Uric acid in serum

Uric acid is a product of the metabolism of purine bases, which are part of complex proteins - nucleoproteins. The resulting uric acid is excreted by the kidneys. Uric acid in the extracellular fluid, including blood plasma, is present in the form of sodium salt (urate) in a concentration close to saturation, so there is a possibility of its crystallization when the maximum normal values are exceeded.

In adult men, the upper limit of normal serum uric acid concentration is considered to be 0.42 mmol/l. In an aqueous solution with a pH of 7.4, at a temperature of 37 °C and an ionic strength equal to that in plasma, the solubility of sodium urate is 0.57 mmol/l; in plasma in the presence of proteins, it is slightly lower. Knowledge of these constants is of great practical importance, as it allows one to determine the goals of treatment of patients with gout, i.e., to what level it is necessary to reduce the concentration of uric acid in the blood serum in order to achieve dissolution of urates in the extracellular fluid and tissues.

Reference values for serum uric acid concentration

	Serum uric acid concentration
Age	Mmol/l	Mg/dl
Up to 60 years: Men Women Over 60 years old: Men Women	0.26-0.45 0.14-0.39 0.25-0.47 0.21-0.43	4.4-7.6 2.3-6.6 4.2-8.0 3.5-4.2

Increased concentration of uric acid in the blood

The main factors that influence uric acid levels are:

1. Diabetes mellitus: Patients with diabetes may have elevated uric acid levels, especially if the diabetes is not well controlled.
2. Metabolic syndrome: Metabolic syndrome, including obesity, high blood pressure, carbohydrate metabolism disorders, and dyslipidemia, can lead to hyperuricemia.
3. Urolithiasis: The formation and accumulation of uric acid can contribute to the formation of urinary stones (urate stones).
4. Food and Drink: Eating foods and drinks rich in purines can increase uric acid levels. Purines are substances that are broken down in the body into uric acid. Examples of such foods include red meat, seafood, alcohol (especially beer), sugar-sweetened beverages, and some vegetables (such as spinach and asparagus).
5. Hyperparathyroidism: Hyperparathyroidism is a condition in which the parathyroid glands produce excess amounts of parathyroid hormone, which can lead to high uric acid levels.
6. Renal failure: In patients with chronic renal failure, hyperuricemia may occur due to impaired renal excretion of uric acid.
7. Genetic factors: Certain genetic mutations may predispose to elevated uric acid levels.
8. Medications: Certain medications, such as diuretics, low-dose aspirin, some cancer drugs, and some antihypertensives, can increase uric acid levels.
9. Alcohol: Drinking alcohol, especially in large quantities, can contribute to elevated uric acid levels.
10. Effects of fasting and starvation: Long-term fasting, fasting or strict dieting can also increase uric acid levels.
11. Kidney failure: When kidney function is impaired, the kidneys may not be able to perform their role in removing uric acid from the body, which can lead to its accumulation in the blood.
12. Post-resuscitation syndrome: Some people may develop temporary increases in uric acid levels after resuscitation and treatment of acute conditions.
13. Kidney disease: Certain kidney diseases, including chronic renal failure and nephrotic syndrome, can lead to hyperuricemia.
14. Enzyme deficiencies: Rare genetic disorders such as Lesch-Nyhan disease and Keltonen-Turner disease can result in deficiencies of enzymes involved in processing uric acid.
15. Consuming large amounts of fructose: Fructose is a type of sugar that can lead to elevated uric acid levels in the blood, especially when consumed in excess from high-fructose syrups, which are used in some industries.
16. Oxidative uric acid syndrome: This is a genetic metabolic disorder in which the body produces too much uric acid.
17. Hypothyroidism: Low thyroid function can also increase uric acid levels.
18. Increased cell destruction: Injuries, tumors, chemotherapy, and some other conditions can contribute to increased cell destruction, which can lead to high uric acid levels.
19. Polycythemia: Polycythemia is an increase in the number of red blood cells in the blood. Some cases of polycythemia can cause hyperuricemia.
20. Obesity: Some people who are obese may have increased uric acid production.
21. Overproduction of uric acid: In rare cases, excess production of uric acid in the body may occur.

Increased uric acid concentration in the blood (hyperuricemia) is of great importance for the diagnosis of gout. A distinction is made between primary gout, in which the accumulation of uric acid in the blood is not caused by any other disease, and secondary gout, which develops as a result of impaired renal function, increased formation of purines in hematological diseases accompanied by the disintegration of many nuclear cells, after exposure to X-rays, in malignant neoplasms, cardiac decompensation, tissue destruction during starvation, and other cases. Thus, primary and secondary gout occur as a result of impaired excretion of uric acid or its excess production.

Primary gout is a consequence of hyperuricemia, which develops with slow excretion (90% of cases) or excessive synthesis (10% of cases) of uric acid. Urate crystals can be deposited in joints, subcutaneous tissue (tophi) and kidneys.

Risk of developing gout depending on the concentration of uric acid in the blood serum

Uric acid concentration	Risk of developing gout,%
In blood serum, mmol/l	Men	Women
Below 0.41 0.42-0.47 0.48-0.53 Above 0.54	2 17 25 90	3 17 No data No data

Determination of uric acid concentration in the blood is of particular importance in the diagnosis of asymptomatic hyperuricemia (uric acid in the blood in men is higher than 0.48 mmol/l, in women higher than 0.38 mmol/l) and the latent development of gouty kidney (in 5% of men). Acute gouty arthritis occurs in 5-10% of patients with asymptomatic hyperuricemia. Hyperuricemia in patients with gout is inconsistent and can be of a wave-like nature. Periodically, the uric acid content can decrease to normal values, but an increase of 3-4 times compared to the norm is often observed. To obtain accurate data on the uric acid content in the blood, most adequately reflecting the level of its endogenous formation, it is necessary to prescribe a low-purine diet to patients for 3 days before the study. In addition, it is necessary to know that during an acute attack of gout, the concentration of uric acid in the blood serum decreases to normal values in 39-42% of patients. Criteria for diagnosing gout:

• the concentration of uric acid in the blood serum in men is higher than 0.48 mmol/l, in women higher than 0.38 mmol/l;
• the presence of gouty nodules (tophi);
• detection of urate crystals in synovial fluid or tissue;
• history of acute arthritis, accompanied by severe pain, which began suddenly and subsided within 1-2 days.

The diagnosis of gout is considered reliable if at least two of any signs are detected.

Secondary gout can develop with leukemia, vitamin _B12 -deficiency anemia, polycythemia, sometimes with some acute infections (pneumonia, erysipelas, scarlet fever, tuberculosis), liver and biliary tract diseases, diabetes mellitus with acidosis, chronic eczema, psoriasis, urticaria, kidney disease, acidosis, acute alcohol intoxication (secondary "alcoholic's gout").

The diagnostic value of determining the uric acid content in the blood in renal failure is minimal.

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