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.

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Obesity should be seen as a potentially chronic disease.🍨🍩🍪

Obesity is not just a physical problem, but a disease that needs attention and treatment. In December 2016, the American Association of Clinical Endocrinologists and the American Endocrinologists Association issued a statement suggesting that a new medical diagnostic term for obesity-based chronic diseases. It was intended to emphasize that obesity affect health and need to control and manage complications as the chronic diseases. 

With the improvement of living standards and changes in lifestyles, the incidence of obesity is showing an obviously increasing. People are paying more and more attention to chronic diseases. The incidences of hypertension, hyperlipidemia and diabetes are also increasing year by year. More researches believe that obesity has become one of the important predisposing factors for many chronic diseases. World Health Organization recognize obesity as the fifth largest risk factor affecting health and can easily lead to many serious complications.

1. Obesity and cardiovascular disease

Obesity can cause the body's fat metabolism disorder which further leads to the occurrence of hyperlipidemia and hypertension. With the increase of BMI, the incidence of hyperlipidemia and hypertension gradually increases.

Adipocytes proliferate and increase in number, the number of insulin receptors on the surface of hypertrophic adipocytes is relatively reduced and insulin affinity decreases. It results in insulin resistance. This may be one of the reasons that obesity leads to abnormal lipid metabolism and causes hyperlipidemia. The mechanism of obesity-induced hypertension may be related to the comprehensive effects of  the immune system, the sympathetic nervous system and the renin-angiotensin system. 

2. Obesity and diabetes

Overweight and obesity are one of the important risk factors related to the onset of diabetes. As the BMI level increases, the risk of disease increases.

The possible mechanism is that excessive eating will cause a large increase in blood sugar and stimulate the islet cells to secrete a large amount of insulin to maintain blood sugar in the normal blood sugar range. It cannot meet the body's requirement for glucose metabolism regulation and cause increased blood sugar. The excess body fat of overweight and obese people leads to the enhancement of fat degradation. Glycogen utilization is impaired, glucose oxidative metabolism decreases and blood sugar rises. In addition, the liver intake of insulin is reduced which leads to an increase in insulin concentration in the body. It leads to hyperinsulinemia and causes down-regulation of insulin receptor expression and insulin resistance.

3. Obesity and hyperuricemia

Uric acid is the end product of purine metabolism which is mainly derived from the enzyme decomposition of nucleic acids and other purine compounds and purine components in food. More and more studies have shown that hyperuricemia is an important component of metabolic syndrome. It has a certain relationship with obesity. Obese people are more likely to suffer from hyperuricemia. Obesity, especially abdominal obesity, is closely related to hyperuricemia. 

The possible mechanisms are: 

1. Too much energy intake, increased purine synthesis in the body and increased uric acid. 

2. Too much eating and too little consumption. It leads to the accumulation of excessive visceral fat and when the liver fatty acid synthesis is hyperactive. It eventually leads to the synthesis of triglyceride and the production of uric acid are hyperactive. 

3. Insulin resistance leads to a decrease in uric acid excretion.

Insulin resistance is one of the main pathophysiological mechanisms of metabolic syndrome and obesity is the theory that leads to the most evidence of insulin resistance.

4. Obesity and other complications

Lungs: The lungs are squeezed by fat. The breathing becomes difficult and it is difficult for the blood to carry out effective oxygen circulation. That can damage the immune system and cause high blood pressure.

Joint: Obesity will increase the weight-bearing of joints such as wrists and knees. It cause osteoarthritis. Obese people are much more likely to develop arthritis than ordinary people.

Intestinal: The fat accumulated around the internal organs will continue to secrete a large number of hormones or chemicals, which will cause changes in metabolism and cause type 2 diabetes. In addition, the secreted hormones can cause endocrine disorders and cause polycystic ovary syndrome, which can have a certain impact on women's future fertility.

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