Gout: why does uric acid still raising although control the diet strictly?😵😵😵

Changes in uric acid can be affected by many factors. Although patients with gout have to control their diet, the effect of controlling uric acid is also uncertain. Some patients even usually do not eat seafood and animal offal, and legumes are rarely high, but uric acid is still increasing. Faced with this situation, should the patient take uric acid-lowering drugs?

1. Although patients have controlled their diet, why are the uric acid still increasing?

Hyperuricemia can be divided into 3 types: high uric acid production, poor uric acid excretion and mixed type. Researches found that 90% of primary hyperuricemia belong to the type of poor uric acid excretion. 80% of blood uric acid comes from the body's synthesis and 20% comes from diet. Therefore, the effect of reducing uric acid only by controlling diet is very limited. However, since high sodium salt can affect the excretion of uric acid, patients with gout should control their salt intake.

2. Why do hyperuricemia and gout cause kidney damage?

In patients with hyperuricemia, if urate crystals are deposited in the joints, it will cause gouty arthritis. If urate crystals are deposited in the kidneys, it will cause kidney stones, interstitial nephritis, acute and chronic renal failure. Kidney damage is the second most common comorbidity of hyperuricemia and gout.

3. Blood uric acid is not too high, why do gout attacks?

20% of patients with gout have a family history. There are three major factors that induce gout attacks: 

The blood uric acid level is too high

• According to statistics, the blood uric acid level at the first attack of gout was 527μmol/L for men and 516μmol/L for women. Therefore, when the blood uric acid level is greater than or equal to 540 μmol/L, uric acid-lowering treatment should be started. The blood uric acid should be controlled to be less than 420 μmol/L.

The blood uric acid level fluctuates too much

• A sudden increase in blood uric acid levels can cause gout attacks. In male patients, the most important factor inducing gout attacks is drinking (25.5%), followed by high-purine diet (22.9%). A sudden drop in blood uric acid levels can also cause gout attacks. For the first 3 to 6 months of taking uric acid lowering drugs, colchicine (0.5 to 1 mg/day) should be taken orally to prevent gout attacks.

A sudden cold of limbs

• At a body temperature of 37°C, the saturated solubility of blood urate is 404.5 μmol/L. The lower the temperature, the lower the solubility of urate. When the blood supply of the foot is poor, the temperature of skin and the pH of the tissue fluid are low and under a great pressure. Most of the joints of first time gout are the first metatarsophalangeal joints.

4. Why must patients with gout avoid from alcohol and lose weight?

Alcohol metabolism requires the participation of adenosine triphosphate. The consumption of adenosine triphosphate can directly increase the production of uric acid. Alcohol also leads to an increase in serum lactic acid levels which can reduce uric acid excretion. Therefore, patients with gout must abstain from alcohol. Obesity can lead to insulin resistance which increases kidney reabsorption of uric acid and increases blood uric acid levels. Therefore, obese hyperuricemia and gout patients must lose weight.

Patients with gout should not eat fruits with high fructose content such as oranges, apples, grapefruits, longans, lychees,  persimmons and pomegranates. Patients with gout should not eat more plant foods with high purine content such as shiitake seaweed, mushrooms, asparagus, straw mushrooms, kelp and grain germs.

Lemons, cherries and olives are relatively beneficial to patients with gout.

5. Which uric acid lowering drug is better for patients with gout?

At present, the commonly used clinically for lowering uric acid are febuxostat, allopurinol and benzbromarone. Uric acid-lowering drugs can be selected according to the following 3 points:

1. Uric acid-lowering effect: febuxostat > allopurinol ≈ benzbromarone.
2. Potential cardiovascular event risk: febuxostat > allopurinol.
3. Fatal exfoliative dermatitis: allopurinol (prohibited for those with positive HLA-B*5801 gene).
4. Hepatotoxicity: benzbromarone> allopurinol ≈ febuxostat.

180μmol/L ≤ blood uric acid ＜ 300μmol/L can promote the dissolution of tophi. The control target of blood uric acid in patients with gout is < 360μmol/L. For patients with hyperuricemia without comorbidities, the control target is < 420μmol/L.

6. Should the patient use uric acid lowering drugs?

For all gout patients, it is recommended to start uric acid-lowering drug treatment when blood uric acid is ≥480μmol/L.

Patients with chronic kidney disease, hypertension, diabetes, dyslipidemia, stroke, ischemic heart disease, heart failure and gout whose age of onset is less than 40 years old. It is recommended to start uric acid-lowering drug treatment when blood uric acid is ≥ 420μmol/L.

The glomerular filtration rate of this patient is less than 60ml/min. The uric acid production inhibitor febuxostat or allopurinol can be preferred.

👉When combined medicines, they should be used that do not affect or reduce the level of uric acid.