echemi logo
  • Product
  • Supplier
  • Inquiry
    Home > Active Ingredient News > Immunology News > High uric acid and "three highs" come together, how to choose medicine?

    High uric acid and "three highs" come together, how to choose medicine?

    • Last Update: 2021-05-09
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit
    *Only for medical professionals to read for reference.
    How to choose medication for hyperuricemia combined with three highs?
    In recent years, with the improvement of social living standards, people's dietary structure has undergone tremendous changes.
    The proportion of high-purine foods has increased significantly.
    High-purine foods are an important reason for the increase in blood uric acid levels in the human body.
    Hyperuricemia The prevalence of gout and gout is increasing year by year, and is showing a younger trend, becoming the second largest metabolic disease after diabetes.

    "China Guidelines for the Diagnosis and Treatment of Hyperuricemia and Gout (2019)" puts forward the concept of "comprehensive treatment" when multiple diseases coexist.

    So when hyperuricemia is combined with three highs (hypertension, hyperlipidemia, hyperglycemia), how should we choose drugs? The “Guidelines for the Diagnosis and Treatment of Hyperuricemia and Gout in China” released in 2019 pointed out: Regardless of men and women, the fasting blood uric acid level on two different days is> 420 μmol/L (previous guide: Men with fasting blood uric acid level on two occasions not on the same day> 420 μmol/L, Female>360 μmol/L) is hyperuricemia.

    If the blood uric acid level is ≥540 µmol/L or ≥480 µmol/L and has one of high blood pressure, abnormal lipid metabolism, diabetes, obesity, etc.
    , uric acid-lowering drug treatment should be initiated.

    1 The choice of uric acid-lowering and anti-gout drugs (1) Uric acid-lowering drugs currently commonly used clinically, such as probenecid, allopurinol, benzbromarone, febuxostat, etc.
    , are not harmful to blood sugar, blood pressure, and blood lipids.
    The impact is even beneficial.

    Allopurinol has a hypotensive effect on adolescent primary hypertension.

    For patients with hypertension and hyperuricemia, the allopurinol treatment group can restore blood pressure to normal better than the placebo group.

    At the same time, studies have also found that the combined application of allopurinol and captopril can improve the blood pressure reduction effect of captopril.

    Febuxostat is suitable for patients who cannot tolerate allopurinol or have contraindications.

    Febuxostat can reduce blood uric acid levels, mainly by inhibiting the renin-angiotensin-aldosterone system (RASS) to reduce blood pressure, and can improve the renal function of patients with hypertension and hyperuricemia.

    Benzbromarone promotes uric acid excretion by inhibiting the reabsorption of uric acid in the renal tubules, and can be used for patients with mild to moderate renal insufficiency.

    However, there are few clinical studies on benzbromarone reducing blood uric acid and blood pressure at the same time.

    Probenecid inhibits the active reabsorption of urate in the renal tubules, increases the excretion of urate and reduces the concentration of urate in the blood, thereby reducing the deposition of uric acid.

    Some studies suggest that it has a better effect on maintaining normal blood pressure in obese adolescents, but the effect of lowering blood pressure on adult primary hypertension is not good.

    In theory, lowering blood uric acid can improve insulin resistance, increase insulin sensitivity, and protect pancreatic β-cell function, which is beneficial to blood sugar control.

    Instead of lowering uric acid levels, nonbuxostat can also regulate blood lipid levels.

    In addition, sodium bicarbonate is used as an auxiliary drug for lowering uric acid.
    It should be noted that it may increase water and sodium retention and heart burden, induce heart failure and increase blood pressure.
    Therefore, patients with hypertension should be used with caution and pay attention to monitoring blood pressure.

    (2) Antigout drugs Clinically, hyperuricemia often causes gout, and gout attacks may also be induced during uric acid-lowering treatment.
    Therefore, in the treatment of people with hyperuricemia and three highs, the application of anti-gout drugs has to be considered The impact on the three highs.

    Commonly used drugs for gout attacks are: colchicine, non-steroidal anti-inflammatory drugs (NSAIDs) or glucocorticoids.

    Generally speaking, colchicine has no adverse effects on blood pressure, blood sugar, and blood lipids, but its adverse reactions should be paid attention to.

    Common adverse reactions of glucocorticoids such as infection, metabolic disorders (water and electrolytes, blood sugar, blood lipids), weight gain, abnormal blood pressure, etc.
    are obviously not conducive to blood pressure, blood sugar, and blood lipid control.

    Therefore, when patients with hyperuricemia and three highs encounter gout attacks, we should try to avoid the use of corticosteroids.

    If you have to use it, you need to closely monitor the changes in blood sugar and blood pressure during the medication.

    (NSAIDs) may induce hypertension.

    Either non-selective NSAIDs or selective COX-2 inhibitors may have adverse effects of elevated blood pressure.

    However, selective COX-2 inhibitors are more likely to have hypertension than non-selective NSAIDs.
    Ibuprofen and naproxen had the lowest proportion of adverse hypertension reactions, which was not significant compared with the non-selective NSAIDs group.
    Sexual difference.

    High-risk factors for NSAIDs to induce hypertension include: advanced age, previous hypertension, renal insufficiency, liver insufficiency and so on.

    The adverse reaction is reversible by stopping or reducing the dose, and the increase is generally 5-10mmHg.

    After the occurrence of hypertension, the drug should be stopped, reduced or actively controlled blood pressure.

    In the past, the domestic and foreign literature has been consulted, and it is not uncommon to use NSAIDs to raise blood pressure, but it is generally 5-10mmHg.

    2 The choice of antihypertensive drugs.
    Hyperuricemia is an independent risk factor for hypertension.
    It has been concluded that hypertension and hyperuricemia interact and interact with each other, forming a vicious circle.

    When the two coexist, the risk of target organ damage is significantly higher than that of patients with simple hypertension or hyperuricemia.

    Therefore, the clinical diagnosis, treatment and management of hyperuricemia combined with hypertension is very important.

    In view of the dual hazards of hyperuricemia and hypertension to the heart, brain, kidney and other target organs, the best medicine should be able to lower blood pressure and blood uric acid at the same time.

    (1) Angiotensin receptor antagonist (ARB): In 1992, it was first reported that Losartan has a dose-dependent effect on lowering blood uric acid, so the uric acid lowering effect of ARB was paid attention to.

    Losartan has the strongest ability to excrete uric acid among all ARBs.
    It is effective in treating hypertension complicated with hyperuricemia and helps reduce the risk of gout in hypertensive patients.

    Studies have compared the antihypertensive and uric acid effects of irbesartan, valsartan, telmisartan and losartan.
    The results show that the antihypertensive effects of the four drugs are basically the same, but the effect of losartan in reducing blood uric acid Better than the other three ARB drugs.

    Therefore, Losartan can be used as the drug of choice for hypertension complicated with hyperuricemia.

    (2) Calcium channel blockers (CCB): Studies have shown that some CCB can lower blood uric acid, which may be related to its renal protection.

    The antihypertensive effects of CCB on different calcium channels are different, and there are also big differences in the effect on blood uric acid levels.

    Long-term oral nifedipine can significantly increase blood uric acid, but nitrendipine has less effect; research has found that amlodipine, in patients with hypertension and hyperuricemia, can lower blood uric acid while lowering blood pressure.

    L-Amlodipine, there are also research reports that can reduce blood uric acid.

    (3) Diuretics: It is a commonly used component of antihypertensive drugs in clinical practice.

    Almost all diuretics and antihypertensive drugs containing diuretics can cause an increase in uric acid, but loop diuretics (such as furosemide), thiazide diuretics (such as hydrochlorothiazide) and indapamide are the most common.

    These drugs can reduce the ability of the kidneys to excrete uric acid, and large doses or long-term use can increase blood uric acid.

    (4) β-receptor blockers: such as propranolol has a significant effect on increasing uric acid, especially when combined with diuretics.

    Metoprolol has less effect on uric acid.

    (5) AECI and α-receptor blockers AECI and α-receptor blockers have no effect on uric acid excretion.

    Therefore, for hyperuricemia combined with hypertension, it is recommended that the antihypertensive drugs should first be Losartan and/or calcium channel blockers and AECIs and α-receptor blockers.
    Thiazides, loop diuretics and β-receptors are not recommended.
    Body blockers, etc.

    3 Choice of lipid-lowering drugs The proportion of hyperuricemia patients with hyperlipidemia and obesity is as high as 68% and 71% in women and men, respectively.
    Obesity has an increase in blood uric acid levels, which are different due to different types of obesity Many patients’ weight has been effectively controlled after effective uric acid-lowering treatment.

    Similarly, lipid-lowering therapy can also assist in uric acid-lowering therapy.

    (1) Atorvastatin is a statin lipid-lowering drug.
    The drug has the effect of promoting uric acid excretion and can lower uric acid.
    The mechanism may be accomplished by inhibiting the reabsorption of uric acid by the kidneys.

    (2) Fenofibrate: Fenofibrate belongs to the fibrate class of lipid-lowering drugs, which can lower blood uric acid while lowering lipids.

    The mechanism of action is believed to increase the elimination of uric acid fragments and purines through the renal bypass pathway.
    Monitoring the urine (liquid) for 24 hours also found that the excretion of uric acid in patients taking the drug increased.

    It is recommended that fenofibrate is the first choice for hyperuricemia combined with hyperlipidemia drugs (especially those with hypertriglyceridemia); for patients with hypercholesterolemia, atorvastatin calcium is the first choice.

    4 The choice of hypoglycemic agents Type 2 diabetes and hyperuricemia can coexist and influence each other.
    Diabetes can lead to hyperuricemia, and hyperuricemia is an independent risk factor for the occurrence and development of diabetes, which can induce type 2 diabetes.
    , Hyperuricemia is not only associated with diabetes, but also has important relevance to diabetes-related complications.

    It is very important to strengthen the blood sugar management of patients with hyperuricemia.

    The effects of commonly used hypoglycemic agents on uric acid are as follows: (1) α-glycosidase inhibitors: suitable for those who rely mainly on carbohydrates and have elevated postprandial blood sugar.

    Acarbose, voglibose and miglitol are listed in the domestic market.

    Among them, acarbose can reduce the increase in blood uric acid levels caused by the decomposition of sucrose.

    (2) Thiazolidinediones (TZDs): These drugs can reduce fasting and postprandial blood sugar, reduce glycosylated hemoglobin, and improve lipid metabolism disorders.

    It may reduce blood uric acid levels by reducing insulin resistance and improving lipid metabolism.

      (3) Metformin: Metformin can reduce appetite to reduce weight and triglycerides, increase insulin sensitivity, reduce renal tubular epithelial cell apoptosis, thereby improve renal function, promote blood uric acid metabolism, and reduce blood Uric acid levels.

    (4) Sodium-glucose cotransporter 2 (SGLT-2) inhibitor: By inhibiting the SGLT-2 activity of the renal proximal tubule reabsorption of glucose, it increases the excretion of glucose in the urine and lowers blood sugar.

    Studies have confirmed that SGLT2 inhibitors can reduce blood uric acid by 10% to 15%.

    Like blood sugar, blood uric acid is also absorbed back in the proximal renal tubules.

    SGLT-2 inhibitors increase urinary sugar excretion, and the body's reactivity increases uric acid secretion in exchange for glucose reabsorption, resulting in increased uric acid excretion.

    (5) Dipeptidyl peptidase (DDP-4) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists: These two types of drugs can improve islet function and reduce insulin resistance without causing Elevated blood uric acid can even reduce blood uric acid to a certain extent by reducing the level of serum insulin and reducing body weight.

    (6) Sulfonylureas: long-term use of glibenclamide, glimepiride, gliclazide and other drugs that are mainly excreted by the kidneys may affect kidney function and reduce the excretion of uric acid, but generally speaking Not big.

    Gliquidone is mainly excreted through bile and has little effect on uric acid.

    (7) Glinides: It is a meal-time blood sugar regulator, which can increase serum insulin concentration and lower blood sugar.
    It is mainly metabolized by the liver and has little effect on uric acid; but it is also believed that it can cause hyperinsulinemia, and insulin can promote kidney The reabsorption of uric acid causes an increase in blood uric acid.

    (8) Insulin: It is a good medicine for the treatment of various types of diabetes, but this medicine can increase the reabsorption of uric acid by the kidneys and increase the blood uric acid level when it participates in the metabolic process of the body.

    Judging from the characteristics of the above-mentioned hypoglycemic agents, metformin, TZDs, α-glycosidase inhibitors, GLP-1 receptor agonists, and DPP-4 inhibitors can improve islet function and reduce insulin resistance, all of which can reduce blood uric acid.

    SGLT-2 inhibitors can directly promote the excretion of uric acid.
    If there are no contraindications, these types of hypoglycemic agents are the first choice for patients with hyperuricemia and hyperglycemia; insulin secretagogues (sulfonylureas and glinides) in general It has little effect on uric acid, but insulin secretagogues can increase serum insulin concentration after all, which may not be conducive to uric acid excretion, so it is not recommended.

    Insulin can promote the reabsorption of uric acid by the kidneys and has an adverse effect on uric acid excretion, so it is not suitable for patients with diabetes and hyperuric acid.

    For insulin secretagogues and exogenous insulin, if it must be used, it is best to use it in combination with metformin or insulin sensitizers and alpha glycosidase inhibitors, and reduce the amount of insulin as much as possible.

    References: [1] Chinese Medical Association Endocrinology Branch.
    Guidelines for the diagnosis and treatment of hyperuricemia and gout in China (2019)[J], Chinese Journal of Endocrinology and Metabolism.
    [2] .
    Li Xiaobin .
    Comparison of efficacy and pharmacoeconomics of losartan and valsartan in the treatment of hypertension complicated with hyperuricemia[J].
    Journal of Chronic Diseases,2019,20(06):928-930.
    [3] .
    Prevention and treatment of hypertension in China Guidelines (Revised in 2018)[J].
    Cardiovascular and Cerebrovascular Disease Prevention and Treatment,2019,19(1):15.
    Multidisciplinary consensus on the diagnosis and treatment of hyperuricemia-related diseases, an expert group on the diagnosis and treatment of hyperuricemia-related diseases in China Multidisciplinary expert consensus Chinese Journal of Internal Medicine, 2017,56(03): 235-248.
    This article is an English version of an article which is originally in the Chinese language on and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.
    Related Articles

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent Echemi's opinion. If you have any queries, please write to It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to with relevant evidence.