Spread the love

With the improvement of modern living standards and changes in dietary structure, gout has gradually extended to young people. We all know that gout is a metabolic disease caused by the deposition of monosodium urate into the joints. It is ultimately related to the reduction of purine metabolism and/or the reduction of uric acid excretion.
Sometimes, even if gout does not have an acute attack, the level of blood uric acid may also be high, namely hyperuricemia (HUA). However, due to the fact that there is no symptoms at ordinary times, no attention is paid to it.
According to statistics, the prevalence of hyperuricemia and gout has generally increased in recent years and has increased with age. Men are higher than women, and coastal areas are higher than inland areas.

The relationship between hyperuricemia and gout

The common feature of both is the effect of serum uric acid (SUA) levels.

Uric acid is produced in the liver by dietary intake and decomposition of purine compounds in the body. About two-thirds of the uric acid is excreted through the kidneys, and the remainder is excreted in the digestive tract. Under normal conditions, the production and excretion of uric acid in the body are kept in balance. Any factor that causes excessive uric acid production and/or reduced excretion can cause HUA.

Urate crystal deposition occurs in patients with HUA, leading to arthritis (gouty arthritis), uric acid nephropathy, and kidney stones known as gout, and some scholars only refer to gouty arthritis as gout.

HUA is the most important biochemical basis and the most direct cause of gout. However, most HUA do not develop gout. Only urate crystals deposit in the body tissue to cause damage and gout; in a few acute patients, SUA levels may also be in the normal range. Therefore, HUA cannot be equated with gout. Neither gout diagnosis nor diagnosis can be ruled out based on SUA levels alone.

Diagnostic criteria for hyperuricemia (HUA)

The diagnostic criteria for HUA were: Normally, fasting blood was collected twice on the same day, and the uric acid enzymatic method was used to measure the blood uric acid value, which was higher in men than in 420 μmol/L or in women over 360 μmol/L. HUA is closely related to gout and is an independent risk factor for diabetes, metabolic syndrome, dyslipidemia, chronic kidney disease, and stroke.

The principle of prevention and treatment of hyperuricemia and gout

Once HUA and gout are diagnosed, they should immediately conduct education and lifestyle interventions, and if necessary, develop appropriate treatment plans.

1. Dietary adjustment

Patients should establish reasonable dietary habits and good lifestyles, limit high-purine animal foods, control the energy and nutrient supply rate, maintain a healthy weight, cooperate with regular reduction of uric acid medications, and regularly monitor follow-up.

Avoid eating liver and kidneys and other animal viscera, shellfish, oysters, and lobsters with crustacean seafood, bouillon, and gravy

Limit food: Animal foods with high purine content a such as beef, mutton, pork, etc.; fish foods; foods containing more fructose and sucrose (such as soft drinks, fruit juices, etc.); various alcoholic beverages, especially beer and distilled spirits (white spirits)

Suggested consumption: Degreasing or low fat and its products; Eggs; Fresh vegetables; Cereal foods with low glycemic index (GI); Full amount of water (more than 2L)

Note:

Alcoholic beverages should be banned in patients with acute gout attacks, poor drug control, or chronic optolithiasis.

Does hyperuricemia require drug treatment without any symptoms?

Some people may ask: I only have high uric acid, but there are no symptoms. In the case of dietary intervention, do I still need medication?

If the gout is confirmed, SUA’s control goal is lower than the diagnostic criteria, that is, long-term control to <360μmol/L to maintain below the saturation point of monosodium urate, and there is evidence that SUA < 300μmol/L will prevent gout Recurrent. Therefore, it is recommended that, as long as gout diagnosis is established, uric acid treatment should be started after acute symptoms are relieved (≥2 weeks); uric acid treatment can also be started immediately on the basis of acute anti-inflammatory treatment to maintain SUA within the target range.

2. Medical treatement

HUA treatment is a key part of gout prevention and treatment. According to studies, the effect of simple dietary control on uric acid is limited, and even a very strict purine diet control can only reduce SUA by 10 to 18% or 70 to 90 μmol/L. Therefore, HUA should be treated with drugs if it is not well treated by non-drug interventions.

Common uric acid lowering drugs mainly include the inhibition of uric acid synthesis and promotion of uric acid excretion drugs. Usually need to choose the medicine according to the cause, complications and liver and kidney function.

1) Uric acid production

Allopurinol

Start with a small dose and gradually increase the amount. The initial dose for adults is 50mg each time, 2~3 times a day, and the blood uric acid level is measured every 2~5 weeks. The non-compliance patients can increase 50~100mg each time and the maximum dose is 600mg/day. Small dose initiation can reduce the burning sensation at the beginning of the early treatment and can also avoid severe allopurinol-related hypersensitivity. The hypersensitivity of allopurinol must be closely monitored during administration, and severe exfoliative dermatitis can occur in severe cases. Studies have shown that allopurinol-related serious hypersensitivity is closely related to the leukocyte antigen HLA-B*5801, so it is recommended that genetic testing be performed prior to the use of the drug when conditions permit, and patients with positive results are prohibited from use.

Case:

The hospital admitted to a male patient. He had taken diclofenac sodium enteric-coated tablets continuously for 4 weeks before the onset of swelling and pain in the joints of both lower extremities and interphalangeal joints. He added allopurinol and cephalexin capsules before 1 month. 5 days before the trunk appeared erythema and papules of rice size, with fever, chills, cough, sputum, diagnosed as “gouty arthritis”, continued oral administration of allopurinol and pulse blood Kang, trunk rash, erythema continued Increased, involving face, limbs, and some of the erythema into a film. Three days ago, the neck was blisters, the wall was loose, and erythema and blisters gradually increased, affecting the entire body. Two days ago, facial edema occurred, mouth, lips, eyes erosion, back and leg exudate. After admission, the doctor saw the symptoms and learned about the medication history. Suddenly he suddenly realized that he was diagnosed as “Euphorbia epidermolysis necrosis type drug eruption”. The allergic possibility was high. He did not rule out diclofenac sodium and cephalexin and immediately stopped all suspicious drugs. , And improve allopurinol-related gene detection.

Follow-up on this case:

The patient was tested for allopurinol-related genes. The results showed that 51 HLA-B*5801 gene mutations were heterozygous and 133 HLA-B*5801 genes were positive, which also strongly validated that the patient’s drug eruption was caused by allopurinol adverse reactions. of.

Special Note: Allopurinol is a first-line medication for the treatment of gout with low price, good efficacy, and clinical use, but allopurinol is prone to serious adverse skin reactions in HLA-B*5801 positive gene population. Therefore, patients are advised to consider HLA-B*5801 allele testing in conditional units before using allopurinol. If the test results are positive, it is highly recommended to use other drugs instead of allopurinol for treatment. If you do not test oral administration of allopurinol, it is advisable to pay close attention to the condition of the skin. If you notice symptoms of skin rash, you should immediately stop the medication and seek medical advice promptly to avoid delaying your illness and causing irreversible consequences.

Femester

The initial dose of 40mg/day, once a day, 2 to 5 weeks after the blood uric acid is not up to the standard, it is recommended to increase to the maximum dose of 80mg/day. Adverse reactions included liver damage, nausea, and rash.

2) Promote uric acid excretion

Benzbromarone

Adult starting dose 50mg/day, once daily, after breakfast. Gastrointestinal discomfort, diarrhea, skin rash, etc. may occur. It is rare and rare liver function damage is rare. During the treatment, a large amount of drinking water is needed to increase urine volume, promote uric acid excretion, and avoid excretion of excessive uric acid to form stones in the urinary system. The sodium bicarbonate or citric acid cocktail may be given as appropriate during the first 2 weeks of starting the medication so that the pH of the patient’s urine is adjusted between 6.2 and 6.9 to increase the uric acid solubility in the urine. Regularly measure the pH of urine.

Probenecul

Adults once 0.25g, 2 times a day, after a week can be increased to 0.5g / time, 2 times a day. The intake of water should also be sufficient when taking, and urine should be basified if necessary.

How to respond to acute gout?

If it is an acute attack of gout, joint symptoms should be quickly controlled. In the acute phase of gout, it is recommended to treat anti-inflammatory and analgesic drugs early (usually within 24 hours). It is recommended to use non-steroidal anti-inflammatory drugs (NSAIDs) such as etoricoxib and celecoxib to relieve symptoms; for NSAIDs In patients with contraindications, it is recommended to use low-dose colchicine alone (1.5 to 1.8 mg/d). If the patient is intolerant to both NSAIDs and colchicine, short-term glucocorticoid alone (30 mg/d for 3 consecutive days) can be selected. Acute attacks involving 1 to 2 large joints, systemic treatment is not effective, may consider intra-articular injection of short-acting glucocorticoids, to avoid repeated use in the short term.

In short, hyperuricemia and gout patients need to pay attention to lifestyle adjustment, low calorie, balanced diet, reduce intake of high purine foods; adequate drinking water (> 2L/day), eat more fruits and vegetables, strict smoking cessation limit alcohol; control weight , Adhere to exercise, daily moderate intensity exercise for more than 30 minutes; also should be regularly monitored, early detection and early treatment, prevention or reduction of cardiovascular, renal function and other complications. Whose life can not be repeated, we should all adhere to a healthy lifestyle and learn to be responsible for our lives!

Leave a Reply

Your email address will not be published. Required fields are marked *