Hyperuricemia - what is it? Types and treatment

An increase in the level of uric acid in a person's blood is classified as hyperuricemia. What it is? This is the result of violation of purine metabolism, more often due to environmental factors (nutrition and others) and genetic factor. This pathology attracted attention after repeated screening studies, which revealed its influence on the course of cardiovascular diseases. It is also considered the leading biochemical sign of gout. Hyperuricemia often occurs asymptomatically, as a result of which it is not always immediately apparent.

When does hyperuricemia occur?

Uric acid is the final product of the metabolism of purine bases. Formed in the liver, it is excreted from the body with urine. An increase in its concentration in the blood plasma indicates the development of some pathological conditions. This leads to hyperuricemia. In the case of a decrease in the level of uric acid, hypouricemia develops. Its normal level is at a maximum of 360 μm / l in women, and in men it is 400 μm / l. Exceeding these indicators requires clarification of the causal factors that result in hyperuricemia. What it is? This is the result of excess uric acid formation and impaired renal function, the main symptom of gout. It can also be evidence of such pathological conditions as lymphoma, leukemia, anemia due to a lack of vitamin B12, bile duct disease, liver, kidney, psoriasis, pneumonia, gestosis, tuberculosis, diabetes, chronic eczema.

At early stages of disturbances of purine metabolism, kidney damage develops, outstripping arthritis attacks and other symptoms. The fact is that the kidneys are the first to be included in the process of compensating for excess uric acid synthesis, increasing the normal excretion of urates, which contributes to the risk of crystallization of these salts in the kidneys. Increased excretion (excretion) of uric acid has a damaging effect on tubules, interstitial kidneys, contributing to the development of diseases such as hyperuricosuria and hyperuricemia. The first pathological condition is due to 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, high protein diet, and alcohol abuse. The second is revealed in the biochemical analysis of blood.

Types of hyperuricemia

Hyperuricemia is primary and secondary. The first is more often due to primary gout, the family-genetic anomaly of purine metabolism (constitutional disparinism). For causal factors, it is divided into three types:

• Metabolic type, caused by the 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;
• Kidney type, caused by impairment of excretion of uric acid by the kidneys and characterized by low clearance;
• Mixed type, which is a combination of the first two states in which the uraturia is reduced or does not exceed the norm, and the clearance is unchanged.

Symptoms of the disease

Recently, often in the course of a medical examination when blood is given for biochemical analysis, hyperuricemia is diagnosed. "What is 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 non-expressed hyperuricemia, the symptoms of which, if manifested, are mostly nonspecific? 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 excessive weight, pain in the lumbar region, itching in the urethra, dyskinesia of the bile ducts. Intoxication and asthenia can be attached to the clinical picture. Interstitial nephritis is formed in adults at an early stage of pathology development . It is able to mutate into secondary type pyelonephritis under the influence of bacterial infection, creating favorable conditions for the formation of kidney stones. It is not uncommon for urolithiasis, or nephrolithiasis. At the heart of the formation of urinary stones should be noted the following metabolic disorders: changes in the acidity of urine, hypercalciuria, hyperoxaluria, hyperphosphaturia, hyperuricuria and hyperuricemia. Hyperuricemia is often combined with various pathologies of the digestive tract.

Risk factors

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

• Involving purine in metabolic processes;
• Impaired renal function;
• Increased fructose in the daily diet.

Causes of hyperuricemia

The main causes of this condition are the abuse of foods saturated with purines, fatty foods. No less dangerous fasting, as well as destruction of tissues, malignant neoplasms. They can promote the development of hyperuricemia of the disease of the lymphatic system, blood.

Treatment

Deterioration of filtration properties and disorders of tubular kidney function is a trigger mechanism provoking such a pathology as hyperuricemia. What is this state, hereditary or acquired? The acquired condition often develops in elderly people as a consequence of sclerosing the vessels of the kidneys. Hyperuricemia is also often a companion of pathologies such as anemia, chronic eczema, acidosis, psoriasis, and toxicosis in pregnancy.

When setting the diagnosis of "hyperuricemia" treatment is appointed based on the obtained data of laboratory tests and other types of additional examination. Its basis is dietotherapy. From the diet of the patient, products containing a significant amount of purine derivatives are excluded, or their use is significantly reduced. The drug course includes uricosodepressor drugs, drugs that have a uricosuric effect. An important aspect of treatment is the achievement of an alkaline urine reaction. Self-medication is unacceptable, even a diet is developed according to an individual plan to prevent one of the serious complications - gout.