HUA is an independent risk factor for many cardiovascular risk factors and related diseases (metabolic syndrome, type 2 diabetes, hypertension, cardiovascular events and death, nephropathy, etc.). Lifestyle guidance and factors that cause HUA are the core strategies for HUA prevention. Gout, as a disease directly related to HUA, should be strictly controlled below 360 μmol/L, preferably up to 300 μmol/L, and maintained for a long time. Asymptomatic HUA should also be treated aggressively in a stratified manner.
Since the 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 has reached 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 in China and abroad. However, no consensus has been reached on whether treatment is necessary for asymptomatic HUA and the treatment criteria. Therefore, the Chinese Society of Endocrinology has organized experts to formulate the “Chinese Expert Consensus on 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, and is higher in men than in women, and there are some regional differences. The higher prevalence in the south and economically developed coastal areas compared with other regions in China during the same period may be related to the consumption of more purine-containing seafood, animal offal, meat and beer in these areas. More importantly, the prevalence of HUA is on the trend of younger people.
According to statistics, the prevalence of HUA in Europe and the United States was 2%-18% in the 1980s. 10.1% in Shanghai in 1998; 13,3% in Nanjing in 2003 [73: 21.8% in Guangzhou in 2004; 16.99% in Shandong in 2009, 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 of HUA in men was as high as 21%.
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, the occurrence of which may be related to insulin resistance. the prevalence of MS increases with the increase of blood uric acid. The prevalence of MS increases with the increase of blood uric acid. When the blood uric acid is <360, 360-414, 420-474, 480-534, 540-594>600μmol/L (Note: The chemical conversion of uric acid unit is 1mg/dl=59.5μmol/L. The incidence of Ms was 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 associated with insulin resistance and 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 diuretic users. The relative risk of hypertension increases by 13% for every 60 μmol/L increase in blood uric acid levels [25,26]. In an animal study, an induction agent increased blood uric acid levels in rats by 96 μmol/L over 7 weeks, with a subsequent average increase in systolic blood pressure of 2.2 mmHg (1 mmHg = 0.133 kPa). When blood uric acid was normalized by concomitant administration of blood uric acid-lowering drugs, blood pressure ceased to rise. This suggests that there is a causal relationship between high uric acid and elevated blood pressure.
Blood uric acid is a predictor of cardiovascular and all-cause mortality and an independent risk factor for cardiovascular events. meta-analysis showed that the overall risk of coronary heart disease (CHD) in patients with HUA was 1.09 and the risk of CHD death in patients with HUA was 1.16 after correcting for age, sex, hypertension, diabetes, smoking and hypercholesterolemia. A 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.
HUA significantly increases the risk of cardiovascular death, which may be associated with a reduced risk of increased blood flow and reperfusion and restenosis after percutaneous coronary intervention (PCI) in patients with CHD. HUA is an independent risk factor for 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 the prevalence of chronic kidney disease (CKD) and diabetic nephropathy increases significantly with increased blood uric acid, and that survival decreases significantly, and that blood uric acid is a strong predictor of acute and chronic renal failure and poor prognosis. In contrast, the risk of gout increases sharply in renal insufficiency with a glomerular filtration rate (eGFR) <60 ml-min-1-1.73 m-2 [50 I. Reducing blood uric acid is beneficial for the control of renal disease. In Japan, for patients with CKD grade 3 or higher, allopurinol and benzbromarone are recommended as conventional treatment regimens to slow 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. Gout refers specifically to acute characteristic arthritis and chronic gouty stone disease, which can be complicated by renal pathology, and in severe cases, joint destruction and impaired renal function. The prevalence of gout increases with increasing blood uric acid levels, but most HUA does not develop gout, but only when urate crystals are deposited in the body’s tissues causing damage: a small percentage of patients in the acute phase. 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 2-10 year follow-up, 87.5% of patients with blood uric acid >360 μmol/L had urate crystals in the knee joint compared to 43.8% (7/16) of those with blood uric acid ≤360 μmol/L. Another study showed 6 instances in patients with control blood uric acid <360 μmol/l 1="">360 μmol/L. During the 3-year clinical observation period, higher blood uric acid levels were associated with a higher rate of gout recurrence 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.
Diagnostic criteria and typing of HUA
Internationally, the diagnosis of HUA is defined as: 2 fasting blood uric acid levels on different days under normal purine diet: >420μmol/L for men and >360μmol/L for women.
Typing diagnosis: 24h urine was collected for uric acid level after 5d of low purine diet in HUA patients. 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 type: 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 x="" cuafccr="" hua="">10% for uric acid overproduction type. < 5% is poor uric acid excretion type, and 5% to 10% is mixed type. < span="">
The results of clinical studies show that 90% of primary HUA are of the poor uric acid excretion type.
Screening and prevention of HUA
High-risk groups for HUA include: advanced age, male, obesity, history of gout in first-degree relatives, and sedentary lifestyle. The following risk factors should be avoided for HUA prevention.
1.Dietary factors: High purine food such as meat, seafood, animal offal, thick broth, 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 at an early stage.
3.Avoid long-term use of drugs that may cause uric acid elevation: It is recommended to remove drugs that may cause uric acid elevation, such as thiazide and tab diuretics, niacin, low-dose aspirin, etc. after weighing the pros and cons. For patients who need diuretics and have HUA, avoid thiazide diuretics. Low-dose aspirin (<325 mg/d) is not recommended to be discontinued as a means of cardiovascular disease control, although it raises blood uric acid. < span="">
IV. Blood uric acid control goals and interventional treatment cut points in patients with HUA
Control target: blood uric acid <360 μmol/L (for patients with gout attacks, blood uric acid <300 μmol/l is appropriate). < span="">
Interventional treatment cut point: blood uric acid >420 p. mol/L (men), >360 μmol/L (women).
In view of the numerous 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 in patients with HUA combined with cardiovascular risk factors and cardiovascular disease, concomitant life coaching and pharmacological uric acid-lowering therapy should be provided to keep blood uric acid under long-term control at <360 μmol/L. In patients with gout attacks, long-term control of blood uric acid at For patients with gout attacks, long-term control of uric acid should be below 300 μmol/L to prevent recurrent attacks. For patients with HUA without cardiovascular risk factors or concomitant cardiovascular diseases, 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 education is needed to raise patients’ awareness of disease prevention and treatment and to improve compliance with treatment. meta-analysis shows that dietary treatment can reduce blood uric acid by approximately 10-18% or 70-90 μmol/L.
(1) Healthy diet: For people 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 daily, preferably >2,000 ml/d. Also, quit smoking, ban beer and white wine, 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, appropriate alkalinization of urine: when the urine pH 6, 0 below, need to alkalinize the urine. Urine pH 6.2-6.9 is conducive to the dissolution of urate crystals and their discharge from the urine, but urine pH>7.0 is prone to the formation of calcium oxalate and other types of stones. Therefore, urine pH should be checked during alkalinization of urine.
Commonly used drugs: sodium bicarbonate or sodium potassium bicarbonate.
Oral sodium bicarbonate (baking soda): 1g per dose, 3 times daily. As this product produces carbon dioxide in the stomach, it can increase gastric pressure and cause belching and secondary increase in gastric acid secretion. Long-term administration of large amounts can cause alkalemia and induce congestive heart failure and edema due to increased sodium load. In case of morning uric acidity, add acetazolamide 250mg at night to increase the solubility of uric acid and avoid stone formation.
Potassium and sodium citrate 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 imbalance (alkaline metabolism) or in 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, lipids, and blood pressure, and are recommended to 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 a gout treatment pathway as shown in Figure 1.
About 11%-49% of gout patients have blood uric acid within the normal range in the acute phase. 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 during acute inflammation and stress; (2) increased renal excretion of uric acid during the acute phase; and (3) discontinuation of HUA-causing factors such as discontinuation of diuretics, weight loss, or abstinence from beer during the gout attack. (3) some patients stop some factors that cause HUA, 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 the diagnosis of gout is lower than the diagnostic criteria. That is, long-term control to <360 μmol/L is required 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)
(E) 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, whose representatives are allopurinol and benzbromarone respectively.
1.Inhibitors of uric acid synthesis, xanthine oxidase inhibitors (XOI): XOI inhibits uric acid synthesis, including allopurinol and febuxostat. Allopurinol and its metabolite oxypurinol reduce uric acid production by inhibiting xanthine oxidase activity (which converts hypoxanthine to xanthine and then xanthine to uric acid).
(1) Allopurinol
Indications.
(1) For the treatment of chronic primary or secondary gout and for the control of acute gout attacks, with concomitant application of colchicine or other anti-inflammatory drugs, especially during the first few months of treatment.
(ii) For the treatment of uric acid nephropathy with or without gout symptoms.
(iii) For patients with recurrent uric acid stones.
④For the prevention of uric acid deposits in tissues and kidney stones secondary to chemotherapy or radiotherapy for leukemia, lymphoma or other tumors.
Dosage and Administration.
①Start with a small dose and gradually increase the dose. The initial dose is 50mg each time, 2-3 times a day. After 2-3 weeks, increase the dose to 200-400mg per day in 2-3 doses; for severe gout, up to 600mg per day; for adults, 100-200mg per dose in 2-3 doses.
If renal function decreases, such as Ccr<60ml/min, allopurinol should be reduced, the recommended dose is 50-100mg/d, and Ccr<15ml/min is prohibited. The usual dosage for the treatment of secondary HUA in children: 50mg per dose up to 6 years of age, 1 to 3 times daily; 100mg per dose from 6 to 10 years of age, 1 to 3 times daily. The dosage can be adjusted as appropriate. Also need to drink more water to alkalize the urine.
Caution: Serious adverse reactions to allopurinol are related to the dose used. When the minimum effective dose is used to achieve the blood uric acid target, try not to increase the dose.
Adverse reactions: include gastrointestinal symptoms, rash, hepatic impairment, and bone marrow suppression and should be monitored. It is not tolerated by about 5% of patients. Occasionally, severe “allopurinol hypersensitivity syndrome” has occurred.
Contraindications: allergy 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. They occur 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, and systemic diseases (eosinophilia, vasculitis, and major organ disease), with a mortality rate of 20% to 25% reported in the literature.
Allopurinol-related severe hypersensitivity reactions have been shown to be strongly associated with leukocyte antigen (HLA)-B*5801, and HLA-B*5801 positivity is higher in Korean CKD stage 3 patients (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 ( The risk of hypersensitivity reactions is greater in whites (HLA, B wood 5801 allele frequency is only 2%). 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, Taiwan has implemented testing for this gene in patients who are ready to use allopurinol, and patients with positive results are prohibited from using it, so it is recommended that genetic testing be performed before using the drug when available.
(2) Febuxostat
In 2009, the U.S. Food and Drug Administration (FDA) approved febuxostat (ULORIC), a gout drug for HUA, and in 2013, the State Food and Drug Administration (CFDA) of China approved febuxostat for marketing 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.
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 the blood uric acid level is not less than 6 mg/dl (approximately 360 μmol/L) after 2 weeks, the recommended dose is increased to 80 mg once every 13 days.
②The effects of food and antacids need not be considered when administering the drug.
(③Patients with mild to moderate renal insufficiency (Clcr30-89ml/min) do not require dose adjustment.
Adverse reactions: Common adverse drug reactions (>1/100, <1/10) mainly include abnormal liver function, nausea, arthralgia, and rash. < span="">
Contraindications: This product is contraindicated in patients being treated with azathioprine and mercaptopurine.
Precautions: Increased frequency of gout attacks is often seen during the initial period of febuxostat administration. This is due to a decrease in blood uric acid concentration, resulting in mobilization of urates deposited in the tissues. To prevent gout attacks during the initial phase of treatment, concomitant administration of NSAIDs or colchicine is recommended. There is no need to discontinue febuxostat therapy if a gout attack occurs during febuxostat treatment. Treatment of gout should be tailored to the patient’s specific situation.
2. Drugs that increase uric acid excretion: Inhibit the active reabsorption of urate in the renal tubules and increase the excretion of urate, 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 due to reduced uric acid excretion by the kidneys, pro-uric acid excretory drugs are more widely used. Typical drugs are benzbromarone and probenecid. When using these drugs, it is important to drink plenty of water and use drugs that alkalize the urine. In addition, urinary uric acid excretion should be measured prior to the use of these drugs and is contraindicated if the 24h urinary uric acid excretion has increased (>3.54 mmol) or if the patient has urinary stones, 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. In adults with Ccr>60ml/min, no dose reduction is needed, 50-100mg daily. 6-8d of benzbromarone usually results in a significant decrease in blood uric acid, and the intensity and rate of uric acid reduction is stronger than that of allopurinol m], and the target blood uric acid level can be maintained. The combination of this drug with antihypertensive, hypoglycemic and lipid-regulating drugs has no drug interactions.
Dosage and Administration: The starting dose for adults is 50 mg orally once a day after breakfast. Blood uric acid concentration should be checked within 1 to 3 weeks of dosing.
Adverse reactions: Gastrointestinal discomfort, diarrhea and rash may occur, but are rare. Hepatic impairment is rare, with an incidence of 1/17,000 reported abroad.
Contraindications.
(1) Hypersensitivity to any of the components of this product.
②Patients with severe renal impairment (glomerular filtration rate less than 20 ml/min) and patients with severe renal calculi.
Pregnant women, women at risk of pregnancy, and women who are breastfeeding are prohibited.
Caution: Drink plenty of water to increase urine volume during the treatment period (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 may be given as appropriate during the first 2 weeks of drug initiation to control 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 per dose, twice a day, which can be increased to 0.5g per dose, twice a day after 1 week. Adjust the dosage according to clinical manifestations and blood and urine uric acid levels, and in principle maintain with the minimum effective amount.
Caution: It should not be taken together with salicylates, aspirin, etanercept, hydrochlorothiazide, protamine, indomethacin and oral hypoglycemic agents. When taking this product, maintain adequate water intake (about 2500ml per day) to prevent the formation of kidney stones, and take drugs to alkalize the urine if necessary. Regularly test blood and urine pH, liver and kidney function, blood uric acid and uric acid, etc.
Contraindications.
①Allergic to this product and sulfonamides.
②Hepatic and renal insufficiency.
(3) Patients with hyperuricemia with tumor, or patients using cytotoxic anticancer drugs or radiation therapy should not use this product because it may cause acute nephropathy. Patients with uric acid stones are relatively contraindicated. It is also not recommended for children, the elderly, or people with peptic ulcers. This product should not be used when the symptoms of acute gouty arthritis are not yet controlled. If an acute attack occurs during treatment with this product, the original dosage may be continued, along with colchicine or other NSAIDs.
(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 glycolated recombinant uric acid oxidase (PEG, uricase), used intravenously. Both have a rapid and potent effect in reducing 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 urate crystallization in patients with gouty stone gout who have acquired treatment disability in Europe. It is not yet available in China.
3. Combination therapy: If monotherapy cannot bring blood uric acid control to the standard, then combination therapy can be considered. That is, XOI 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 it still cannot reach the standard, it can also be combined with pegolase.
4, uric acid-lowering drugs should be used continuously: studies have confirmed that continuous uric acid-lowering treatment is more effective in controlling gout attacks than those who take it intermittently. Consensus suggests that after the blood uric acid reaches the standard, it should be used continuously and monitored regularly.
5.Chinese medicine treatment: Chinese medicine treatment for gout and HUA is gaining attention. Certain herbs are reported to have anti-inflammatory, analgesic, blood activating, anti-swelling and blood uric acid lowering effects, and it is hoped that there will be rigorously designed evidence-based medical evidence to confirm this.