Hyperuricemia is an increased level of uric acid in the blood compared to normal. The normal uric acid content is considered to be 240-400 µm/l.
?By the nature of its occurrence, the primary and secondary forms of the disease are determined.
Primary hyperuricemia is idiopathic in nature, i.e. occurs for unclear, undetected reasons. It is believed that it arises as a consequence of a violation of biosynthesis at the molecular level and the breakdown of nucleids as a result of the pathology of purine metabolism (purines are vital substances found in all cells of the human body).
Secondary hyperuricemia is observed with accelerated breakdown of adenosine phosphate and occurs as a consequence of any disease. This form is often observed with hypoxia of various types, as well as with an imbalance of lactate and glucose in the blood, and also with alcohol abuse.
Secondary hyperuricemia can be the result of a tumor process in myelo- and lymphoproliferative diseases, infectious mononucleosis, pernicious anemia and other diseases with tissue proliferation through cell division.
Treatment of tumor processes can also cause secondary hyperuricemia.
A common consequence of this form is kidney failure, which occurs as a result of uric acid crystals blocking the kidney tubules.
Based on the provoking factors, the causes of hyperuricemia are divided into forms that lead to an increase in the level of uric acid in the blood.
One of the reasons is the excessive formation of uric acid, which results in metabolic or metabolic hyperuricemia.
If the excretion of uric acid by the kidneys is impaired, renal hyperuricemia is determined. Renal hyperuricemia can develop as a hereditary predisposition or be acquired. In both cases, the development of the disease occurs when renal function is impaired according to the filtration-tubular type.
An acquired form of hyperuricemia usually develops in older people due to the growth of scar tissue in the walls of the renal vessels, causing their narrowing - vascular sclerosis.
In addition, the causes of acquired hyperuricemia can be atherosclerosis, arterial hypertension, and diabetes mellitus. Often, long-term and sometimes unjustified use of aspirin, diuretics or other medications also leads to the development of hyperuricemia.
Hyperuricemia resulting from impaired excretion of uric acid from urine, i.e. its accumulation in the urine leads to the formation of sand and kidney stones.
When purine metabolism is disrupted, gout develops - an inflammatory disease of the joints, accompanied by their deformation and acute pain.
The causes of hyperuricemia can be diseases of the blood and lymphatic system, psoriasis, sarcoidosis and other factors that impair kidney function.
Asymptomatic hyperurecemia is the process of increasing uric acid without signs of crystal formation and inflammatory arthritis. Asymptomatic hyperuricemia rarely requires medical intervention and is often referred to as gout without symptoms. With this form of hyperuricemia, there are no manifestations such as tophi, urate stones, urate nephropathy, gouty arthritis, but there is an increased level of uric acid.
Asymptomatic hyperuricemia occurs in 5% of the world's inhabitants, with consequences occurring in approximately 10-20% of them. With this type, there is no impairment of kidney function, and a decrease in the amount of uric acid does not produce any changes in the condition of the body.
Most often, the factors influencing its occurrence are arterial hypertension, obesity, and increased levels of lipids and/or lipoproteins.
Hyperuricemia is one of the factors in the development of gout, a disease of the most well-known types of arthritis. As a result of gout, there is permanent damage to the joints and kidneys. Gout and hyperuricemia are closely related because An increased level of uric acid in the blood leads to the deposition of its crystals in the periarticular tissues. Uric acid penetrates the joint fluid through the bloodstream and forms crystals that destroy and deform them.
For many years, gout was considered a hereditary disease. Approximately 20% of patients have a family predisposition.
But, based on modern research, a connection has been established between purine metabolism and the formation of urate stones. In addition, impaired purine metabolism leads to the inability of pancreatic beta cells to synthesize insulin.
Therefore, gout may be associated with urolithiasis and diabetes.
But gout does not always develop only as a result of excess uric acid production. Its occurrence can be simultaneously caused by reduced filtration of urate by the kidneys or under the influence of various third-party factors.
Signs of gout are acute inflammatory processes, redness of the skin in the affected area, swelling and pain, hyperuricemia, and unilateral joint damage.
Therefore, gout and hyperuricemia must be treated simultaneously.
Symptoms of hyperuricemia vary depending on the origin of the disease, and the main criterion is an elevated level of uric acid. Therefore, for successful treatment of hyperuricemia, it is necessary to undergo appropriate diagnostics to identify the causes and form of development of the disease.
Modern medicine uses several methods to treat hyperuricemia. The main criterion for reducing uric acid levels is adherence to a diet that involves excluding foods high in purines from the diet.
Alcohol and beer, steep meat and fish soups are completely excluded. You should not eat fried, stewed or baked meat and fish dishes. It is not recommended to eat liver, heart, kidneys, sausages, smoked meats, and legumes. The consumption of chocolate, cheeses, cauliflower, sorrel, spinach, and radishes is limited.
The diet includes rabbit, turkey, chicken, soups cooked in recycled broth, fermented milk and dairy products. It is recommended to consume vegetables and fruits rich in potassium - sweet peppers, pumpkin, cucumbers, eggplants, carrots, apricots, pears, apples, grapes, etc.
Useful for hyperuricemia - cherries, viburnum, lingonberries, cranberries, hawthorns and other dark, bright red and blue berries that help reduce uric acid levels.
It is necessary to consume at least 2-2.5 liters of fluid daily, because... water prevents the formation of stones. In addition, it is useful to spend fasting days.
Drug treatment involves the use of probenecid, which helps reduce the level of uric acid in the blood. In addition, xanthine oxidase inhibitors and allopurinol are prescribed.
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 a violation of purine metabolism, most often caused by environmental factors (diet and others) and genetic factors. This pathology attracted attention after repeated screening studies, which revealed its effect on the course of cardiovascular diseases. It is also considered the leading biochemical sign of gout. Hyperuricemia is often asymptomatic, as a result of which it is not always immediately detected.
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 the blood plasma indicates the development of certain pathological conditions. This leads to hyperuricemia. If the level of uric acid decreases, hypouricemia develops. Its normal level is 360 µm/l in women, and 400 µm/l in men. Exceeding these indicators requires clarification of the causative factors that result in hyperuricemia. What it is? This is the result of excess uric acid production and impaired kidney function, the main symptom of gout. This may also be evidence of pathological conditions such as lymphoma, leukemia, anemia caused by a lack of vitamin B12, diseases of the biliary tract, liver, kidneys, psoriasis, pneumonia, preeclampsia, tuberculosis, diabetes mellitus, chronic eczema.
In the early stages of purine metabolism disorders, kidney damage develops, ahead of attacks of gouty arthritis and other symptoms. The fact is that the kidneys are the first to join 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 (secretion) of uric acid has a damaging effect on the tubules and 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 poor nutrition, rich in purine bases, a high-protein diet, and alcohol abuse. The second is revealed by a biochemical blood test.
Hyperuricemia can be primary or secondary. The first is more often caused by primary gout, a family-genetic abnormality of purine metabolism (constitutional dyspurinism). Based on causal factors, it is divided into three types:
Recently, hyperuricemia is often diagnosed during a medical examination when donating blood for biochemical analysis. "What it is?" is the first question that patients ask, since they have not noticed any signs of the disease. The disease, in fact, is often virtually asymptomatic.
How harmless is such mild hyperuricemia, the symptoms of which, even when they appear, are mostly nonspecific? In childhood, this pathological condition can be expressed by constipation, abdominal pain, nocturnal enuresis, logoneurosis, tics, and excessive sweating. Adolescents more often show signs of hyperuricemia such as excess weight, pain in the lumbar region, itching in the urethra, and biliary dyskinesia. Intoxication and asthenia may be added to the clinical picture. In adults, interstitial nephritis forms at an early stage of pathology development. It can transform into secondary type pyelonephritis under the influence of a bacterial infection, creating favorable conditions for the formation of kidney stones. Urolithiasis, or nephrolithiasis, is also not uncommon. The following metabolic disorders are the basis for the formation of urinary stones: changes in urine acidity, hypercalciuria, hyperoxaluria, hyperphosphaturia, hyperuricuria and hyperuricemia. Hyperuricemia is often often combined with various pathologies of the digestive tract.
The disease, developing against the background of accelerated formation of uric acid, is often caused by the influence of such factors:
The main causes of this condition are the abuse of foods rich in purines and fatty foods. No less dangerous is fasting, as well as tissue destruction and malignant neoplasms. Diseases of the lymphatic system and blood can contribute to the development of hyperuricemia.
Deterioration of the filtration properties and disorders of the tubular functions of the kidneys is a trigger that provokes such pathology as hyperuricemia. What kind of condition is this, is it inherited or acquired? The acquired condition often develops in older people as a consequence of hardening of the renal vessels. Hyperuricemia is also often a companion to pathologies such as anemia, chronic eczema, acidosis, psoriasis, and toxicosis during pregnancy.
When a diagnosis of hyperuricemia is made, treatment is prescribed based on the data obtained from laboratory tests and other types of additional examination. Its basis is diet therapy. Products containing significant amounts of purine derivatives are excluded from the patient’s diet, or their consumption is significantly reduced. The drug course includes uricodepressor drugs and drugs that have a uricosuric effect. An important aspect of treatment is to achieve an alkaline urine reaction. Self-medication is unacceptable, even the diet is developed according to an individual plan in order to prevent one of the serious complications - gout.
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If excess uric acid accumulates in the blood, the development of hyperuricemia begins. Such a failure indicates problems with purine metabolism. Diet for hyperuricemia is one of the main methods of treatment. Diet therapy is necessarily accompanied by drug treatment, since as a result of the progression of this disorder, gout develops, a type of arthritis that affects the kidneys and joints.
It is the kidneys that remove the final product of purine metabolism - uric acid. If this process is disrupted, it accumulates in the blood plasma. As a result, the renal tubular system is damaged and disorders such as hyperuricemia and hyperuricosuria develop. If the amount of uric acid decreases, hypouricemia appears. The upper limit of concentration for females is 360 µm/l, for males - 400 µm/l, for children - 320 µm/l.
If a blood test reveals a value higher than the permissible maximum, then the functioning of the kidneys is impaired. This may indicate the progression of gout, and it is also possible to diagnose diabetes mellitus, lymphoma, anemia, gestosis and other diseases. Hyperuricmia can also manifest itself in such ailments and conditions as:
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Correct identification of the type and causes of hyperuricemia plays an important role in diagnosis and selection of medical treatment tools. Based on the nature of its occurrence, the disease is divided into the following forms:
Based on the reasons for their appearance, the following types are distinguished:
Hyperuricemia usually develops asymptomatically, so its detection may be incidental. More often it is diagnosed during the transition to other pathologies, such as pyelonephritis (infectious inflammation in the kidneys), nephrolithiasis (deposition of stones in the kidneys). The onset of stone formation is triggered by the following disorders in the body's metabolism:
A decrease in the body's immunity can further lead to the development of glomerulonephritis (an inflammatory process in the glomeruli of the kidneys). Children with hyperuricemia may experience the following symptoms:
At older ages the following are added:
In adults, hyperuricemia is often asymptomatic. Sometimes accompanied by pain. Disturbances in the digestive tract and metabolism in the myocardium may be recorded. During pregnancy, this disease significantly increases the risk of developing all kinds of fetal pathologies.
The development of hyperuricemia is based on increased excessive formation of uric acid. The following factors can lead to such a metabolic disorder:
The first common cause of this disease is a failure in purine metabolism, which leads to increased accumulation of uric acid in the blood. This occurs against the background of various diseases or hereditary deficiency of the enzyme hypoxanthine-guanine-phosphoribosyltransferase. The second reason is a violation of the excretory function of the kidneys. Both reasons are associated with the problem of filtration-tubular functions of the kidneys.
Secondary hyperuricemia in old age can accompany sclerosis of the renal vessels due to hypertension, atherosclerosis and diabetes mellitus. Sometimes it can be the result of prolonged or improper use of medications such as diuretics and salicylates. Poor nutrition is also considered to be the main factor in the secondary form of hyperuricemia. Eating fatty, heavy foods with a high purine content and alcohol increase the synthesis of uric acid and affect the excretion of urates. Therefore, therapy for this disease begins with a diet.
The main thing in diagnosing such a disorder is donating blood for biochemical analysis. In addition, they take a urine test and do an ultrasound of the kidneys and ureters. If the doctor suspects the development of gout, x-rays of the affected joints and kidneys are prescribed. Correct determination of the cause of hyperuricemia and its type greatly facilitates the further process of normalizing metabolism in the body. When donating blood and urine for analysis, it is recommended to adhere to the following rules:
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Therapy for this disease begins with a strict diet that eliminates or minimizes the consumption of foods containing purine bases. Drug treatment of hyperuricemia consists of prescribing drugs that improve kidney function and accelerate the excretion of uric acid, such as:
A diet for this disease involves reducing the amount of protein foods . It is recommended to eat in small portions, but often. You should avoid alcohol, fried and stewed meat, fish dishes, smoked foods, fatty meat broths, hard cheese, cocoa, chocolate, and canned food. The list of unacceptable foods also includes mushrooms, radishes, legumes, sorrel, cauliflower, and spinach.
It should be remembered that all medications and dietary prescriptions are carried out by a specialist who treats metabolic disorders. It is recommended to drink at least 2.5 liters of liquid. It dilutes urine well and has a preventive effect on the deposition of kidney stones. It is recommended to drink alkaline mineral water for no longer than 2 weeks. Fasting days have a beneficial effect. Light varieties of meat (chicken, rabbit, turkey), acid-urinary low-fat products, boiled eggs, berries, vegetable soups, fruit drinks, fresh juices and compotes are allowed in the diet.
During therapy, the alkaline reaction of urine is monitored using test strips. Treating hyperuricemia on your own, like any other disease, is dangerous to your health. This can lead to complication of the disease and its transformation into other more severe pathologies with further development.
Hyperuricemia is a condition characterized by elevated levels of uric acid in the blood. The pathology belongs to the category of factors that increase the risk of developing gout, one of the most common types of arthritis, which affects the kidneys and joints.
Uric acid is the end product of the metabolism of purines - vital components of any cell of the human body and, first of all, its nucleus. In cases where there is any disruption in the normal course of metabolic processes, uric acid and its acid salts begin to accumulate in the blood, which leads to the development of various pathologies in a person, in particular this contributes to the formation of stones in the urinary tract (kidneys and urinary tract). bladder), gouty deposits, as well as hyperuricemia.
Statistics from recent years indicate that hyperuricemia is observed in almost every fifth adult member of the population and in approximately 3% of children. Moreover, the frequency of cases of development of this condition increases significantly every year, which is due to the negative impact of the deteriorating environment on the human body. Thus, one of the prerequisites for impaired metabolism of purine bases and, consequently, the cause of hyperuricemia is the increased content in the air of large cities of products produced by gasoline car engines.
Hyperuricemia develops against the background of accelerated formation of uric acid, which may be due to the following factors:
The main causes of hyperuricemia are:
In addition, diseases of the blood and lymphatic system, as well as other diseases that impair renal excretion and are characterized by massive breakdown of nucleotides in cell nuclei, can give impetus to the development of hyperuricemia.
Renal hyperuricemia can be either an inherited or acquired condition. However, regardless of the etiology, the trigger mechanism that provokes the pathology is considered to be a deterioration in filtration properties and a violation of the tubular functions of the kidneys. As an acquired condition, hyperuricemia in most cases develops in old age as a result of hardening of the renal vessels. Quite often it is a companion to the following pathologies:
In the pathogenesis of a pathological condition, determining its type is considered extremely important. Hyperuricemia is classified as:
The metabolic type is characterized by increased production of uric acid, its high concentration in the urine (uricosuria) against the background of normal or slightly increased clearance of uric acid.
A distinctive feature of renal type hyperuricemia is a violation of the secretion of uric acid against the background of reduced levels of these parameters.
As for the mixed type, which is a combination of metabolic and renal, such a condition is diagnosed if the patient’s uraturia (excretion of urates and uric acid in the urine) is within normal limits or slightly reduced, and the clearance of uric acid is not changed.
In the early stages of the development of the pathological process, interstitial nephritis forms, which, under the influence of a bacterial infection, can transform into secondary type pyelonephritis. If favorable conditions are created for this, the process of formation of kidney stones also starts.
In addition, it is noted that uric acid can affect the function of the immune system. It is for this reason that the main symptoms of hyperuricemia, in particular in children, include a significant decrease in the protective properties of the body, against which glomerulonephritis often develops.
The pathology is also accompanied by abdominal symptoms, which are expressed in the form of pain. As for young children, their symptoms of hyperuricemia manifest themselves in the form of:
It should also be noted that hyperuricemia that occurs in a pregnant woman is a serious threat to the development of a large number of various pathologies in the fetus. This is due to the fact that uric acid and its salts have a strong teratogenic and nephrotoxic effect.
The main direction of treatment for hyperuricemia is diet therapy, which involves eliminating from the diet or significantly reducing food products containing a large amount of purine bases.
Drug treatment of hyperuricemia involves prescribing to patients:
In addition, ensuring an alkaline urine reaction is considered an important point in treatment.
A diet for hyperuricemia involves reducing protein intake. At the same time, it is recommended to eat food often, but in small portions. The daily diet should be based on the principle: three main meals (and the last of them should be no later than 3.5-4 hours before going to bed) and two or three snacks.
The main requirements of the diet for hyperuricemia are:
Eating meat, fish, seafood and poultry is allowed no more than twice a week. Dairy products should be chosen with minimal fat content (it is better to give preference to fermented milk). You can eat no more than three fruits per day.
In every cell of the human body and in the intercellular space, a constant internal environment is normally maintained. All substances - organic and inorganic - must remain in a strictly defined concentration.
When this balance is disturbed, dangerous diseases and pathological conditions develop that affect all organs and systems.
The body can correct small shifts in the concentration of biochemical compounds on its own, through nervous or humoral self-regulation, and then the person does not feel discomfort. If the regulatory system does not work, deviations from the norm begin to manifest themselves as noticeable symptoms. Hyperuricemia and hyperuricuria are one of these metabolic disorders.
Hyperuricemia, also known as hyperuricosuria, is an excess of uric acid concentration in the blood of more than 360 µM/L in women or more than 420 µM/L in men.
This acid appears in the body due to the metabolism of purine compounds.
This disease is very common - it affects about a fifth of the adult population and about 3% of children, but as a rule, patients rarely know about it.
Most people who have not encountered this diagnosis in their lives do not know what hyperuricosuria and hyperuricemia are and how they differ. Hyperuricosuria is a condition in which the content of uric acid in urine increases.
If the doctor has diagnosed “hyperuricemia”, you should ask him in detail about this disease, clarify all the unclear nuances in order to avoid errors in treatment.
Depending on the underlying causes of the increase in uric acid, three types of hyperuricemia are distinguished:
The type and cause of hyperuricemia can only be determined after a comprehensive diagnosis and consultation with specialists.
Hyperuricemia has the following causes:
Many causes of hyperuricemia depend on a person's behavior and lifestyle, so the risk of developing the disease can be reduced by avoiding such factors.
Hyperuricosuria and hyperuricemia have few symptoms.
Exceeding the normal level of uric acid in the blood is the only symptom.
The indicator can be determined using laboratory tests. Otherwise, the disorder manifests itself when gout, nephrolithiasis or other diseases develop against its background.
Therefore, in most cases, asymptomatic hyperuricemia is detected by chance, during the diagnosis of other diseases. Doctors characterize this condition as the first stage of the development of hyperuricemia. It can last for several decades.
The second stage is accompanied by pathological changes in organs. In childhood, hyperuricemia can manifest as disruption of the digestive, urinary, nervous system, and skin functioning. In this case, constipation, speech defects, nervous tics, severe sweating, nocturnal enuresis, pain in joints and muscles develop.
Even states of intoxication may occur.
In adolescents, other manifestations occur: itching in the urethra, lower back pain, biliary dyskinesia, and accumulation of excess weight.
In adults, an increase in uric acid levels is often provoked by pathologies of the digestive tract. Patients with hyperuricemia are more likely to experience metabolic disorders in the myocardium.
If this phenomenon occurs in the body of a pregnant woman, the likelihood of multiple developmental pathologies in the fetus increases, since uric acid salts have a strong toxic effect on the tissue.
There is also the concept of intercritical hyperuricemia. Doctors use this term to refer to signs of the condition between exacerbations. Remission for this disease can last up to two years.
The symptoms of hyperuricemia are nonspecific, that is, they are characteristic of many other diseases, so it is impossible to independently identify the pathology by external manifestations.
The risk of developing hyperuricemia increases if a person's body is exposed to risk factors. These include:
To prevent the development of hyperuricemia, you should try to avoid the effects of these factors. This is a truly dangerous condition that can provoke the development of severe incurable illnesses or diseases that become chronic.
Due to the accumulation of uric acid, tubulointerstitial nephritis, kidney stones, gouty arthritis and other pathologies develop. This pathology has an extremely negative impact on the developing fetus.
The increase in uric acid is very dependent on nutrition, so you need to plan your diet wisely.
The main ways to eliminate hyperuricemia are diet and medication. Only an integrated approach can have a therapeutic effect and prevent the development of dangerous diseases against the background of impaired metabolism.
The diet for hyperuricemia should be designed in such a way that the patient’s diet contains as little as possible purine compounds and substances involved in the accumulation of uric acid.
The patient's diet should not contain the following foods:
You should limit the consumption of greens and some vegetables (spinach, cauliflower, sorrel, radishes), chocolate, and cheese.
To improve the condition of the body and prevent the accumulation of uric acid, the following products are introduced into the diet:
Potassium-containing plant products are very useful for this disease - white cabbage, peaches, zucchini, melons, bananas, carrots, lemon, pears, cucumbers, green peas, pumpkin, eggplant.
It is better to choose berries that are dark in color (blue, red) - cherries, cranberries, blueberries, lingonberries, cherries. You should drink a lot of fluid (at least 2.5 liters), but if swelling occurs, it is better to consult a doctor about the daily intake.
You can add berry juice to water, this helps remove uric acid from tissues. One day a week should be a fasting day so that the body can cleanse itself of harmful metabolites that contribute to the development of hyperuricemia.
Allopurinol Sandoz tablets
Hyperuricemia treatment also includes medications. It is recommended to take drugs that accelerate the excretion of uric acid and prevent its formation in the body from purine compounds. Allopurinol and Probenecid are used as medications .
If any symptoms of concomitant illnesses or complications develop, they need to be eliminated with the help of special therapy. Constant monitoring of the patient’s condition is necessary, for which he undergoes examinations of internal organs, blood tests, and laboratory tests of urine.
Therefore, only a doctor can prescribe a complete and only correct treatment; self-medication can lead to a worsening of the condition, the appearance of other diseases, and their transition to a chronic form.
Negligence in drug treatment and non-compliance with diet can lead to a deterioration in the patient’s condition; an advanced disease is much more difficult and expensive to treat.
About the connection between obesity and hyperuricemia:
If symptoms of hyperuricemia appear, or the fact of an increase in uric acid is detected by chance during an examination, this should not be ignored. The diet and drug therapy prescribed by your doctor should be followed carefully. With timely treatment, the risk of pathological changes in vital organs is reduced. If hyperuricemia is accompanied by gout or kidney disease, the body requires even more attention.
Hyperuricemia is an increased level of uric acid in the blood. Normally, its content should not exceed 360 micromol/liter (6 mg/dL) for women and 400 micromol/liter (6.8 mg/dL) for men
The most common cause of hyperuricemia is disorders of purine metabolism in the body, as a result of which the formation of uric acid is accelerated, caused by various diseases or congenital deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase. Another common cause is weakened kidney function.
Excessive consumption of foods rich in fructose and purine compounds (primarily canned fish in oil, fatty meat and fish, caviar, almost all offal) also leads to hyperuricemia. Its occurrence is also provoked by fasting and overly strict diets, in which muscle mass begins to be wasted to produce energy, as a result of the “processing” of which a large amount of purines enters the blood.
Almost all symptoms of hyperuricemia are nonspecific, that is, they do not clearly indicate this particular pathology. Patients often experience abdominal pain, constipation, myalgia and arthralgia, increased sweating, excess body weight, itching in the urethra, biliary dyskinesia, lower back pain, and in children nocturnal enuresis. Many patients suffering from hyperuricemia are prone to blood pressure disorders (hyper- or hypotension).
Very often, hyperuricemia in the early stages does not manifest itself at all, and the only way to detect it is a biochemical blood test.
Treatment of hyperuricemia should be comprehensive; its main components are diet and drug therapy.
First of all, it is necessary to exclude foods high in purines from the diet. These are fatty fish and meat dishes, offal, canned food, sausages, as well as alcoholic drinks (including beer). You should limit your consumption of spinach, sorrel, cheese, radishes, cocoa, chocolate, and cauliflower.
The basis of the diet for hyperuricemia should be lean poultry, dairy and fermented milk products, fruits, vegetables and herbs (except for those mentioned above). It is especially important to enrich your diet with foods rich in potassium (eggplant, pumpkin, white cabbage, cucumbers, carrots, sweet peppers, apricots, green peas, grapes, melons, pears, apples, cherries, cranberries, blueberries, lingonberries).
If you have hyperuricemia, you need to drink plenty of fluids; it is recommended to drink at least 2 liters of water daily (of course, if there are no contraindications due to other diseases). It is also good to have fasting days that are not too strict once a week.
The main goal of urate-lowering therapy is to maintain serological urate levels, which requires regular monitoring and, if necessary, dose adjustment of the drug. Xanthine oxidase inhibitors are used in patients with excessive synthesis and decreased excretion of urate, but they are used with caution in combination with azathioprine and 6-mercaptopurine, since xanthine oxidase is involved in their metabolism.
Allopurinol is the first choice drug for uricodepressive therapy in patients with hyperuricemia and gout. Allopurinol is also used with caution in patients with renal failure (CC is taken as a basis). The maximum daily dose can reach 800 mg. Adverse reactions may manifest as a rash in 2% of patients, and the risk of their development increases with concurrent use of amoxicillin, ampicillin, thiazide diuretics or ACE inhibitors. Hypersensitivity to allopurinol is rare (in 0.1% of patients), but can be fatal (mortality rate is 20%).
Considering that adverse reactions of allopurinol can be very serious and even life-threatening in patients, especially with renal failure, there is a need to find an alternative drug for use in such patients.
Probenecid is a drug used for uricosuric therapy.
Among the new drugs to lower uric acid levels and reduce the development of tophi is pegloticase. The drug requires preliminary premedication with antihistamines and corticosteroids. Among the main disadvantages of the drug are: high cost, administration, formation of antibodies, decreased effectiveness in some patients, general reactions to the infusion.
At one of the last scientific congresses in Los Angeles, modern aspects regarding the principles of treatment of hyperuricemia and gout were considered. Scientists have come to the conclusion that today it is necessary to abandon the “old” therapy for this pathology and move on to “new” therapy. A number of modern drugs were presented that need to be introduced into practice and their advantages and effectiveness should be intensively studied. Specifically, these include anakinra, rilonacept, canakinumab, pegloticase and lesinurad. Unfortunately, the high cost of these drugs does not allow them to be widely used and studied, but scientists are confident that the future of medicine depends primarily on the introduction of new things and the abandonment of old ones.
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Uricemia is the level of uric acid in the blood. Uric acid is the end product of purine metabolism. Normally, uricemia does not exceed 0.5 mmol/l. If the uric acid content is exceeded, hyperuricmia develops. In this case, uric acid salts can be deposited in tissues, in particular in joints. Also, in parallel, patients develop hyperuricosuria - an increase in the content of uric acid in the urine. This condition promotes the formation of stones (urates) in the urinary tract. This condition can develop in adults or children.
Increased uricemia can be temporary, caused by excessive consumption of nitrogen-containing foods (meat, fish, legumes) or be a symptom of some pathology. The causes of the disease are associated with metabolic failures (impaired purine metabolism) or kidney diseases. Symptoms of the disease are nonspecific: it can be pain in the abdomen, muscles, joints, nervous tics, headache, nausea. Treatment consists of reducing the level of uric acid in the blood, for which it is necessary to follow a diet and take traditional medicines: tinctures and decoctions of medicinal herbs. This treatment has a gentle effect on the body and does not cause side effects.
Hyperuricemia can be primary or secondary. Primary elevated uricemia is associated with genetic metabolic disorders and is congenital. The secondary form of the disease is a sign of some disease.
Depending on the etiology, there are metabolic, renal and mixed hyperuricemia.
The most common causes of the disease are metabolic. Hyperuricemia and hyperuricosuria develop due to impaired purine metabolism. In this case, there is an increased formation of uric acid, which simply does not have time to be excreted by the kidneys.
Another common cause of pathology is disruption of normal kidney function. Renal increased uricemia develops due to impaired filtration in the renal glomeruli. The following factors may contribute to this:
Increased uricemia develops in humans due to the abuse of certain foods rich in purine bases. Such products include fatty meats and fish, offal (liver, kidneys, heart), canned fish, caviar. However, the opposite condition can also increase the level of uric acid in the blood - fasting and following strict diets.
Effective treatment of the disease is only possible with an accurate determination of the cause of the pathology, since it is important not only to remove excess uric acid from the body, but also to prevent a further increase in this indicator.
The following symptoms of the disease are distinguished:
Increased uricemia is diagnosed using a laboratory biochemical blood test. Such an analysis will also help assess the functioning of the kidneys and gastrointestinal tract. Hyperuricosuria is diagnosed using a biochemical urine test.
The test is taken in the morning on an empty stomach. It is prohibited to consume alcohol or protein-rich foods before donating blood, as this may distort the picture.
An x-ray examination of the joints is carried out to determine the presence of deposits of uric acid salts in them.
Treatment of the disease must be comprehensive. Folk remedies are used to remove uric acid from the blood and other tissues of the body. Traditional treatment is safer, has a mild effect and does not cause side effects.
In therapy, it is important to follow a diet. It is necessary to exclude foods high in purines from your diet. Such products include canned meat and fish, fatty meats and fish, offal, fish caviar, sausages and smoked meats. It is not recommended to eat fried, fatty foods and smoked foods. Spinach, sorrel, radishes, cauliflower, cocoa, and cheese are also contraindicated in this condition. Patients with hyperuricemia are prohibited from drinking alcoholic beverages, especially beer.
It is best to stick to a vegetarian diet, eat fresh vegetables and fruits, cereals, and herbs. It is allowed to eat lean meats and fish, but not more than three times a week.
It is important to eat foods rich in potassium. A lot of potassium is found in vegetables (eggplant, pumpkin, cucumbers, white cabbage, carrots, bell peppers) and fruits (melon, grapes, apricots, apples, pears, berries).
Patients with hyperuricemia need to drink a lot and drink at least 2 liters of clean water per day.
Artichokes have a diuritic effect. This plant is consumed boiled. It is also useful to drink artichoke broth or cook soups or porridges with it.
Apples are also useful for removing uric acid. Drink 1 glass of freshly squeezed sweet apple juice daily. It is also useful to make dessert from this fruit: lightly fry apples sprinkled with sugar in a frying pan.
Strawberries reduce uric acid content. Fresh berries are eaten in the summer, and at other times of the year you can cook compotes from dried or frozen berries.
It is useful to arrange fasting days once a week. It is best to choose a day off for these purposes, when you can completely relax. In the morning on such a day, you need to do an enema with a decoction of chamomile or calendula. During the day you need to drink water, herbal teas or green tea without sugar and honey. In the evening they do the enema again. For the next two days after the fasting day, you should eat only steamed vegetables or cereals without milk, and do not eat “heavy” foods.
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