Lifestyle guidance and factors causing HUA are the core strategies for HUA prevention. As a disease directly causally related to HUA, gout should be strictly controlled below 360 μmol/L of blood urine, preferably up to 300 μmol/L, and maintained for a long time. For asymptomatic HUA, it should also be treated aggressively in a stratified manner.
Since 1980s, with the continuous improvement of people’s living standard in China, the prevalence of hyperuricemia (HUA) has been increasing year by year, especially in economically developed cities and coastal areas, the prevalence of HUA reaches 5%-23.5%, which is close to the level of western developed countries.
HUA is inseparable from gout and is an independent risk factor for metabolic diseases [diabetes, metabolicsyndrome (MS), hyperlipidemia, etc.], chronic kidney disease, cardiovascular disease and stroke.
In recent years, there are more new studies and understanding on the correlation between HUA and metabolic diseases and other systemic diseases at home and abroad. However, no consensus has been reached on whether treatment is necessary for asymptomatic HUA and the treatment criteria. Therefore, the Endocrinology Branch of the Chinese Medical Association has organized experts to jointly develop the Chinese Expert Consensus on the Treatment of Hyperuricemia and Gout to provide guidance for effective clinical control of HUA.
I. Epidemiology of HUA and its hazards
The prevalence of HUA shows an overall trend of increasing year by year, with men being higher than women, and there are certain regional differences. The high prevalence rate in southern and economically developed coastal areas is higher than that in other regions of China during the same period, which may be related to the intake of more purine-containing seafood, animal offal, meat food and large amount of beer consumption in the region. What’s more, the prevalence of HUA is showing a trend of young people.
According to statistics, the prevalence of HUA in Europe and America in 1980s was 2%~18%. 1998 HUA prevalence in Shanghai was 10.1%; 2003 HUA prevalence in Nanjing was 13,3% [73: 2004 HUA prevalence in Guangzhou was as high as 21.8%; 2009 HUA prevalence in Shandong was 16.99%, which was significantly higher than the data in 2004 in the same region, and increased with age.
In 2010, the prevalence of HUA in rural Jiangsu reached 12.2%. In the same period, the prevalence of HUA in Heilongjiang and Inner Mongolia reached 13.7%, and the prevalence in men was as high as 21%. 2006, the prevalence age of HUA in Ningbo was (43.6±12.9) and (55.7±12.4) for men and women respectively, which was 15 and 10 years earlier than that in Shanghai in 1998.
The high prevalence of HUA is accompanied by a large body of research evidence highlighting the dangers of HUA, which is closely associated with MS, type 2 diabetes, hypertension, cardiovascular disease, chronic kidney disease, and gout, and is an independent risk factor for the development of these diseases.
MS is a complex group of metabolic disorders whose occurrence may be related to insulin resistance. the prevalence of MS increases with the increase of blood uric acid.
When blood uric acid is <360, 360-414, 420-474, 480-534, 540-594 and >600μmol/L (Note: the chemical conversion relationship of uric acid unit is 1mg/dl=59.5μmol/L, with reference to the new literature and clinical convenience, the incidence of MS is converted by 1mg/dl=60μmol/L in this paper). were 18.9%, 36.0%, 40.8%, 59.7%, 62.0% and 70.7%, respectively, with a significant positive correlation.
Blood uric acid levels were significantly correlated with insulin resistance, positively correlated with body mass index and waist circumference, total cholesterol, triglycerides, and LDL cholesterol, and negatively correlated with HDL cholesterol.
HUA is an independent risk factor for the development of type 2 diabetes, and the risk of developing type 2 diabetes increases with the increase of blood uric acid level. A national study found that patients with HUA had a 95% increased risk of developing diabetes compared to those with normal blood uric acid. When blood uric acid was stratified by quartiles, the risk of diabetes increased by 145% (men) and 39% (women) in the highest quartile compared to the lowest quartile, respectively. For every 60 μmol/L increase in blood uric acid levels in the general population, the risk of new-onset diabetes increased by 17%.
Blood uric acid is an independent risk factor for the development of hypertension, and there may be a causal relationship between the two. Uric acid is associated with renal arterial hypertension, especially in those who use diuretics. The relative risk of developing hypertension increases by 13% for every 60 μmol/L increase in blood uric acid level [25,26]. In an animal study, blood uric acid levels in rats were increased by 96 μmol/L over 7 weeks by induction agents, with a subsequent average increase in systolic blood pressure of 2.2 mmHg (1 mmHg = 0.133 kPa). If blood uric acid was normalized by concomitant administration of blood uric acid-lowering drugs, the blood pressure no longer increased. This suggests that there is some causal relationship between high uric acid and elevated blood pressure.
Blood uric acid predicts cardiovascular and all-cause mortality and is an independent risk factor for cardiovascular events. meta-analysis showed that after correcting for age, sex, hypertension, diabetes, smoking, and hypercholesterolemia, patients with HUA had a higher risk of coronary heart disease (CHD).
The overall risk of coronary heart disease (CHD) in patients with HUA was 1.09 and the risk of death from CHD in patients with HUA was 1.16. Each 60 μmol/L increase in blood uric acid was associated with a 12% increase in the risk of death from CHD compared with normal blood uric acid.
The correlation was more significant in female patients.HUA significantly increased the risk of cardiovascular death, which may be related to the fact that HUA reduces the risk of percutaneous coronary intervention (PCI) in CHD patients.
HUA is an independent risk factor for the development of heart failure, ischemic stroke and death. Lowering blood uric acid significantly improves coronary flow and left ventricular function in dilated cardiomyopathy and reduces the risk of cardiovascular and all-cause mortality in patients with hypertensive nephropathy.
Elevated blood uric acid levels can lead to acute uric acid nephropathy, chronic uric acid nephropathy and kidney stones, increasing the risk of renal failure. Renal insufficiency, in turn, is an important risk factor for gout. Numerous studies have confirmed that with increased blood uric acid, the prevalence of chronic kidney disease (CKD) and diabetic nephropathy significantly increases, while the survival rate significantly decreases, and that blood uric acid is also a strong predictor of the development of acute and chronic renal failure and poor prognosis. While renal insufficiency, with glomerular filtration rate (eGFR) <60 ml?min-1?1.73
m-2 the risk of gout increases sharply [50I.
Lowering blood uric acid is beneficial for the control of kidney disease. In Japan, for patients with CKD grade 3 or higher, allopurinol and benzbromarone are recommended as conventional treatment regimens to delay the progression of CKD and prevent cardiovascular events through uric acid-lowering therapy.
HUA is the most important biochemical basis and the most direct cause of gout development. Gout refers specifically to acute characteristic arthritis and chronic gout stone disease, which can be complicated by renal lesions, and in severe cases, joint destruction and impaired renal function. With the increase of blood uric acid level, the prevalence of gout increases gradually, but most HUA does not develop gout, and gout appears only when urate crystals are deposited in the tissues of the body causing damage: a small number of patients in the acute stage.
The blood uric acid level can also be in the normal range, therefore, HUA cannot be equated with gout. The diagnosis can neither be established nor excluded on the basis of blood uric acid levels alone. To dissolve urate crystals, blood uric acid levels must be reduced.
In a study with a follow-up of 2 to 10 years, knee fluid urate crystals were seen in 87.5% of patients with blood uric acid >360 μmol/L, compared with 43.8% (7/16) of those with blood uric acid ≤360 μmol/L. Another study showed that when controlling for blood uric acid <360 μmol/L, there was only 1 episode of gouty arthritis in the last 1 year, compared with 6 episodes in patients with blood uric acid >360 μmol/L. During the 3-year clinical observation period, the higher the blood uric acid level, the higher the recurrence rate of gout after 1 year, showing a significant correlation between blood uric acid of 360 μmol/L and gout attacks. The control of blood uric acid below 300μmol/L is beneficial to the dissolution of gout stones.
Second, the diagnostic criteria and typing of HUA
Internationally, the diagnosis of HUA is defined as: fasting blood uric acid level on 2 non-same days under normal purine diet: men >420μmol/L, women >360μmol/L.
Typing diagnosis: After 5 d of low purine diet in HUA patients, 24-h urine was collected to detect urinary uric acid level. According to the blood uric acid level and urinary uric acid excretion, they were classified into three types as follows.
(1) Poor uric acid excretion type: uric acid excretion <0.48mg?kg-1?h-1, uric acid clearance rate <6.2ml/min.
(2) Excessive uric acid production: uric acid excretion >0.51mg?kg-1?h-1, uric acid clearance rate ≥6.2ml/min.
(3) Mixed type: uric acid excretion >0.51mg?kg-1?h-1, uric acid clearance <6.2
Note: uric acid clearance (Cua) = uric acid X urine volume per minute / blood uric acid] Considering the influence of renal function on uric acid excretion, corrected by creatinine clearance (Ccr), the HUA was classified according to the CuafCcr ratio as follows: >10% as excessive uric acid production type. <5% is the type of poor uric acid excretion, and 5% to 10% is the mixed type.
Clinical research results show that 90% of primary HUA belong to the type of poor uric acid excretion.
Screening and prevention of HUA
The high-risk groups of HUA include: advanced age, male, obesity, history of gout in first-degree relatives, sedentary lifestyle, etc. For the high-risk group, regular screening is recommended to detect HUA early by testing blood uric acid.The prevention of HUA should avoid the following risk factors
1. dietary factors: High purine food such as meat, seafood, animal offal, thick broth, drinking alcohol (especially beer) can increase the blood uric acid level.
2. Disease factors: HUA is mostly accompanied by cardiovascular and metabolic diseases, which interact with each other and influence each other. Therefore, attention should be paid to the blood uric acid test for these patients to detect HUA early.
3.
Avoid the long-term use of drugs that may cause elevated uric acid in the treatment of co-morbidities: It is recommended to remove drugs that may cause elevated uric acid after weighing the pros and cons, such as thiazide and tab diuretics, niacin, low-dose aspirin, etc. For patients who need to take diuretics with HUA, avoid thiazide diuretics. Although low-dose aspirin (<325mg/d) increases blood uric acid, it is not recommended to stop using it as a means of cardiovascular disease prevention and treatment.
Fourth, the control goal of blood uric acid in HUA patients and the cut point of intervention treatment
Control target: blood uric acid <360μmol/L (for patients with gout attack, blood uric acid <300μmol/L is appropriate).
Interventional treatment cut point: blood uric acid >420 p. mol/L (men), >360 μmol/L (women).
In view of the large number of studies confirming the increased risk of multiple co-morbidities when blood uric acid levels exceed the normal range or the high limit of normal (Table 1), it is recommended that for those with HUA combined with cardiovascular risk factors and cardiovascular disease, life coaching and pharmacological uric acid-lowering therapy should be administered simultaneously to keep blood uric acid under long-term control at <360 μmol/L. For patients with gout attacks, long-term control of blood uric acid at 300 μmol/L or less to prevent recurrent attacks.
For patients with HUA without cardiovascular risk factors or cardiovascular co-morbidities, the following intervention programs are recommended for these patients.
V. Treatment of HUA
(I) General treatment
1.
Lifestyle guidance: Lifestyle changes include: healthy diet, restriction of smoking and alcohol, exercise and weight control, etc. Lifestyle changes are also beneficial to the management of co-morbidities (such as CHD, obesity, MS, diabetes, hyperlipidemia and hypertension). Active patient medical education to raise patients’ awareness of disease prevention and treatment and improve treatment compliance. meta-analysis shows that dietary treatment can reduce blood uric acid by approximately 10-18% or 70-90 μmol/L.
(1) Healthy diet: For those with existing gout, HUA, metabolic and cardiovascular risk factors and middle-aged and elderly people, diet should be based on low purine foods, as recommended in Table 2.
(2) Drink more water, quit smoking and limit alcohol: drink more than 1,500 ml/d of urine per day, preferably >2,000 ml/d. Also, quit smoking, ban beer and liquor, and drink red wine in moderation.
(3) Adhere to exercise and weight control: daily moderate intensity exercise for more than 30min. Obese people should lose weight, so that the weight control in the normal range.
2.
Proper alkalinization of urine: when urine pH 6,0 or below, alkalinization of urine is needed. Urine pH 6.2-6.9 is good for urate crystals to dissolve and be excreted from urine, but urine pH>7.0 is easy to form calcium oxalate and other types of stones. Therefore, urine pH should be tested during alkalinization of urine.
Commonly used drugs: sodium bicarbonate or sodium potassium bicarbonate citrate.
Oral sodium bicarbonate (baking soda): 1g per dose, 3 times daily. As this product produces carbon dioxide in the stomach, it can increase the intragastric pressure and cause belching and secondary increase in gastric acid secretion. Long-term administration in large amounts can cause alkalemia and induce congestive heart failure and edema due to increased sodium load. In case of morning uric acidity, acetazolamide 250mg is added at night to increase uric acid solubility and avoid stone formation.
Potassium sodium citrate combination Shohl solution (140g potassium citrate, 98g sodium citrate, add distilled water to 1000ml): 10-30ml each time, 3 times daily. Blood potassium concentration should be monitored during use to avoid hyperkalemia.
Sodium potassium hydrogen citrate granules: This drug should not be used in patients with acute or chronic renal failure, or when sodium chloride is absolutely prohibited. Sodium potassium hydrogen citrate is also contraindicated in severe acid-base balance disorders (alkaline metabolism) or chronic urinary tract ureolytic bacterial infections.
(ii) Aggressive treatment of metabolic and cardiovascular risk factors associated with elevated blood uric acid Aggressive control of obesity, MS, type 2 diabetes, hypertension, hyperlipidemia, CHD or stroke, chronic kidney disease, etc. Metformin, atorvastatin, fenofibrate, cloxacin and amlodipine have different degrees of uric acid-lowering effects while lowering glucose, lipid regulation and blood pressure, and it is suggested that they can be used appropriately according to the patient’s condition.
(C) Treatment path of gout
Treatment of HUA is a key part of gout prevention and treatment. This consensus recommends the gout treatment pathway as shown in Figure 1.
About 11%-49% of gout patients have blood uric acid within the normal range at the acute stage. A retrospective analysis found that 81% of newly diagnosed gout patients with normal blood uric acid had elevated uric acid for about 1 month.
Possible reasons for normal blood uric acid in the acute/exacerbation phase of gout include: (1) a temporary decrease in blood uric acid as a “negative” acute phase reactant in acute inflammatory and stressful situations; (2) increased renal excretion of uric acid during the acute phase; (3) some patients have stopped some HUA-causing factors during the gout attack, such as stopping diuretics , losing weight or giving up beer. Therefore, blood uric acid is of limited value as a diagnosis of acute gout attack.
The goal of blood uric acid control after diagnosis of gout is lower than the diagnostic criteria. That is, all should be controlled over time to <360 μmol/L to maintain it below the saturation point of monosodium urate, and there is evidence that blood uric acid <300 μmol/L will prevent recurrent gout attacks. Therefore, it is recommended that uric acid-lowering therapy be started as soon as the gout diagnosis is established and after the acute symptoms have resolved (≥2 weeks): it can also be started immediately on the basis of anti-inflammatory therapy in the acute phase to maintain blood uric acid within the target range.
(iv) HUA treatment pathway (Figure 2)
(V) Selection of uric acid-lowering drugs
The selection and application of drugs can be based on the patient’s condition and HUA typing, the indications and contraindications of drugs and their precautions. At present, the common clinical drugs include drugs that inhibit uric acid synthesis and drugs that increase uric acid excretion, the representative drugs are allopurinol and benzbromarone respectively.
1. Inhibitors of uric acid synthesis: xanthine oxidase inhibitors (XOI)
Inhibitors (XOI): XOI inhibits uric acid synthesis, including allopurinol and febuxostat. Allopurinol and its metabolite oxypurinol reduce uric acid production by inhibiting the activity of xanthine oxidase (which converts hypoxanthine to xanthine, which in turn converts xanthine to uric acid).
(1) Allopurinol
Indications: ① treatment of chronic primary or secondary gout, control of acute gout attacks with concomitant application of colchicine or other anti-inflammatory drugs, especially during the first few months of treatment: ② for the treatment of uric acid nephropathy with or without gout symptoms: ③ for patients with recurrent uric acid stones: ④ for the prevention of uric acid salts in tissues secondary to chemotherapy or radiotherapy for leukemia, lymphoma or other tumors deposition, kidney stones, etc.
Usage and dosage: ①Start with small dose and gradually increase the dosage. The initial dose is 50mg each time, 2-3 times a day. After 2-3 weeks, increase to 200-400mg daily in 2-3 doses; for severe gout, up to 600mg daily; for adults, 100-200mg twice to three times daily. (2) In case of decreased renal function, such as Ccr<60ml/min, allopurinol should be reduced to the recommended dose of 50-100mg/d.
Ccr<15ml/min is prohibited. Common dosage for children with secondary HUA: 50mg per dose within 6 years of age, 1 to 3 times daily; 100mg per dose between 6 and 10 years of age, 1 to 3 times daily. The dose can be adjusted as appropriate. It is also necessary to drink more water to alkalize the urine.
Precautions: Serious adverse reactions to allopurinol are related to the dose used; try not to increase the dose when the minimum effective dose is used to bring the blood uric acid to the standard.
Adverse reactions: including gastrointestinal symptoms, rash, hepatic impairment, and bone marrow suppression, should be monitored. It is not tolerated by about 5% of patients. Occasionally, severe “allopurinol hypersensitivity syndrome” has occurred.
Contraindications: hypersensitivity to allopurinol, severe hepatic. Allopurinol is contraindicated in patients with severe hepatic and renal insufficiency and significant hematocrit, pregnant women, women at risk of pregnancy, and nursing mothers.
Monitor closely for hypersensitivity reactions to allopurinol. It occurs primarily within the first few months of use, most commonly as exfoliative dermatitis. The use of thiazide diuretics and renal insufficiency are risk factors for hypersensitivity reactions. The incidence of hypersensitivity reactions is 1:1000 in the U.S. The more severe cases include Stevens-Johnson syndrome, toxic epidermolysis bullosa, systemic diseases (eosinophilia, vasculitis, and diseases of major organs), with a mortality rate of 20% to 25% reported in the literature.
It has been demonstrated that allopurinol-related severe hypersensitivity reactions are closely associated with leukocyte antigen (HLA)-B*5801, and that HLA-B*5801 positivity is higher in Korean patients with stage 3 CKD (HLA-B*5801 allele frequency of 12%) or Chinese Han and Thai (HLA, B wood 5801 allele frequency of 6% to 8%) than in whites ( Whites HLA, B wood 5801 allele frequency is only 2%) and have a greater risk of hypersensitivity reactions. Therefore, in 2012, the American College of Rheumatology (ACR) recommended that Asian populations should undergo rapid PCR testing for HLA-B*5801 before using allopurinol, and in 2008, testing for this gene was implemented in Taiwan for patients who were ready to use allopurinol, and use was prohibited for patients with positive results, so it is recommended that genetic testing be performed prior to drug administration when available.
(2) Febuxostat
In 2009, the U.S. Food and Drug Administration (FDA) approved the marketing of febuxostat (trade name ULORIC), a gout drug for the treatment of HUA, and in 2013, the State Food and Drug Administration (CFDA) of China approved the marketing of febuxostat in China. It is a non-purine xanthine oxidase selective inhibitor that does not inhibit other enzymes involved in purine and pyrimidine synthesis and metabolism at conventional therapeutic concentrations, and reduces serum uric acid concentration by inhibiting uric acid synthesis.
Indications: Indicated for the long-term treatment of hyperuricemia in patients with gout. Not recommended for hyperuricemia without clinical symptoms.
Dosage and Administration: ① The recommended oral dose of febuxostat tablets is 40mg or 80mg once daily. The recommended starting dose of febuxostat tablets is 40mg once daily. If after 2 weeks, the blood uric acid level is still not less than 6mg/dl (about 360μmol/L), the recommended dose is increased to 80mg every 13
1 time. ②The effect of food and antacids need not be considered when administering the drug. (③Patients with mild to moderate renal insufficiency (Clcr30-89ml/min) do not need to adjust the dose.
Adverse reactions: Common adverse drug reactions (>1/100, <1/10) mainly include abnormal liver function, nausea, arthralgia, rash.
Contraindications: This product is contraindicated in patients being treated with azathioprine and mercaptopurine.
Precautions: During the initial period of febuxostat administration, an increase in the frequency of gout attacks is often observed. This is due to a decrease in blood uric acid concentration, resulting in mobilization of urate deposited in the tissues. To prevent gout attacks during the initial phase of treatment, concomitant administration of a non-steroidal anti-inflammatory drug or colchicine is recommended. There is no need to discontinue febuxostat treatment if a gout attack occurs during febuxostat treatment. Gout should be treated accordingly to the patient’s specific condition.
2.
Drugs that increase uric acid excretion: Inhibit active reabsorption of urate in the renal tubules and increase urate excretion, thus reducing the concentration of urate in the blood. It can alleviate or prevent the production of urate crystals, reduce the damage of joints, and also promote the dissolution of formed urate crystals. Since more than 90% of HUA is caused by reduced uric acid excretion in the kidneys, pro-uric acid excretion drugs are more widely used. The representative drugs are benzbromarone and propofol.
When using these drugs, it is important to drink more water and use drugs that alkalize the urine. In addition, urinary uric acid excretion should be measured before using these drugs. If the 24h urinary acid excretion has increased (>3.54 mmol) or if the patient has urinary stones, these drugs are contraindicated and should be used with caution in cases of ulcer disease or renal insufficiency.
(1) Benzbromarone
Indications: Primary and secondary hyperuricemia, intermittent gouty arthritis and gouty nodular swelling. Long-term use has no significant effect on the kidney and can be used in patients with renal insufficiency with Ccr>20ml/min. For adults with Ccr>60ml/min no dose reduction is required, 50 to 100mg daily.
Usually, the blood uric acid decreases significantly in 6-8 d of benzbromarone, and the intensity and attainment rate of blood uric acid reduction is stronger than that of allopurinolm], and adherence to it can maintain the blood uric acid level in the body to reach the target value. Long-term treatment for more than 1 year (average 13.5 months) can effectively dissolve gout stones [67I. The drug has no drug interaction with the combination of antihypertensive, hypoglycemic and lipid-regulating drugs.
Dosage and Administration: The starting dose for adults is 50 mg per oral dose, once daily, after breakfast. Blood uric acid concentrations are checked 1 to 3 weeks after administration. In follow-up treatment, adults and patients over 14 years of age are given 50 to 100g daily.
Adverse reactions: Gastrointestinal discomfort, diarrhea, and rash may occur, but are relatively uncommon. Rare hepatic impairment, with an incidence of 1/17,000 reported abroad.
Contraindications: ① Hypersensitivity to any of the ingredients in this product. ②Patients with severe renal impairment (glomerular filtration rate less than 20 ml/min) and patients with severe kidney stones. ③Pregnant women, women at risk of pregnancy and lactating women are prohibited.
Precautions: Drink plenty of water during the treatment period to increase urine output (not less than 1500-2000m1 at the beginning of treatment) to promote uric acid excretion. Avoid the formation of stones in the urinary system due to excessive excretion of uric acid. Sodium bicarbonate or citrate combination can be given as appropriate during the first 2 weeks of starting medication to keep the pH of the patient’s urine between 6.2 and 6.9. Measure the pH of the urine regularly.
(2) Propofol
Dosage and Administration: Adults 0,25g once, twice a day, which can be increased to 0.5g once, twice a day after 1 week. Adjust the dosage according to clinical manifestations and blood and uric acid levels, and in principle, maintain with the minimum effective amount.
Precautions: It should not be taken with salicylates, aspirin, etanercept, hydrochlorothiazide, protamine, indomethacin and oral hypoglycemic agents. Maintain adequate water intake (about 2500ml per day) when taking this product to prevent the formation of kidney stones, and take drugs that alkalize urine at the same time if necessary. Regularly test blood and urine pH, liver and kidney function, and blood uric acid and uric acid, etc.
Contraindications: ①Allergic to this product and sulfonamides. ②Persons with hepatic or renal insufficiency. ③Patients with hyperuricemia with tumor, or patients using cytotoxic anticancer drugs or radiation therapy should not use this product because it can cause acute nephropathy. Patients with uric acid stones are a relative contraindication. It is also not recommended for use in children, the elderly, or those with peptic ulcers. This product should not be used when the symptoms of gouty arthritis are not yet controlled. If there is an acute attack during the treatment of this product, continue to apply the original dosage and give colchicine or other non-steroidal anti-inflammatory drugs at the same time.
(3) Uricase (uricase)
Uricase catalyzes the oxidation of uric acid to the more soluble allantoin, thereby reducing blood uric acid levels. The main biosynthetic uric acid oxidase enzymes are.
①Recombinant Aspergillus flavus uric acid oxidase (Rasburicase), also known as labile lyase, powder injection, is currently indicated for patients with chemotherapy-induced hyperuricemia. ②Polyethylene glycolized recombinant uric acid oxidase (PEG, uricase), used intravenously. Both have the efficacy of rapid and potent reduction of SUA. It is mainly used for patients with severe HUA, refractory gout, and especially tumor lysis syndrome. Pegloticase, a polyglycolylated uric acid-specific enzyme, has been marketed in the United States and Europe for lowering uric acid and reducing the deposition of urate crystals in patients with gouty stone gout who have acquired therapeutic disability in Europe. It is not yet available in China.
3.
Combination therapy: If monotherapy does not bring blood uric acid control up to the standard, combination therapy can be considered. That is, XOI is combined with drugs that promote uric acid excretion, while other uric acid excreting drugs can also be used as a reasonable supplement (applied under indications), such as cloxacitant, fenofibrate, etc. Crosartan and fenofibrate can assist in reducing uric acid levels in patients with gout.
Patients with hypertension with increased blood uric acid, the choice of crosartan anti-hypertension at the same time, can also reduce blood uric acid: In addition, crosartan treatment combined with elevated blood uric acid in patients with chronic cardiac insufficiency can lead to a decrease in blood uric acid. Fenofibrate can be the first choice for the treatment of hypertriglyceridemia with hyperuricemia. If the target is still not reached, pegolase can also be combined.
4. Uric acid-lowering drugs should be used continuously: studies have confirmed that continuous uric acid-lowering therapy is more effective in controlling gout attacks than those who take it intermittently. The consensus recommendation is that they should be used continuously and monitored regularly after the blood uric acid standard has been reached.
5.
Chinese herbal medicine treatment: Chinese herbal medicine for gout and HUA is receiving increasing attention. Certain herbal medicines are reported to have anti-inflammatory, analgesic, blood-activating, anti-swelling and blood uric acid-lowering effects, which hopefully will be confirmed by rigorously designed evidence-based medical evidence.
List of the expert group participating in the preparation (in order of last name) Lulu Chen, Zhengnan Gao, Xiaowei Guo, Tianbei Hong, Qiuhe Ji, Changgui Li, Chunlin Li