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    Home > Active Ingredient News > Endocrine System > 7 general directions, direct targeted treatment of gout and hyperuricemia

    7 general directions, direct targeted treatment of gout and hyperuricemia

    • Last Update: 2021-04-19
    • Source: Internet
    • Author: User
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    *For medical professionals to read only for reference.
    Hyperuricemia is inseparable from gout and is an independent risk factor for metabolic diseases, chronic kidney disease, cardiovascular disease, and stroke.

    With the changes in living and eating habits in recent years, the incidence of gout and hyperuricemia in China has been increasing year by year, showing a trend of younger age, higher males than females, and higher coastal areas than inland areas.

    The earliest gout guidelines were proposed by the European Union Against Rheumatism (EULAR) in 2006.
    The early gout treatment guidelines emphasize the treatment of acute attacks and complications.
    The recent guidelines not only emphasize the treatment of the acute phase, but also begin to focus on the reduction of the remission phase.
    Uric acid treatment, especially stratified uric acid lowering treatment.

    At present, it is believed that the best treatment for gout is a comprehensive standardized treatment combining drug therapy and non-drug therapy.

    Adhering to standardized treatment can gradually reduce gout attacks, lower uric acid, and ultimately reverse and cure gout.

    The standardized treatment of gout and hyperuricemia includes the following 7 aspects: 1 Four formulas for non-pharmacological treatment: control your mouth, open your legs, control your weight, and drink more water.
    Both foreign EULAR/ACR guidelines and domestic guidelines emphasize non-drug treatment.
    The importance of medication.

    Diet control, especially a continuous low-purine diet, can reduce the source of uric acid in food.

    It is worth noting that strict diet control can only reduce blood uric acid by 70-90μmol/L, and cannot over-control diet.
    Eating only vegetables and fruits will increase lactic acid due to excessive hunger, leading to gout attacks.

    In addition, it is necessary to maintain proper exercise, control weight, and ensure that you drink 2000-3000ml of water per day.
    The best alkaline water can increase the excretion of uric acid and reduce the chance of urinary calculi.

    2.
    What alkalinize you? When the pH value of my urine is less than 5.
    5, uric acid is supersaturated, and the dissolved uric acid is less.
    When the pH value is 6.
    2-6.
    9, most of the uric acid is in the form of anionic urate.
    Exist, uric acid stones are most easily dissolved and excreted in urine. Therefore, maintaining the urine pH at around 6.
    5 is most conducive to the dissolution and discharge of uric acid stones.

    At present, the commonly used drugs to alkalinize urine are sodium bicarbonate (baking soda) and potassium citrate.
    Because sodium bicarbonate is irritating to the stomach, it is recommended to take it intermittently.

    3 Refusal of high metabolic risk factors A large amount of research evidence shows that hyperuricemia is an independent risk factor leading to diabetes, hypertension, cardiovascular disease, and chronic kidney disease, and it often coexists with these diseases.

    Therefore, patients with hyperuricemia and gout should actively control hyperlipidemia, hypertension, hyperglycemia, obesity, and quit smoking.

    Metformin, atorvastatin, fenofibrate, losartan, and amlodipine all have different levels of uric acid-lowering effects while reducing blood sugar, lipids, and blood pressure.
    It is recommended to choose first.

    4 To make things worse, avoid the use of drugs that increase uric acid.
    Some commonly used drugs in clinical practice can lead to increased blood uric acid, including aspirin, diuretics, cyclosporine, tacrolimus, nicotine, alcohol, levodopa, pyrazinamide, Ethambutol and so on.

    It is recommended that patients use drugs rationally under the guidance of doctors, and try to avoid using drugs that increase uric acid after weighing the pros and cons.

    For patients with hyperuricemia who need to take diuretics, thiazide diuretics should be avoided.

    Although low-dose aspirin can increase blood uric acid, it is not recommended to stop using it as a preventive measure for cardiovascular disease.

    5 Reasonable use of medications, and when patients with gout and hyperuricemia need to use uric acid-lowering drugs are the issues of concern for both patients and doctors.

    Domestic guidelines recommend that patients with gout symptoms and signs should be treated with uric acid-lowering drugs; for patients with hyperuricemia who have not yet experienced gout attacks, cardiovascular risk factors or metabolic diseases, blood uric acid in men exceeds 420μmol/L or in women Uric acid-lowering treatment should be started at 360 μmol/L.
    For those without high risk factors, uric acid-lowering treatment should be used when blood uric acid exceeds 540 μmol/L.

    Note: Uric acid-lowering treatment cannot be started during the acute attack of gout.

    Anti-inflammatory and analgesic drugs should be given first until relief is 1-2 weeks before uric acid-lowering treatment.

    In the early stage of uric acid lowering treatment, it is possible that the rapid decrease in blood uric acid may induce an acute attack of gout.
    There is no need to stop the drug at this time, and anti-inflammatory analgesics can be used to control symptoms.

    Once the uric acid lowering treatment is started, it is recommended not to stop the drug by itself, and the medication should be administered under the guidance of a doctor.

    For ordinary patients, the target of blood uric acid control is 360μmol/L.
    For patients with tophi, it is recommended that blood uric acid be controlled below 300μmol/L to promote the dissolution of tophi.

    The lower the blood uric acid, the less likely to have gout attacks, and the faster the tophus shrinks.

    At present, the commonly used drugs for lowering uric acid include drugs that inhibit the synthesis of uric acid and drugs that increase the excretion of uric acid.

    The former includes allopurinol and febuxostat, and the latter includes benzbromarone and probenecid.

    In addition, uricase can rapidly oxidize uric acid into allantoin, which is not absorbed by the renal tubules but excreted, thereby reducing the blood uric acid level.
    It has not yet been marketed in China.

    6 Long-term maintenance, refusal of gout recurrence.
    After the blood uric acid reaches the standard and the symptoms and signs of gout disappear, some patients will relax their vigilance or even stop the medication by themselves, which finally causes gout to swept through again.

    It is recommended that after the blood uric acid reaches the standard, you should continue to use uric acid-lowering drugs, and perform regular tests.
    Under the guidance of a doctor, you can try to reduce the amount of the drug and find the minimum dose that can maintain the target value of blood uric acid.

    7 Be the master of your own blood uric acid, self-management and regular review is an important part of the standardized treatment of gout and hyperuricemia.
    Understanding the relevant knowledge of gout, participating in the formulation of comprehensive treatment plans, preventing possible adverse drug reactions, etc.
    will help improve patient treatment The compliance and treatment effect of the disease, and fully mobilize patients' enthusiasm for self-management of the disease, can often get twice the result with half the effort.

    Regular review of blood uric acid, liver and kidney function and other indicators is beneficial to adjust the dose of the drug and prevent drug side effects.

    Therefore, only by paying attention to the standardized treatment of gout and hyperuricemia, cooperating with patients and doctors, and combining drug treatment and non-drug treatment, can we achieve the goal of eliminating gout attacks and maintaining blood uric acid standards.

    Source of this article: Medical Reference News Rheumatism Channel Review of this article: Wang Jianhua Editor in charge: Xiao Ma Ma copyright statement  
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