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    Home > Active Ingredient News > Endocrine System > I didn’t answer these 5 questions correctly, don’t say you understand uric acid and gout

    I didn’t answer these 5 questions correctly, don’t say you understand uric acid and gout

    • Last Update: 2021-04-28
    • Source: Internet
    • Author: User
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    *It is only for medical professionals to read for reference.
    The treatment of hyperuricemia and gout may seem simple, but in fact it is "hidden.

     Do gout patients only require a low-purine diet in terms of diet? no.

    We all know that uric acid is a product of purine metabolism, so foods rich in purines (various meats, animal offal, etc.
    ) need to be avoided in life as much as possible.

    However, there are two types of food ingredients that are also prone to induce gout, that is-fructose and alcohol.

    Although high-sugar beverages and snacks themselves contain low amounts of purines.

    However, the intake of high fructose syrup is positively related to the content of uric acid in the blood, and fructose may accelerate the metabolism of purines.

    Of course, long-term excessive intake of high-sugar beverages can also cause obesity and insulin resistance.

    Therefore, sweet drinks cannot be drunk too much.

    In addition, alcoholic beverages are also a major risk factor.

    Drinking a lot of alcohol can accelerate the decomposition of purines and accelerate the production of uric acid.
    At the same time, alcoholic beverages are not conducive to the filtration of uric acid by the renal tubules, which reduces the excretion of uric acid.

    Therefore, for gout patients, not only beer needs to be consumed less, but also red wine and white wine also need attention.

    We all know that obesity can easily cause gout, so are people with normal BMI less likely to suffer from gout? no.

    On the one hand, in theory, obesity does promote hyperuricemia.
    The reasons are divided into two main aspects: 1.
    Increased uric acid synthesis: due to the increase of free fatty acids, the de novo synthesis of 5-phosphoribose to phosphoribose pyrophosphate is hyperactive; 2.
    Decrease in uric acid excretion: Obesity causes insulin resistance, which in turn affects the hyperactivity of Na+/H+ pump, activation of the sympathetic nervous system and renin-angiotensin system, and renal body fluid disturbances, resulting in increased uric acid reabsorption.

    Therefore, the greater the BMI, the higher the incidence of gout.

    The figure below shows a clinical study of "Am J Med" in 2012.
    The results show that women with a larger BMI have a higher incidence of gout in the 50-70 age group.

    The larger the BMI, the higher the incidence of gout.
    However, on the other hand, BMI cannot completely determine people's risk of gout, because there is another indicator that is very important-waist-to-hip ratio.

    This truth is also easy to understand.

    Waist-to-hip ratio is an indicator of central obesity.
    The higher the indicator, the more obvious the accumulation of visceral fat.

    Therefore, the higher the waist-to-hip ratio (especially >0.
    95), the greater the risk of gout.

    Therefore, to reduce the risk of gout, it is not enough to look at BMI.
    "A4 waist" is also very important! How to distinguish whether there is hyperuricemia or nephropathy first? In clinical practice, hyperuricemia can cause these kidney damages: 1.
    Chronic uric acid nephropathy; 2.
    Uric acid kidney stones; 3.
    Acute hyperuric acid nephropathy.

    Among them, chronic uric acid nephropathy is the most common, that is, urate is deposited in the renal interstitium, leading to chronic tubulointerstitial nephritis.
    In severe cases, it may cause glomerular ischemic sclerosis.

    However, renal insufficiency can also be secondary to hyperuricemia.

    And, the higher the uric acid level, the more obvious the decrease in eGFR.

    The following table (Table 1) can help you distinguish these two types of diseases with different causes: Table 1 Differentiation of uric acid nephropathy and secondary hyperuricemia.
    Is the goal of alkalized urine to be the more "alkaline" the better? It's not.

    When the urine pH value is less than 6.
    0, sodium bicarbonate can be added to promote the excretion of uric acid.

    When pH>7.
    0, calcium oxalate and other crystals are easily formed.

    Therefore, urine pH needs to be monitored when alkalizing urine, and the urine pH level that is most conducive to the dissolution of urate and excreted in urine is between 6.
    2 and 6.
    9.

    Do antihypertensive drugs affect hyperuricemia? some.

    It has been confirmed that β-blockers, loop diuretics, and thiazide diuretics can increase the risk of hyperuricemia.

    However, losartan, certain ACEIs (such as captopril, enalapril, ramipril), and CCB drugs (such as amlodipine, felodipine) can reduce the risk of uric acid.

    In addition, low-dose aspirin, cyclosporine A, mycophenolate mofetil, ethambutol, pyrazinamide, etc.
    tend to increase uric acid levels.

    Table 2 The effects of different drugs on uric acid levels.
    Through the above five questions, we can see that for patients with hyperuricemia and gout, not only should they apply uric acid-lowering drugs, but also "just keep your mouth open and open your legs".
    Alkalize urine and avoid drugs that raise uric acid levels.

    In short, when it comes to hyperuricemia and gout, lifestyle improvement is as important as medication.

     
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