Hyperuricemia - what is it? Types and treatment

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Hyperuricemia - what is it? Types and treatment
Hyperuricemia - what is it? Types and treatment

Video: Hyperuricemia - what is it? Types and treatment

Video: Hyperuricemia - what is it? Types and treatment
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Increased levels of uric acid in a person's blood are classified as hyperuricemia. What it is? This is the result of a disorder of purine metabolism, more often due to environmental factors (nutrition and others) and a genetic factor. This pathology attracted attention after repeated screening studies that revealed its impact on the course of cardiovascular diseases. It is also considered the leading biochemical sign of gout. Hyperuricemia is often asymptomatic and therefore not always immediately detected.

When does hyperuricemia occur?

What is hyperuricemia
What is hyperuricemia

Uric acid is the end product of the metabolism of purine bases. Formed in the liver, it is excreted from the body in the urine. An increase in its concentration in blood plasma indicates the development of certain pathological conditions. It leads tohyperuricemia. In the case of a decrease in the level of uric acid, hypouricemia develops. Its normal level is 360 µm/l in women, and 400 µm/l in men. Excess of these indicators requires clarification of the causative factors, the result of which is hyperuricemia. What it is? This is the result of excess uric acid production and impaired kidney function, the main symptom of gout. It may also be evidence of such pathological conditions as lymphoma, leukemia, anemia due to a lack of vitamin B12, diseases of the biliary tract, liver, kidneys, psoriasis, pneumonia, preeclampsia, tuberculosis, diabetes mellitus, chronic eczema.

Hyperuricosuria and hyperuricemia
Hyperuricosuria and hyperuricemia

In the early stages of disorders of purine metabolism, kidney damage develops, ahead of attacks of gouty arthritis and other symptoms. The fact is that the kidneys are the first to be included in the process of compensating for excess synthesis of uric acid, increasing the normal excretion of urates, which contributes to the risk of crystallization of these s alts in the kidneys. Increased excretion (release) of uric acid has a damaging effect on the tubules, interstitium of the kidneys, contributing to the development of diseases such as hyperuricosuria and hyperuricemia. The first pathological condition is caused by an increased concentration of uric acid in the urine, which is caused by a violation of purine metabolism due to malnutrition, rich in purine bases, a high-protein diet, and alcohol abuse. The second is detected by a biochemical blood test.

Types of hyperuricemia

Hyperuricemia is primary and secondary. The first is more often caused by primary gout, a family genetic anomaly of purine metabolism (constitutional dyspurinism). According to causal factors, it is divided into three types:

  • metabolic type, due to an increase in the synthesis of endogenous purines and characterized by high uricosuria and the rate of purification of biological tissues and body fluids (clearance) of uric acid;
  • renal type, caused by impaired renal excretion of uric acid and characterized by low clearance;
  • mixed type, which is a combination of the first two conditions, in which the uraturia is reduced or does not exceed the norm, and the clearance is unchanged.
Hyperuricemia symptoms
Hyperuricemia symptoms

Symptoms of disease

Recently, hyperuricemia is often diagnosed during a medical examination when donating blood for biochemical analysis. "What it is?" - the first question asked by patients, since they did not notice any signs of the disease. The disease, indeed, often passes almost asymptomatically.

How harmless is this unexpressed hyperuricemia, the symptoms of which, and when they appear, are mostly non-specific? In childhood, this pathological condition can be expressed by constipation, abdominal pain, nocturnal enuresis, logoneurosis, tics, excessive sweating. Adolescents often show signs of hyperuricemia, such as overweight, pain in the lumbar region, itching in the urethra, biliary dyskinesiaways. The clinical picture may be accompanied by intoxication and asthenia. In adults, interstitial nephritis is formed at an early stage in the development of pathology. It is able to mutate into secondary pyelonephritis under the influence of a bacterial infection, creating favorable conditions for the formation of kidney stones. Not uncommon is urolithiasis, or nephrolithiasis. At the basis of the formation of urinary stones, the following metabolic disorders should be noted: modifications of the acidity of urine, hypercalciuria, hyperoxaluria, hyperphosphaturia, hyperuricuria and hyperuricemia. Hyperuricemia is often often combined with various pathologies of the digestive tract.

Risk factors

Hyperuricuria and hyperuricemia
Hyperuricuria and hyperuricemia

The disease, developing against the background of accelerated formation of uric acid, is more often caused by the influence of such factors:

  • participation of purine in metabolic processes;
  • impaired kidney function;
  • high fructose in the daily diet.

Causes of hyperuricemia

The main causes of this condition are the abuse of foods rich in purines, fatty foods. No less dangerous is starvation, as well as tissue destruction, neoplasms of a malignant nature. Can contribute to the development of hyperuricemia diseases of the lymphatic system, blood.

Treatment

Deterioration of the filtration properties and violations of the tubular functions of the kidneys is a trigger that provokes such a pathology as hyperuricemia. What is this conditionIs it hereditary or acquired? The acquired condition often develops in older people as a result of sclerosis of the kidney vessels. Hyperuricemia is also often a companion of such pathologies as anemia, chronic eczema, acidosis, psoriasis, toxicosis during pregnancy.

Hyperuricemia treatment
Hyperuricemia treatment

When a diagnosis of "hyperuricemia" is established, treatment is prescribed based on the data obtained from laboratory tests and other types of additional examinations. Its basis is diet therapy. Foods containing a significant amount of purine derivatives are excluded from the patient's diet, or their use is significantly reduced. The drug course includes uricosodepressor drugs, drugs with uricosuric action. An important aspect of treatment is the achievement of an alkaline urine reaction. Self-medication is unacceptable, even the diet is developed according to an individual plan to prevent one of the serious complications - gout.

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