is the early stage of gout. In addition to the elevated blood uric acid level, patients in this stage have no symptoms and signs of gout, but about 20% of patients will eventually develop gout. The focus of this treatment is to control blood uric acid , avoiding the precipitation of crystals when the blood uric acid level reaches or exceeds the saturation, causing an acute attack of gout.
As people's life pace accelerates and their dietary habits change, gout is very common in diagnosis and treatment. Let's take a look at the causes, pathogenesis, clinical manifestations of gout, diagnosis and treatment, and dietary precautions. 01 Concept
02 uric acid production process
uric acid is the terminal product of purine metabolism in the human body. The synthesis of uric acid is jointly participated by the human body's amino acid , carbon dioxide , ribose phosphate and adenosine triphosphate (ATP), and adenine is formed through the action of certain enzymes in the human body, which then produces uric acid under the action of xanthine oxidase or hypoxanthine converting enzyme.
03 The relationship between gout and hyperuricemia
Hyperuricemia does not equal gout! Hyperuricemia is the basis of gout. When the uric acid level in the blood is relatively high, urate crystals will be produced. Urate crystals are deposited in the joints, which can cause local inflammatory reactions, destroy local tissues, and induce gout.
, but Not every patient with hyperuricemia will have gout , and some patients will never show up in their lifetime. The onset of gout is closely related to uric acid levels. The higher the uric acid and the longer the duration, the greater the risk of gout.
So when you are detected to have hyperuricemia, you need to pay more attention to your daily diet and life, and don’t let hyperuricemia continue to worsen, which will turn into gout.
04 Clinical stage of gout
Gout manifests as an intermittent onset of severe painful arthritis (gout attacks), which is caused by the innate immune response to deposited monosodium urate crystals.
▸ Features: Pain, swelling, burning, beating, etc.
One or more joints suddenly have severe pain, swelling, redness and tenderness, which can occur in joints or tissues around the joints (for example, burses, tendons and tendons). Pain includes tingling, gnawing, burning or thrusting. One or more of the affected joints become swollen, tender, warm and red. Over time, it may cause bone and soft tissue damage and joint deformities.
Gout is most common to affect the big toe, but other joints in may also be affected, including:
Other joints on the feet, ankles, knees, elbows, wrists, fingers, and kidneys.
gout attacks are mainly divided into five stages, namely asymptomatic hyperuricemia, acute gout arthritis, gout intermittent period, chronic arthritis, and gout kidney disease period.
Asymptomatic hyperuricemia phase is the early stage of gout. In addition to the elevated blood uric acid level, patients in this stage have no symptoms and signs of gout, but about 20% of patients will eventually develop gout. The focus of this treatment is to control blood uric acid , avoiding the precipitation of crystals when the blood uric acid level reaches or exceeds the saturation, causing an acute attack of gout.
Initiative causes: drinking alcohol with a lot of food, eating high-purine foods, overwork, damage, etc.
Attack characteristics: onset is acute, often onset at midnight, often without signs
Pain site: The first metatarsophalal joint is the most common
Duration: Most of them relieve themselves, usually no more than 2 weeks
Systemic manifestations: low fever, fatigue, palpitations , etc.
refers to the interval between two gout. During this period, the patient had obvious symptoms of gout, such as redness, swelling, fever, tenderness, etc. Blood collection tests will detect hyperuricemia. The interval can last for months or years. When encountering triggering factors, such as alcohol consumption, overeating, and excessive fatigue, it can lead to acute attacks of gout.
As the disease progresses, the interval period will gradually shorten. If preventive treatment is not carried out, the number of attacks will increase every year, the duration of attack will be prolonged, and even the attack will not be completely relieved after the attack, and the involved joints will also increase accordingly. The slower the onset, the worse the symptoms, the more joints accumulated, the slower the relief.
, chronic gout stage
also known as chronic gout lesions. gout is a characteristic change during this period. Repeated deposition of urate causes chronic foreign body-like reactions in local tissues. The sediment is surrounded by monocytes, epithelial cells, and macrophages, and fibrous tissues proliferate to form nodules, , called gout stone.
Common sites of subcutaneous gout are the auricle, around the recurrent joints, as well as the eagle beak, Achilles tendon, patellar bursal, etc. The appearance is yellow-white growths of different sizes with different sizes under the skin. After rupture, white powder or paste is discharged, which is not easy to heal. Chronic gout arthritis is the deposit of a large amount of MSU crystals in the joints, which leads to the formation of gout, manifested as continuous joint swelling, tenderness, deformity and functional disorders, which can cause damage to joint bones, fibrosis of the surrounding tissues of the joints, secondary degenerative changes, etc.
, gouty nephropathy stage
clinically, about 1/3 of patients will have symptoms of kidney damage, and their manifestations are mainly as follows:
05 When will gout patients start treatment
According to my country's "Guidelines for Diagnosis and Treatment of Hyperuric Acidemia and Gout", those who meet one of the following conditions should be given uric acid-lowering drugs:
If the risk factors for cardiovascular disease or cardiovascular disease are not combined, the blood uric acid 540umol/ L, uric acid-lowering drugs should also be given;
For men who have no cardiovascular risk factors and have blood uric acid between 420 and 540umol/L (or women between 360 and 540umol/L) who have simple hyperuricemia, lifestyle intervention should be given for 3 to 6 months. If blood uric acid is still high, uric acid-lowering drugs should be initiated.
06 Common medicines for gout (endocrine time)
colchicine
is metabolized in the liver meridian P-glycoprotein and cell color P450 (CYP)3A4, mainly excreted through the bile tract, about 20% from the kidney. Gout attacks The most obvious effect is within 24 hours.
Common dosage: colchicine first dose 1 mg, add 0.5 mg after 1 h, and change to 0.5 mg qd or bid after 12 h until the symptoms are relieved.
ACR Guidelines Recommended:
- without the above gout symptoms, small dose of colchicine is recommended to treat for at least 6 months;
- without gout stone, small dose of colchicine is recommended to treat for 3 months after blood uric acid level meets the standard;
- with gout stone, small dose of colchicine is still needed after blood uric acid meets the standard 6 Months;
Note: Patients with renal insufficiency are advised to adjust the dosage of colchicine according to eGFR.
Table 1 Adjust the dosage of colchicine
Precautions: Nausea, vomiting, diarrhea, abdominal pain and other gastrointestinal reactions, stop the medication immediately if symptoms appear. At the same time, liver and kidney damage and myelosuppression may occur. Regular monitoring of liver and kidney function, blood is routinely .
Nonsteroidal anti-inflammatory drug (NSAID)
NSAID mainly inhibits the synthesis of prostaglandins by inhibiting the activity of cyclooxygenase (COX), thereby blocking the inflammatory response process, and exerting the anti-inflammatory and analgesic effects.
Table 2 List of drugs for commonly used treatment of gout
Recommended Early sufficient and full treatment course Until acute gout arthritis is completely relieved, usually takes several days to 2 weeks.
NSAIDs may cause renal ischemia to induce and aggravate acute and chronic renal insufficiency. It is recommended to use NSAIDs with caution or disable NSAIDs in patients with gout combined with renal insufficiency.
- eGFR 60 mL•min-1 •(1.73m2)-1 is not recommended for long-range use;
- eGFR 30 mL•min-1 •(1.73m2)-1 is disabled.
Notes: Pay attention to gastrointestinal risks such as gastrointestinal tract ulcers, bleeding, perforation, etc.; it may increase the risk of cardiovascular events, and be cautious when applying it to high-risk groups.
glucocorticoid
European and American guidelines mostly recommend glucocorticoids as first-line anti-inflammatory and analgesic drugs.
Studies show that patients with long-term use of glucocorticoids (prednisone 15 mg/d or more, for more than 3 months of continuous use) have a 5-fold increase in the risk of gout stones. The expert group of my country recommends glucocorticoids as a second-line analgesic drug. Only when the acute attack of gout involves multiple joints, large joints or combined with systemic symptoms are recommended for systemic glucocorticoid treatment.
How to use:
- prednisone 0.5 mg /(kg • d), course 5 to 10 days, stop the medication directly; or 0.5 mg/(kg • d), course 2 to 5 days, then gradually reduce the dose, stop the medication 7 to 10 days.
- methylprednisolone Intramuscular or intravenous injection of methylprednisolone, the starting dose is 0.5 ~ 2 mg/kg.
- dexamethasone 5 ~ 10 mg of intravenous infusion, and stop the medication for 3 ~ 5 days.
Table 3 Glucocorticoid classification
Notes: may have adverse reactions such as hypertension , hyperglycemia , hyperlipidemia, infection, gastrointestinal risk, water and sodium retention, osteoporosis , etc.
For severe acute gout attacks (pain VAS ≥7), polyarthritis or involvement of ≥2 large joints, 2 or more analgesics are recommended to treat, including colchicine combined with NSAID, colchicine combined with oral glucocorticoids, and articular glucocorticoid injection and any other form, but oral NSAID combined with systemic glucocorticoids are not recommended.
Drugs for lowering uric acid in patients with hyperuricemia and gout
When choosing a drug for lowering uric acid, the classification of hyperuricemia, the indications and contraindications of the drug should be comprehensively considered.
Hyperuricemia was classified clinically according to the 24-h uric acid excretion (UUE) and renal uric acid excretion fraction (FEUA).
Table 4 Clinical classification of hyperuricemia
xanthine oxidase inhibitor is a first-line drug for uric acid reduction treatment in patients with hyperuricemia and gout. It is suitable for patients with uric acid production polytype. After oral administration,
Usage: The initial dose for adults is 50~100 mg/d, and the blood uric acid level is measured once every 4 weeks. Patients who do not meet the standards can increase by 50~100 mg each time, and the maximum dose is 800 mg/d.
When renal insufficiency is easily accumulated in the body, the starting and maximum dose of the drug can be adjusted reasonably according to the renal function stage.
Table 5 Allopurine dose for patients with different renal functions
Precautions: can cause skin allergic reactions, and in severe cases, fatal exfoliation dermatitis and other hypersensitivity syndromes may occur. Before taking allopurinol treatment, renal, liver, and blood routines should be checked. If conditions permit, screens for HLA-B∗5801 gene . It is not recommended for those who are positive for genes. Other adverse reactions include inducing gout attacks, liver function abnormalities, leukopenia, thrombocytopenia, thrombocytopenia, drug heat , diarrhea, rash, etc.
specific xanthine oxidase inhibitor is a first-line uric acid-lowering drug for gout patients and is suitable for patients with increased uric acid production.
This product has a bioavailability in the intestine after oral administration, and a plasma protein binding rate in the blood is 99.2%, mainly in the liver metabolization, and a half-life of 5 to 8 hours. The metabolites in the liver are inactive substances, 49% are excreted through the kidneys, and 45% are excreted through the feces, which are dual-channel excretion drugs.
Recommendation eGFR 30 mL•min-1 •(1.73m2)-1 for uric acid-lowering drugs. However, it is not recommended for the treatment of asymptomatic hyperuricemia.
Usage: The initial dose is 20 mg/d. After 2 to 4 weeks, the blood uric acid level still does not meet the standard, which can increase by 20 mg/d, and the maximum dose is 80 mg/d. For patients with stage 4 to 5 CKD, the recommended starting dose is 20 mg/d and the maximum dose is 40 mg/d.
Note: febulista can cause liver function damage. If it exceeds the upper limit of the normal reference value by 3 times, the dosage or stop the medication as appropriate. In the elderly with cardiovascular and cerebrovascular diseases, they should be used with caution and pay close attention to cardiovascular events.
inhibits reabsorption of renal proximal tubules urate transporter 1 (URAT-1) to promote uric acid excretion. Especially suitable for patients with reduced renal uric acid excretion.
Usage: The initial dose for adults is 25 mg/d. After 2 to 4 weeks, the blood uric acid level still does not meet the standard, which can increase by 25 mg/d, and the maximum dose is 100 mg/d.
benbromalone is absorbed 50% of its metabolites, mainly through the biliary tract excretion, and has a good uric acid-lowering effect in patients with mild and moderate renal insufficiency and does not lead to drug accumulation and further damage to the kidneys. For CKD periods 4 to 5 [eGFR 30 mL•min-1 •(1.73m2)-1] Patients do not recommend using
Precautions:
- Precautions for pregnant women, pregnant women and breastfeeding women;
- Hydroneal , polycystic kidney , sponge kidney, etc. cause urine elimination Diseases that are not affected are prohibited; large-scale production or excessive excretion of uric acid caused by abnormal purine metabolic enzymes, blood diseases or sharp weight loss are relatively contraindicated; patients with uriconephrolithiasis are prohibited; patients with uriconephrolithiasis are closely monitored during use, and benzylbromalone should be used with caution in patients with chronic liver disease.
At the same time, it should be noted that:
. Alkaline urine drug
When patients with hyperuricemia and gout have a pH of 6.0, especially when taking uric acid excretion drugs, it is recommended to take citric acid preparations and sodium bicarbonate to alkalize the urine to maintain the pH of morning urine at 6.2~6.9, to reduce the risk of uric acid kidney stones and facilitate the dissolution of uric acid kidney stones.
(1) Sodium bicarbonate
is suitable for patients with chronic renal insufficiency and metabolic acidosis
(2) Citrate preparation
is mainly used in patients with uricidal kidney stones, cystine stones and
07 Misunderstandings about gout
Misunderstanding 1: Hyperuricemia = gout
Outpatient clinics often come to the clinic and say that their physical examination found increased blood uric acid. Is it gout? In fact, hyperuricemia represents the level of uric acid metabolism in the body. Blood uric acid in men > 420 μmol/L or above, and women > 360 μmol/L or above, which represents hyperuricemia.
But gout refers to crystalline arthritis caused by the deposition of urate crystals in the joints, which is directly related to hyperuricemia, but gout is also accompanied by the manifestations of onset joint redness, swelling, heat and pain. About 10% of patients with hyperuricemia develop gout. Therefore, hyperuricemia and gout cannot be completely equated.
Misconception 2: Gout is an "old man's disease"
With the improvement of national living conditions, the epidemic of hyperuricemia and gout is showing an increasing trend year by year, and the patient population is getting younger and younger. Gout patients are not all elderly men, and young people and postmenopausal women also suffer from gout. Female women rarely suffer from primary gout during the reproductive period, but secondary gout can occur at all ages and women also suffer from illness.
Overall, the prevalence of hyperuricemia and gout increases with age, with men higher than women, cities higher than rural areas, and coastal areas higher than inland.
Misconception 3: Gout is joint pain
Gout can not only cause painful arthritis, but also cause gout stones, uric nephropathy , gout urinary stones, hyperuricemia, arteriosclerosis, etc.; gout is often accompanied by hypertension , diabetes, coronary heart disease , dyslipidemia, arteriosclerosis, etc.; gout is involved in the occurrence and progression of diseases such as diabetes, arteriosclerosis, hypertension, and heart failure .
Misconception 4: If you don’t hurt gout, it’s not a disease
Asymptomatic hyperuricemia, gout remission period, intermittent period, there may be no symptoms or the symptoms are not obvious. However, hyperuricemia can still promote the recurrence of gout and aggravate Gout nephropathy , uric stones, hypertension, coronary heart disease, arteriosclerosis, diabetes and other diseases. Even if it is "unpainful gout", it requires non-drug and drug treatment to reduce uric acid.
Misconception 5: Uric acid must be high during gout attack
Uric acid level may not increase during gout. In acute attacks of gout, uric acid will be deposited at the joints and temporarily reduced as an acute phase reactant. At the same time, renal excretion of uric acid increases in acute stage. In addition, some gout patients have paused some factors that cause hyperuricemia during the acute attack, including diuretics, weight loss or alcohol withdrawal.
Misconception 6: Drug treatment is needed only during the attack of gout
Outpatient clinics often have gout patients taking allopurinol or benbromalon for gout during the attack of joint redness, swelling, heat and pain. The symptoms worsen.
There are two misunderstandings here. On the one hand, during the acute attack of gout, you need to take anti-inflammatory and pain-relieving drugs, colchicine or hormones and other drugs to control the attack of redness, swelling, heat and pain in the joints, rather than taking uric acid-lowering drugs directly.
On the contrary, during the acute attack period, taking uric acid-lowering drugs aggravate uric acid fluctuations in the body, which will lead to worsening joint swelling and pain or difficult to control. On the other hand, uric acid-lowering drugs require long-term use to control uric acid levels to reduce the onset of repeated acute arthritis.
Misconception 7: After the gout attack is relieved, it is cured.
Gout arthritis has a characteristic, which is that it can occur repeatedly. Current medical technology cannot completely cure gout. It is necessary to control blood uric acid in the normal range for a long time to avoid risk factors and prevent recurrence of gout.
Misconception 8: The lower the blood uric acid level, the better
The lower the blood uric acid level, the better. Uric acid is an important biochemical substance in the human body and has an important physiological effect. Appropriate blood uric acid concentration is conducive to antioxidant, balance immune function, and increase the ability to fight infection in the body. Too low blood uric acid is related to many neurological diseases.
Misconception 9: When gout occurs, you should take uric acid-lowering drugs to treat
When gout is acute, you should not use uric acid-lowering drugs. If you just start to treat uric acid-lowering drugs, you also need to temporarily stop taking uric acid-lowering drugs. For long-term use, you can decide specifically based on the condition and dosage to avoid aggravate gout arthritis and prevent metastatic gout. Uric acid-lowering drugs should start from a small dose after the acute attack of gout is relieved, and the dose should be gradually increased until the blood uric acid level is normal and the treatment is maintained at a low dose.
Misconception 10: Avoiding food means not eating meat, while eating vegetables and fruits casually
Diet control includes alcohol restriction, low-purine diet and drinking more water.
needs to strictly limit various alcoholic beverages, especially beer and distilled liquor (white wine). It is recommended that the overall alcohol consumption is ≤2 alcohol units/day for men and ≤1 alcohol units/day for women. (One alcohol unit is approximately 14g pure alcohol, equivalent to 145ml of 12° red wine, 497ml of 3.5° beer, and 43ml of 40° distilled liquor).
The diet should be balanced, and the daily total calorie intake should be restricted, and the low-purine diet should be mainly used to restrict the intake of high-purine foods such as animal offal, seafood and meat. Encourage foods such as fresh vegetables, low-fat or skim milk, eggs, and other foods, and consume beans and soy products in moderation.
Some vegetables contain purine , including lettuce, spinach, mushrooms, cauliflower, etc. It is currently believed that there is no obvious correlation with hyperuricemia and gout attacks. In addition, establish good eating habits and avoid overeating or eating a lot of meat within a meal. It is recommended to cook seafood, meat and plant-based foods with high purine to reduce the purine content in the food.
Drinking a lot of water can shorten the onset of gout and relieve symptoms. It is recommended that people with normal heart and kidney function drink more water and maintain a daily urine volume of 2000~3000ml. Avoid beverages with high fructose (such as orange juice, apple juice, etc.) and sugary soft drinks (Cola, etc.). It can be replaced with fresh fruits with low fructose, such as cherries, strawberry , pineapple, peach, etc. At the same time, it is necessary to properly alkalize the urine to maintain the urine pH between 6.2 and 6.9, which is conducive to the dissolution of urate crystals and excretion from the urine.
Misconception 11: The greater the exercise intensity, the better
Rgitative exercise can reduce the number of gout attacks, but the greater the intensity, the better. You should insist on moderate exercise, and you should reduce your activity during the acute attack of gout and braking is required if necessary. In terms of exercise intensity and time, it is recommended to perform moderate-intensity aerobic exercise at least 150 minutes (30 minutes/d, 5 days/w) per week. Medium intensity refers to the range of heart rate = (220-age) × (50~70%) times/minute during exercise.
Note: Strong exercise or sudden cold can induce acute attacks of gout.
In addition to diet control and proper exercise, lifestyle intervention also includes weight control and smoking cessation.
Misconception 12: If uric acid drops to normal, it can be
Simple hyperuricemia patients generally require blood uric acid to be controlled within 420 μmol/L; if gout attacks, blood uric acid is generally required to be controlled within 360 μmol/L; if gout patients are also associated with gout stones, blood uric acid is required to be controlled within 300 μmol/L.
08 How should we pay attention to
alcohol can significantly increase the risk of gout recurrence, especially white wine, beer, and rice wine. The red wine may be slightly better, and it is still controversial.
As for why drinking alcohol is closely related to uric acid, its mechanism may be because ethanol in alcohol will quickly consume energy ATP during the metabolism process, which increases the production of uric acid; and the acetic acid produced by ethanol metabolism can inhibit the kidney's excretion of uric acid.
Because the beverage contains a lot of fructose, the intake of a large amount of fructose will inhibit the excretion of blood uric acid from the kidneys, causing uric acid to accumulate in the body and cause hyperuricemia.
Therefore, it is best for gout kidney friends not to drink beverages, and it is better to use white water, tea, sugar-free soda water, etc. as daily drinks.
The main causes of gout are purine metabolism disorders and (or) abnormal uric acid excretion in the body, and the intake of high-purine foods is often one of the important factors in the onset of gout.
Heart, liver, kidney, intestine and other animals contain super high purines, so Kids with high uric acid should be avoided as much as possible.
. Stay away from Dabu Soup
Because after the meat is cooked, many purines are dissolved in the soup, so it is best to avoid fish soup, broth, chicken soup, and hot pot soup. Gout patients can choose to eat only meat and not drink soup.
ACR Guidelines Recommended:
- without the above gout symptoms, small dose of colchicine is recommended to treat for at least 6 months;
- without gout stone, small dose of colchicine is recommended to treat for 3 months after blood uric acid level meets the standard;
- with gout stone, small dose of colchicine is still needed after blood uric acid meets the standard 6 Months;
Note: Patients with renal insufficiency are advised to adjust the dosage of colchicine according to eGFR.
Table 1 Adjust the dosage of colchicine
Precautions: Nausea, vomiting, diarrhea, abdominal pain and other gastrointestinal reactions, stop the medication immediately if symptoms appear. At the same time, liver and kidney damage and myelosuppression may occur. Regular monitoring of liver and kidney function, blood is routinely .
Nonsteroidal anti-inflammatory drug (NSAID)
NSAID mainly inhibits the synthesis of prostaglandins by inhibiting the activity of cyclooxygenase (COX), thereby blocking the inflammatory response process, and exerting the anti-inflammatory and analgesic effects.
Table 2 List of drugs for commonly used treatment of gout
Recommended Early sufficient and full treatment course Until acute gout arthritis is completely relieved, usually takes several days to 2 weeks.
NSAIDs may cause renal ischemia to induce and aggravate acute and chronic renal insufficiency. It is recommended to use NSAIDs with caution or disable NSAIDs in patients with gout combined with renal insufficiency.
- eGFR 60 mL•min-1 •(1.73m2)-1 is not recommended for long-range use;
- eGFR 30 mL•min-1 •(1.73m2)-1 is disabled.
Notes: Pay attention to gastrointestinal risks such as gastrointestinal tract ulcers, bleeding, perforation, etc.; it may increase the risk of cardiovascular events, and be cautious when applying it to high-risk groups.
glucocorticoid
European and American guidelines mostly recommend glucocorticoids as first-line anti-inflammatory and analgesic drugs.
Studies show that patients with long-term use of glucocorticoids (prednisone 15 mg/d or more, for more than 3 months of continuous use) have a 5-fold increase in the risk of gout stones. The expert group of my country recommends glucocorticoids as a second-line analgesic drug. Only when the acute attack of gout involves multiple joints, large joints or combined with systemic symptoms are recommended for systemic glucocorticoid treatment.
How to use:
- prednisone 0.5 mg /(kg • d), course 5 to 10 days, stop the medication directly; or 0.5 mg/(kg • d), course 2 to 5 days, then gradually reduce the dose, stop the medication 7 to 10 days.
- methylprednisolone Intramuscular or intravenous injection of methylprednisolone, the starting dose is 0.5 ~ 2 mg/kg.
- dexamethasone 5 ~ 10 mg of intravenous infusion, and stop the medication for 3 ~ 5 days.
Table 3 Glucocorticoid classification
Notes: may have adverse reactions such as hypertension , hyperglycemia , hyperlipidemia, infection, gastrointestinal risk, water and sodium retention, osteoporosis , etc.
For severe acute gout attacks (pain VAS ≥7), polyarthritis or involvement of ≥2 large joints, 2 or more analgesics are recommended to treat, including colchicine combined with NSAID, colchicine combined with oral glucocorticoids, and articular glucocorticoid injection and any other form, but oral NSAID combined with systemic glucocorticoids are not recommended.
Drugs for lowering uric acid in patients with hyperuricemia and gout
When choosing a drug for lowering uric acid, the classification of hyperuricemia, the indications and contraindications of the drug should be comprehensively considered.
Hyperuricemia was classified clinically according to the 24-h uric acid excretion (UUE) and renal uric acid excretion fraction (FEUA).
Table 4 Clinical classification of hyperuricemia
xanthine oxidase inhibitor is a first-line drug for uric acid reduction treatment in patients with hyperuricemia and gout. It is suitable for patients with uric acid production polytype. After oral administration,
Usage: The initial dose for adults is 50~100 mg/d, and the blood uric acid level is measured once every 4 weeks. Patients who do not meet the standards can increase by 50~100 mg each time, and the maximum dose is 800 mg/d.
When renal insufficiency is easily accumulated in the body, the starting and maximum dose of the drug can be adjusted reasonably according to the renal function stage.
Table 5 Allopurine dose for patients with different renal functions
Precautions: can cause skin allergic reactions, and in severe cases, fatal exfoliation dermatitis and other hypersensitivity syndromes may occur. Before taking allopurinol treatment, renal, liver, and blood routines should be checked. If conditions permit, screens for HLA-B∗5801 gene . It is not recommended for those who are positive for genes. Other adverse reactions include inducing gout attacks, liver function abnormalities, leukopenia, thrombocytopenia, thrombocytopenia, drug heat , diarrhea, rash, etc.
specific xanthine oxidase inhibitor is a first-line uric acid-lowering drug for gout patients and is suitable for patients with increased uric acid production.
This product has a bioavailability in the intestine after oral administration, and a plasma protein binding rate in the blood is 99.2%, mainly in the liver metabolization, and a half-life of 5 to 8 hours. The metabolites in the liver are inactive substances, 49% are excreted through the kidneys, and 45% are excreted through the feces, which are dual-channel excretion drugs.
Recommendation eGFR 30 mL•min-1 •(1.73m2)-1 for uric acid-lowering drugs. However, it is not recommended for the treatment of asymptomatic hyperuricemia.
Usage: The initial dose is 20 mg/d. After 2 to 4 weeks, the blood uric acid level still does not meet the standard, which can increase by 20 mg/d, and the maximum dose is 80 mg/d. For patients with stage 4 to 5 CKD, the recommended starting dose is 20 mg/d and the maximum dose is 40 mg/d.
Note: febulista can cause liver function damage. If it exceeds the upper limit of the normal reference value by 3 times, the dosage or stop the medication as appropriate. In the elderly with cardiovascular and cerebrovascular diseases, they should be used with caution and pay close attention to cardiovascular events.
inhibits reabsorption of renal proximal tubules urate transporter 1 (URAT-1) to promote uric acid excretion. Especially suitable for patients with reduced renal uric acid excretion.
Usage: The initial dose for adults is 25 mg/d. After 2 to 4 weeks, the blood uric acid level still does not meet the standard, which can increase by 25 mg/d, and the maximum dose is 100 mg/d.
benbromalone is absorbed 50% of its metabolites, mainly through the biliary tract excretion, and has a good uric acid-lowering effect in patients with mild and moderate renal insufficiency and does not lead to drug accumulation and further damage to the kidneys. For CKD periods 4 to 5 [eGFR 30 mL•min-1 •(1.73m2)-1] Patients do not recommend using
Precautions:
- Precautions for pregnant women, pregnant women and breastfeeding women;
- Hydroneal , polycystic kidney , sponge kidney, etc. cause urine elimination Diseases that are not affected are prohibited; large-scale production or excessive excretion of uric acid caused by abnormal purine metabolic enzymes, blood diseases or sharp weight loss are relatively contraindicated; patients with uriconephrolithiasis are prohibited; patients with uriconephrolithiasis are closely monitored during use, and benzylbromalone should be used with caution in patients with chronic liver disease.
At the same time, it should be noted that:
. Alkaline urine drug
When patients with hyperuricemia and gout have a pH of 6.0, especially when taking uric acid excretion drugs, it is recommended to take citric acid preparations and sodium bicarbonate to alkalize the urine to maintain the pH of morning urine at 6.2~6.9, to reduce the risk of uric acid kidney stones and facilitate the dissolution of uric acid kidney stones.
(1) Sodium bicarbonate
is suitable for patients with chronic renal insufficiency and metabolic acidosis
(2) Citrate preparation
is mainly used in patients with uricidal kidney stones, cystine stones and
07 Misunderstandings about gout
Misunderstanding 1: Hyperuricemia = gout
Outpatient clinics often come to the clinic and say that their physical examination found increased blood uric acid. Is it gout? In fact, hyperuricemia represents the level of uric acid metabolism in the body. Blood uric acid in men > 420 μmol/L or above, and women > 360 μmol/L or above, which represents hyperuricemia.
But gout refers to crystalline arthritis caused by the deposition of urate crystals in the joints, which is directly related to hyperuricemia, but gout is also accompanied by the manifestations of onset joint redness, swelling, heat and pain. About 10% of patients with hyperuricemia develop gout. Therefore, hyperuricemia and gout cannot be completely equated.
Misconception 2: Gout is an "old man's disease"
With the improvement of national living conditions, the epidemic of hyperuricemia and gout is showing an increasing trend year by year, and the patient population is getting younger and younger. Gout patients are not all elderly men, and young people and postmenopausal women also suffer from gout. Female women rarely suffer from primary gout during the reproductive period, but secondary gout can occur at all ages and women also suffer from illness.
Overall, the prevalence of hyperuricemia and gout increases with age, with men higher than women, cities higher than rural areas, and coastal areas higher than inland.
Misconception 3: Gout is joint pain
Gout can not only cause painful arthritis, but also cause gout stones, uric nephropathy , gout urinary stones, hyperuricemia, arteriosclerosis, etc.; gout is often accompanied by hypertension , diabetes, coronary heart disease , dyslipidemia, arteriosclerosis, etc.; gout is involved in the occurrence and progression of diseases such as diabetes, arteriosclerosis, hypertension, and heart failure .
Misconception 4: If you don’t hurt gout, it’s not a disease
Asymptomatic hyperuricemia, gout remission period, intermittent period, there may be no symptoms or the symptoms are not obvious. However, hyperuricemia can still promote the recurrence of gout and aggravate Gout nephropathy , uric stones, hypertension, coronary heart disease, arteriosclerosis, diabetes and other diseases. Even if it is "unpainful gout", it requires non-drug and drug treatment to reduce uric acid.
Misconception 5: Uric acid must be high during gout attack
Uric acid level may not increase during gout. In acute attacks of gout, uric acid will be deposited at the joints and temporarily reduced as an acute phase reactant. At the same time, renal excretion of uric acid increases in acute stage. In addition, some gout patients have paused some factors that cause hyperuricemia during the acute attack, including diuretics, weight loss or alcohol withdrawal.
Misconception 6: Drug treatment is needed only during the attack of gout
Outpatient clinics often have gout patients taking allopurinol or benbromalon for gout during the attack of joint redness, swelling, heat and pain. The symptoms worsen.
There are two misunderstandings here. On the one hand, during the acute attack of gout, you need to take anti-inflammatory and pain-relieving drugs, colchicine or hormones and other drugs to control the attack of redness, swelling, heat and pain in the joints, rather than taking uric acid-lowering drugs directly.
On the contrary, during the acute attack period, taking uric acid-lowering drugs aggravate uric acid fluctuations in the body, which will lead to worsening joint swelling and pain or difficult to control. On the other hand, uric acid-lowering drugs require long-term use to control uric acid levels to reduce the onset of repeated acute arthritis.
Misconception 7: After the gout attack is relieved, it is cured.
Gout arthritis has a characteristic, which is that it can occur repeatedly. Current medical technology cannot completely cure gout. It is necessary to control blood uric acid in the normal range for a long time to avoid risk factors and prevent recurrence of gout.
Misconception 8: The lower the blood uric acid level, the better
The lower the blood uric acid level, the better. Uric acid is an important biochemical substance in the human body and has an important physiological effect. Appropriate blood uric acid concentration is conducive to antioxidant, balance immune function, and increase the ability to fight infection in the body. Too low blood uric acid is related to many neurological diseases.
Misconception 9: When gout occurs, you should take uric acid-lowering drugs to treat
When gout is acute, you should not use uric acid-lowering drugs. If you just start to treat uric acid-lowering drugs, you also need to temporarily stop taking uric acid-lowering drugs. For long-term use, you can decide specifically based on the condition and dosage to avoid aggravate gout arthritis and prevent metastatic gout. Uric acid-lowering drugs should start from a small dose after the acute attack of gout is relieved, and the dose should be gradually increased until the blood uric acid level is normal and the treatment is maintained at a low dose.
Misconception 10: Avoiding food means not eating meat, while eating vegetables and fruits casually
Diet control includes alcohol restriction, low-purine diet and drinking more water.
needs to strictly limit various alcoholic beverages, especially beer and distilled liquor (white wine). It is recommended that the overall alcohol consumption is ≤2 alcohol units/day for men and ≤1 alcohol units/day for women. (One alcohol unit is approximately 14g pure alcohol, equivalent to 145ml of 12° red wine, 497ml of 3.5° beer, and 43ml of 40° distilled liquor).
The diet should be balanced, and the daily total calorie intake should be restricted, and the low-purine diet should be mainly used to restrict the intake of high-purine foods such as animal offal, seafood and meat. Encourage foods such as fresh vegetables, low-fat or skim milk, eggs, and other foods, and consume beans and soy products in moderation.
Some vegetables contain purine , including lettuce, spinach, mushrooms, cauliflower, etc. It is currently believed that there is no obvious correlation with hyperuricemia and gout attacks. In addition, establish good eating habits and avoid overeating or eating a lot of meat within a meal. It is recommended to cook seafood, meat and plant-based foods with high purine to reduce the purine content in the food.
Drinking a lot of water can shorten the onset of gout and relieve symptoms. It is recommended that people with normal heart and kidney function drink more water and maintain a daily urine volume of 2000~3000ml. Avoid beverages with high fructose (such as orange juice, apple juice, etc.) and sugary soft drinks (Cola, etc.). It can be replaced with fresh fruits with low fructose, such as cherries, strawberry , pineapple, peach, etc. At the same time, it is necessary to properly alkalize the urine to maintain the urine pH between 6.2 and 6.9, which is conducive to the dissolution of urate crystals and excretion from the urine.
Misconception 11: The greater the exercise intensity, the better
Rgitative exercise can reduce the number of gout attacks, but the greater the intensity, the better. You should insist on moderate exercise, and you should reduce your activity during the acute attack of gout and braking is required if necessary. In terms of exercise intensity and time, it is recommended to perform moderate-intensity aerobic exercise at least 150 minutes (30 minutes/d, 5 days/w) per week. Medium intensity refers to the range of heart rate = (220-age) × (50~70%) times/minute during exercise.
Note: Strong exercise or sudden cold can induce acute attacks of gout.
In addition to diet control and proper exercise, lifestyle intervention also includes weight control and smoking cessation.
Misconception 12: If uric acid drops to normal, it can be
Simple hyperuricemia patients generally require blood uric acid to be controlled within 420 μmol/L; if gout attacks, blood uric acid is generally required to be controlled within 360 μmol/L; if gout patients are also associated with gout stones, blood uric acid is required to be controlled within 300 μmol/L.
08 How should we pay attention to
alcohol can significantly increase the risk of gout recurrence, especially white wine, beer, and rice wine. The red wine may be slightly better, and it is still controversial.
As for why drinking alcohol is closely related to uric acid, its mechanism may be because ethanol in alcohol will quickly consume energy ATP during the metabolism process, which increases the production of uric acid; and the acetic acid produced by ethanol metabolism can inhibit the kidney's excretion of uric acid.
Because the beverage contains a lot of fructose, the intake of a large amount of fructose will inhibit the excretion of blood uric acid from the kidneys, causing uric acid to accumulate in the body and cause hyperuricemia.
Therefore, it is best for gout kidney friends not to drink beverages, and it is better to use white water, tea, sugar-free soda water, etc. as daily drinks.
The main causes of gout are purine metabolism disorders and (or) abnormal uric acid excretion in the body, and the intake of high-purine foods is often one of the important factors in the onset of gout.
Heart, liver, kidney, intestine and other animals contain super high purines, so Kids with high uric acid should be avoided as much as possible.
. Stay away from Dabu Soup
Because after the meat is cooked, many purines are dissolved in the soup, so it is best to avoid fish soup, broth, chicken soup, and hot pot soup. Gout patients can choose to eat only meat and not drink soup.
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