Types of dyslipidemia and its causes. Hyperlipidemia - what is it? Hyperlipidemia: causes, symptoms, treatment Hyperlipidemia types

Nevertheless, hyperlipidemia is a risk factor for the development of cardiovascular diseases, especially atherosclerosis, and needs to be controlled, corrected and treated.

Types of hyperlipidemias

The classification of types of hyperlipidemias was developed by Donald Fredikson in 1965 and has been adopted by the World Health Organization as an international standard. It is still in use today. According to Fredikson's classification, there are five types of hyperlipidemias.

Type I. This is a rare type of hyperlipidemia that occurs when lipoprotein lipase is deficient or there is a defect in the lipoprotein lipase activator protein. In this type of disease, levels of chylomicrons (lipoproteins that carry lipids from the intestines to the liver) are elevated. Hyperlipidemia worsens after fatty foods and decreases after fat restriction, so diet is the main treatment.

Type II. A common type of hyperlipidemia in which low-density lipoprotein levels are elevated. It is subdivided into two subtypes depending on the presence of high triglycerides, which require the additional administration of gemfibrozil during treatment. Hyperlipidemia of this type leads to the development of atherosclerosis after years and can cause a heart attack in older men and women.

Type III. A type of hyperlipidemia also called dys-beta lipoproteinemia. The disease is characterized by hereditary causes, and is associated with a defect in Apolipoprotein E, and is also characterized by an increase in the level of high density lipoproteins. Carriers of hyperlipidemia are prone to obesity, gout, mild diabetes mellitus and are at risk for atherosclerosis.

Type IV. A type of hyperlipidemia characterized by elevated levels of triglycerides. Their levels rise after taking carbohydrates and alcohol. Against the background of this syndrome, atherosclerosis, obesity, diabetes mellitus and pancreatitis can develop.

Type V. A type of hyperlipidemia, similar to the first, but in contrast to it, not only the level of chylomicrons, but also very low density lipoproteins increases. Therefore, as in the case of the first type, the fat content in the blood jumps after eating fatty and carbohydrate foods. Hyperlipidemia of this type is fraught with the development of severe pancreatitis, which develops against the background of eating too fatty foods.

In addition to this classification, there are two more types of hyperlipidemia - hypo-alpha-lipoproteinemia and hypo-beta-lipoproteinemia.

Symptoms

Hyperlipidemia is mostly asymptomatic and is most often detected during a general biochemical blood test. Preventive analysis for cholesterol levels should be carried out from the age of 20 at least once every five years. Sometimes, with hyperlipidemia, fatty bodies are formed in the tendons and skin of the patient, which are called xanthomas. An enlarged liver and spleen, as well as signs of pancreatitis, can serve as a pathological symptom.

Causes of the disease

The level of blood lipids depends on a number of factors, which include the presence of saturated fatty acids and cholesterol in the daily diet, body weight, level of physical activity, age, diabetes, heredity, medication, blood pressure disorders, kidney and thyroid disease, smoking and drinking alcoholic beverages.

Treatment of hyperlipidemia

Depending on the type of hyperlipidemia, either a diet with increased physical activity alone or a specific combination of drugs can be prescribed, the choice of which can only be made by the attending physician. Treatment of hyperlipidemia is almost always accompanied by a low-fat diet and control of blood lipids. To reduce the level of cholesterol and triglycerides, a course of exercise therapy is prescribed, aimed at weight loss. The well-being of the patient is well affected by the elimination of bad habits, as well as therapeutic cleansing procedures.

Treatment for hyperlipidemia may include statins, which lower blood cholesterol levels and keep cholesterol from being deposited in the liver. Additionally, fibrates and choleretic drugs may be prescribed. In the treatment of hyperlipidemia, vitamin B5 has proven itself well.

This article is posted for educational purposes only and does not constitute scientific material or professional medical advice.

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What happened?

Type V. A type of hyperlipidemia, similar to the first, but in contrast to it, not only the level of chylomicrons, but also very low density lipoproteins increases. Treatment for hyperlipidemia depends on the level of lipids in the blood, the risk of developing heart disease, and general health.

In addition, some hyperlipidemias affect the development of acute pancreatitis. This hyperlipidemia can be sporadic (due to malnutrition), polygenic, or hereditary.

Treatment for this hyperlipidemia includes dietary modification as a major component of therapy. This form of hyperlipidemia is manifested by an increase in chylomicrons and LPP, therefore it is also called dis-beta-lipoproteinenia. In this article, we will talk about what hyperlipidemia is, describe the symptoms of this phenomenon and see how this disease is treated. Primary hyperlipidemia is genetically inherited, but the genetic defect is found in only a small number of patients with atherosclerosis.

Diagnosis of hyperlipidemia

Hyperlipidemia is a group of disorders characterized by an increase in the level of blood cholesterol, especially its LDL fractions and/or triglycerides. It is believed that hyperlipidemia is inherited from parents, but the following factors influence its development: certain diseases and drugs, unhealthy diet and alcohol.

All this only worsens the course of hyperlipidemia. If a patient has hyperlipidemia, he is referred to a cardiologist, neurologist, vascular surgeon, depending on the organs most affected by atherosclerosis. Nevertheless, hyperlipidemia is a risk factor for the development of cardiovascular diseases, especially atherosclerosis, and needs to be controlled, corrected and treated. The classification of types of hyperlipidemias was developed by Donald Fredikson in 1965 and has been adopted by the World Health Organization as an international standard.

Type I. This is a rare type of hyperlipidemia that occurs when lipoprotein lipase is deficient or there is a defect in the lipoprotein lipase activator protein. In this type of disease, levels of chylomicrons (lipoproteins that carry lipids from the intestines to the liver) are elevated. Hyperlipidemia of this type leads to the development of atherosclerosis after years and can cause a heart attack in older men and women. Carriers of hyperlipidemia are prone to obesity, gout, mild diabetes mellitus and are at risk for atherosclerosis.

How to treat hyperlipidemia?

In addition to this classification, there are two more types of hyperlipidemia - hypo-alpha-lipoproteinemia and hypo-beta-lipoproteinemia. Hyperlipidemia type I is characterized by a high content of triglycerides in the blood, including chylomicrons. However, most often this term means an increased level of cholesterol and triglycerides in the blood, which are related to lipids. Most hyperlipidemia is a consequence of lifestyle, habitual diet or medications taken.

In this situation, the patient may have a normal weight, and his relatives also suffer from hyperlipidemia. The higher your risk of developing heart disease, the more intense the treatment for hyperlipidemia. These are LDL - low density lipoproteins ("bad cholesterol"), HDL - high density lipoproteins ("good cholesterol"), total cholesterol and triglycerides.

The main goal of the treatment of hyperlipidemia is to reduce the level of "bad cholesterol" - low-density lipoprotein. Most often, candidates for drug treatment are men over 35 years of age and women during menopause. Excess weight also contributes to an increase in the level of low-density lipoproteins in the blood and a decrease in high-density lipoproteins.

What is hyperlipidemia and why is it dangerous?

Smoking is also one of the main factors of hyperlipidemia and atherosclerosis, so it is recommended to stop smoking immediately as soon as you are diagnosed with hyperlipidemia. All of these activities contribute to the normalization of blood lipid levels and the prevention of the development of cardiovascular diseases. This common pathology, also called familial combined hyperlipidemia, is inherited as an autosomal dominant trait.

An increase in plasma cholesterol and/or triglyceride levels is detected at puberty and persists throughout the patient's life. Mixed hyperlipidemia is found in approximately 10% of all patients with myocardial infarction.

Diabetes, alcoholism and hypothyroidism increase the severity of hyperlipidemia. Diagnostics. There are no clinical or laboratory methods that would reliably diagnose multiple hyperlipidemia in a patient with hyperlipidemia. However, multiple-type hyperlipidemia should be suspected in every patient with mild hyperlipoproteinemia, the type of which varies over time.

Hyperlipidemia (hyperlipoproteinemia, dyslipidemia) is an abnormally elevated level of lipids and / or lipoproteins in human blood. Hyperlipidemia is not a disease, but a complex of symptoms and conditions. There is no hyperlipidemia in childhood. There are five types of hereditary or primary hyperlipidemia. By itself, hyperlipidemia does not manifest itself in any way. Type III. A type of hyperlipidemia also called dys-beta lipoproteinemia.

Diseases associated with changes in cholesterol levels

As noted earlier, both an increase and a decrease in cholesterol levels are harmful to health. In this part of the book, the main diseases associated with lipid metabolism disorders and methods for their diagnosis will be considered.

Excess cholesterol

Hyperlipidemia

Elevated levels of lipids - triglycerides and cholesterol - in the blood is called hyperlipidemia. This condition is often due to heredity.

There are five types of hereditary or primary hyperlipidemia.

Hyperlipidemia type I is characterized by a high content of triglycerides in the blood, including chylomicrons. This can lead to the development of pancreatitis.

The diagnosis of type II hyperlipidemia is made in cases of high levels of low-density lipoproteins in the blood.

The level of triglycerides in the blood can be either normal (type Pa) or elevated (type Pb). Clinically, the disease is manifested by atherosclerotic disorders, sometimes coronary heart disease (CHD) develops. With this condition, heart attacks often occur in men over 40 years of age and women over 55 years of age.

Hyperlipidemia type III is called an increased content of very low density lipoproteins and triglycerides in the blood. They accumulate in the blood due to a violation of the conversion of VLDL to LDL. This type of disease is often combined with various manifestations of atherosclerosis, including coronary artery disease and damage to the vessels of the legs. These patients are prone to gout and diabetes.

Hyperlipidemia type IV - an excess of triglycerides in the blood with normal or slightly elevated cholesterol levels - is a risk factor for atherosclerosis, obesity and mild diabetes.

Type V hyperlipidemia - the inability of the body to use and excrete triglycerides from food - can be both hereditary and caused by an unhealthy lifestyle (alcohol abuse, unhealthy diet, etc.). Ischemic heart disease with this type of hyperliidemia is not observed.

However, this classification does not cover all possible variants of deviations from the norm in the content of lipids and lipoproteins in blood plasma. In particular, it does not take into account changes in the concentration of HDL, a low content of which is an independent risk factor for the development of atherosclerosis and IVS, and an increased one, on the contrary, plays the role of a protective factor.

The causes of high triglycerides in the blood can be as follows:

Too high calorie or unbalanced diet;

Taking certain medications (estrogens, oral contraceptives, corticosteroids, etc.).

Treatment of hyperlipidemia

Cholesterol on the vessels - the cause of hyperlipidemia

Hyperlipidemias are common: in almost 25% of the adult population, plasma cholesterol levels exceed 5 mmol / l. Since this increases the risk of cardiovascular disease, timely treatment of hyperlipidemia is very important. When examining a patient with hyperlipidemia, first of all, its secondary origin should be excluded, that is, the causes should be established, for example, diseases of the liver and biliary system, obesity, hypothyroidism, diabetes mellitus, malnutrition and alcohol abuse. In most cases, hyperlipidemia is multifactorial, i.e. due to both external causes and genetic predisposition. Some forms of hyperlipidemia are primary, genetically determined. This fact is the basis of their classification. When confirming the diagnosis of hyperlipidemia, all members of the patient's family should be examined.

Risk factors

In most patients, hyperlipidemia can only be corrected by an appropriate diet. Significant efforts in clinics in the treatment are aimed at eliminating other risk factors in patients with lipid metabolism disorders, such as hypertension, diabetes mellitus, thyroid disease, smoking, as well as correcting impaired lipid metabolism. The use of lipid-lowering drugs is justified only in a relatively small number of patients with large changes in the lipid profile in order to reduce the risk of coronary heart disease.

Biochemical diagnosis is based on the results of a blood test taken from a patient 14 hours after eating. If there is a question about treatment throughout the life of the patient, the study is repeated 2-3 times with a weekly interval. In patients with recurrent myocardial infarction and other severe diseases, the concentration of triglycerides in plasma is increased, and cholesterol is reduced. Their lipid profile is not stable for 3 months after the acute period of the disease. However, the indicators obtained in the first 24 hours after the development of the pathological process, when significant changes in metabolism have not yet occurred, can be considered quite informative.

Lipoproteins and hyperlipidemia

Dietary triglycerides in the bloodstream are converted into chylomicrons, the number of which progressively decreases during lipolysis. This process is carried out with the participation of the enzyme lipoprotein lipase associated with the capillary endothelium in certain tissues, including adipose, skeletal muscle and myocardium. Fatty acids released during lipolysis are taken up by the tissues, and the remaining chylomicrons are eliminated by the liver. Endogenous triglycerides are synthesized by the liver and circulate bound to very low density lipoproteins (VLDLs). They are eliminated from the bloodstream using the same lipolytic mechanism that is involved in the elimination of exogenous triglycerides. Low-density lipoproteins (LDL) formed during the metabolism of triglycerides are the main delivery system for cholesterol in human tissues. These are rather small molecules that, passing through the vascular endothelium, bind to specific receptors with high affinity for LDL on cell membranes and enter the cells by pinocytosis. Intracellular cholesterol is necessary for the growth and repair of membrane structures, as well as for the formation of steroids.

High-density lipoproteins (HDL) are cholesterol-rich particles that act as transport intermediaries that mobilize peripheral cholesterol, for example from the vascular wall, and transport it to the liver for elimination. Thus, they perform the function of protectors in coronary heart disease.

Types of hyperlipidemia

There are several types of hyperlipidemia. Type 1 (rare) is characterized by high levels of chylomicrons and triglycerides in the blood due to lipoprotein lipase deficiency and is accompanied by abdominal pain, pancreatitis, and xanthomatous rashes.

Type 2a (common) is characterized by high blood levels of both LDL and cholesterol and is associated with a risk of coronary heart disease. These patients make up 0.2% of the population, and their familial hypercholesterolemia is inherited in a heterozygous monogenic type, which leads to the premature development of severe heart disease and xanthomatosis.

Type 2b (common) is characterized by a high concentration of LDL and VLDL, cholesterol and triglycerides in the blood and is associated with the risk of coronary heart disease.

Type 3 (rare) is characterized by a high level of so-called floating 3-lipoproteins, cholesterol and triglycerides in the blood due to a hereditary apo-lipoprotein anomaly, combined with xanthomatosis on the palmar surfaces, coronary heart disease and peripheral vascular disease.

Type 4 (common) is characterized by high levels of VLDL and triglycerides in the blood, may be accompanied by obesity, diabetes and alcoholism, leads to the development of coronary heart disease and peripheral vascular disease.

Type 5 (rare) is characterized by high blood levels of chylomicrons, VLDL, and triglycerides. Some of these metabolic changes may be due to alcohol abuse or diabetes. Patients of this type often develop pancreatitis.

Drugs for the treatment of hyperlipidemia

Cholestyramine (Questran) is available in the form of packages containing 4 g of the drug, and is an ion-exchange resin that binds bile acids in the intestine. Bile acids formed in the liver from cholesterol enter the intestine with bile and are reabsorbed in the upper small intestine. In total, the body contains 3-5 g of bile acids, but due to enterohepatic recirculation, which occurs 5-10 times a day, an average of 20-30 g of bile acids enters the intestine daily. By binding with cholestyramine, they are excreted in the feces and the depletion of their reserves in the depot stimulates the conversion of bile acids into cholesterol, as a result of which the level of the latter, in particular LDL, in plasma decreases by 20-25%. However, in some patients in the liver, cholesterol biosynthesis can be increased compensatory. The daily dose of cholestyramine is 16-24 g, but sometimes up to 36 g / day is required to correct the lipid profile. Such a dose is too large (9 packets of 4 g per day), which is inconvenient for patients. Almost half of those who take cholestyramine develop side effects (constipation, sometimes anorexia, bloating, rarely diarrhea). Since the drug binds anions, when combined with warfarin, digoxin, thiazide diuretics, phenobarbital and thyroid hormones, it should be borne in mind that their absorption is reduced, so these drugs should be taken one hour before taking cholestyramine.

Colestipol (Colestid) is similar to cholestyramine.

Nicotinic acid (available in 100 mg) lowers plasma cholesterol and triglyceride levels. Perhaps its action is due to the anti-lipolytic effect in adipose tissue, resulting in a decrease in the level of non-esterified fatty acids, which are the substrate from which lipoproteins are synthesized in the liver. For the treatment of patients with hyperlipidemia, 1-2 g of nicotinic acid is used 3 times a day (normally, the body's need for it is less than 30 mg / day). In this case, the patient often has reddening of the skin of the face and the function of the digestive tract is disturbed. With a gradual increase in dose over 6 weeks, adverse reactions are less pronounced and tolerance develops.

Nicofuranose (tetranicotinoylfructose, Bradilan), a fructose nicotinic acid ester, may be better tolerated by patients.

Clofibrate (Atromid; available in 500 mg doses) inhibits hepatic lipid synthesis, lowering plasma cholesterol levels by 10-15%. In patients with type 3 hyperlipidemia, the effect may be twice as pronounced. Clofibrate is readily absorbed from the gastrointestinal tract and is largely bound to plasma proteins. Its action is terminated as a result of metabolism in the liver, in addition, it is excreted unchanged in the urine. In the amount of 500 mg, it is taken 2-3 times a day after meals. Side effects are mild, but sometimes acute myalgia develops, especially in hypoproteinemic conditions, such as nephrotic syndrome, when the concentration of free substance is unusually high. The results of a placebo-controlled study in which patients participated indicate that when using clofibrate for the purpose of primary prevention of myocardial infarction, the incidence of myocardial infarction was 25% lower in patients who received the active drug. However, an increase in the frequency of deaths from diseases not associated with coronary heart disease was unexpected, which remained without explanation (report of the Committee of Leading Investigators. Br. Heart J., 1978; Lancet, 1984). In patients taking clofibrate, the incidence of calculous cholecystitis, which required surgical treatment, increased. When combined with oral anticoagulants, furosemide and sulfourea derivatives, interactions may occur as a result of their competition with clofibrate for association with plasma albumins. In this regard, the concentration in the blood of pharmacologically active non-protein compounds increases, which leads to an increase in the effects of these drugs when administered in therapeutic doses. In many countries, clofibrate is banned for long-term use as a lipid-lowering agent.

Benzafibrate (Bezalip) is similar in action to clofibrate. It lowers plasma levels of triglycerides and cholesterol.

Probucol (Lurcell) increases the excretion of bile acids and reduces the biosynthesis of cholesterol, resulting in a decrease in the concentration of lipids in plasma, both low and high density, with protective properties. Usually the drug is well tolerated by patients, but some of them develop disorders of the digestive tract and abdominal pain.

Treatment of hyperlipidemia depending on its type

Treatment for hyperlipidemia should be carried out taking into account some general provisions. First, you must first try to influence any pathology that can cause lipid metabolism disorders, such as diabetes mellitus, hypothyroidism.

Secondly, they correct the diet: a) reduce the amount of calories consumed in case of excess body weight until it normalizes (of course, it is necessary to reduce the consumption of alcohol and animal fats); the cessation of alcohol consumption is accompanied by a decrease in the level of triglycerides in the blood; b) patients who do not lose body weight or it already corresponds to the norm should eat less fat, animal fats should be replaced with polyunsaturated fats or oils. Adherence to a special diet, such as the exclusion of egg yolk, sweets, meat, is not necessary, since reducing fat intake is quite effective.

Thirdly, appropriate treatment is recommended for certain types of hyperlipidemias.

Type 1 (sometimes type 5). They reduce the amount of dietary fat to 10% of the total calories consumed, which can be achieved by partial replacement of fats with medium chain triglycerides, which, without entering the general circulation as part of chylomicrons, enter directly into the liver through the portal system.

Type 2a. Usually hyperlipidemia is corrected by diet, but in the hereditary form it is almost always necessary to prescribe ion exchange resins (cholestyramine or colestipol), and often other agents.

Types 2b and 4. As a rule, patients suffer from obesity, diabetes, alcoholism, they have nutritional errors. These disorders can be corrected by diet. In resistant cases, nicotinic acid, clofibrate or bezafibrate are additionally prescribed.

Type 3. Diet is usually sufficient for patients, but sometimes they have to prescribe drugs clofibrate or bezafibrate, which are highly effective in this type of hyperlipidemia. Hereditary hyperlipidemias of type 2a and severe types 3, 4 and 5 are difficult to correct; these patients should be examined by a specialist.

What should you do after reading this article? If you suffer from hyperlipidemia, first of all try to change your lifestyle, and then, according to the doctor's recommendation, select the drug. If you are over 40 and you do not know your cholesterol status, do not be too lazy to take a blood test. It is possible that timely treatment of hypercholesterolemia will become an important method for the prevention of cardiovascular diseases. Be healthy!

2 comments

My diagnosis is hyperlipidemia and vascular atherosclerosis. True, IHD has not yet reached, but the state of the coronary vessels is also not ideal. I had to immediately quit smoking, eliminate alcohol, reduce fatty foods - the result was not so effective. LDL didn't go up, but it didn't go down either. Together with this, statins were prescribed - they acted differently. Sometimes I felt uncomfortable, especially from simvastatin. But I continue to take - now it's Rosuvastatin-SZ. Everything gave excellent results - LDL - 4.1, I take the medicine in courses, I tolerate it well.

I take Rosuvastatin Severnaya Zvezda after a heart attack every day, in addition to cardiomagnyl.

Hyperlipidemia: what is it, why does it occur, how dangerous is it and how to treat it?

The syndrome of hyperlipidemia develops in many diseases, makes them more severe and leads to the development of complications. Prevention and treatment of hyperlipidemia is very important for the prevention of atherosclerosis, the normal functioning of organs, a long and active life.

What are lipids, lipoproteins and hyperlipidemia?

There is an opinion that fats are harmful to the body. It's not like that at all. Fats are the most important component of all living organisms, without which life is impossible. They are the main “energy station”, they produce the energy necessary for metabolism and cell renewal during chemical reactions.

Fats become harmful when their content is excessive, especially certain types that lead to atherosclerosis and other diseases - low-density lipids, or atherogenic ones. All fatty substances in the body are divided into 2 groups according to their chemical composition:

Lipids

The name comes from the Greek lipos - fat. This is a whole group of fat-forming substances in the body, including:

• fatty acids (saturated, monounsaturated, polyunsaturated);
• triglycerides;
• phospholipids;
• cholesterol.

Fatty acids, which everyone knows about and which play a big role in the development of atherosclerosis, are precisely saturated ones. They are found in animal products. Unsaturated acids, on the contrary, prevent the development of atherosclerosis, are found in vegetable oils, seafood (omega 3, omega 6, omega 9 and others).

Triglycerides are neutral fats derived from glycerol, which are the main energy providers. Their high content contributes to the development of diseases. Phospholipids contain a phosphoric acid residue and are essential for the maintenance of nervous tissue.

Finally, well-known cholesterol is the main culprit of many diseases, and the most common "disease of the century" - atherosclerosis. It is of 2 types: high density, or "good cholesterol", and low density, or "bad cholesterol". It is he who is deposited in the organs, causing fatty degeneration, in the vessels, causing circulatory disorders.

Lipoproteins

These are more complex compounds, including lipids and protein molecules. They are divided into:

• chylomicrons, which perform a transport function, deliver fat from the intestines to tissues and organs, including contributing to its deposition in the subcutaneous tissue;
• lipoproteins of various density - high (HDL), low (LDL), intermediate (LDL) and very low (LDL).

Lipoproteins and low-density lipids, chylomicrons contribute to the accumulation of fatty substances, “bad” cholesterol in the body, that is, the development of hyperlipidemia, against which diseases develop.

The normal content of essential fatty substances in the blood is presented in the table:

Low density lipoproteins (LDL)

High density lipoproteins (HDL)

What are the causes of hyperlipidemia?

Many organs play a role in the metabolism of fats in the body: the liver, kidneys, endocrine system (thyroid gland, pituitary gland, gonads), as well as lifestyle, nutrition, and so on. We also recommend that you study the information about the symptoms of hyperkalemia on our portal. Therefore, the causes of hyperlipidemia can be the following:

• malnutrition, excessive intake of fatty substances;
• abnormal liver function (with cirrhosis, hepatitis);
• impaired renal function (with hypertension, pyelonephritis, renal sclerosis);
• decreased thyroid function (myxedema);
• dysfunction of the pituitary gland (pituitary obesity);
• diabetes;
• decreased function of the sex glands;
• long-term use of hormonal drugs;
• chronic alcohol intoxication;
• hereditary features of fat metabolism.

Important: You should not think that the listed reasons necessarily lead to obesity. We are talking about hyperlipidemia - an increased content of fatty substances in the blood, organs, and not about subcutaneous fat deposits.

Classification, types of hyperlipidemia

For the reasons for the increase in lipids in the body, 3 types of pathology are distinguished:

• primary hyperlipidemia (hereditary, familial) associated with the genetic characteristics of fat metabolism;
• secondary, developing against the background of diseases (liver, kidneys, endocrine system);
• alimentary, associated with excessive consumption of fat.

There is also a classification of hyperlipidemia, depending on which fraction of lipids is in high concentration in the blood:

1. With an increase in the concentration of triglycerides.
2. With an increased concentration of "bad" cholesterol (LDL) - type 2a hyperlipidemia, the most common.
3. With an increase in the content of chylomicrons.
4. With an increased concentration of triglycerides and cholesterol.
5. With an increased concentration of triglycerides, cholesterol and chylomicrons.
6. With an increase in triglycerides and a normal content of chylomicrons.

This distribution is important from a clinical point of view, that is, a blood test doctor can navigate which disease may be more likely in a given patient. Most often in practice, hyperlipidemia of a mixed nature occurs, that is, with an increase in the content of all fatty components.

Symptoms and Diagnosis of Hyperlipidemia

By itself, hyperlipidemia is not a disease, but a syndrome against which other diseases develop. Therefore, it as such does not have any symptoms, but the diseases already caused by it appear.

For example, an increased concentration of cholesterol leads to atherosclerotic lesions of blood vessels - the arteries of the heart, brain, kidneys, limbs. Accordingly, clinical symptoms appear:

• with atherosclerosis of the coronary vessels - pain in the heart area (angina attacks), shortness of breath, rhythm disturbances, in severe cases, memory loss, sensitivity disorders, speech disorders, mental disorders may develop, acute cerebrovascular accident (stroke) may develop;
• with atherosclerosis of the vessels of the extremities - muscle pain, increased chilliness, thinning of the skin, nails, trophic disorders, areas of necrosis on the fingers, gangrene;
• with atherosclerosis of the renal vessels - a violation of glomerular filtration, arterial hypertension, the development of renal failure, wrinkling of the kidney.

We have previously written about high cholesterol during pregnancy and recommended bookmarking the article.

Important: With an increase in lipid levels, not only the listed diseases develop. Almost any organ can be affected due to atherosclerosis of the vessels feeding it and fatty degeneration, for example, liver hyperlipidemia.

Diagnosis of hyperlipidemia is carried out by a biochemical blood test, which takes into account the following main indicators:

• cholesterol (cholesterol) - "bad", that is, low density (LDL), its content should not exceed 3.9 mmol / l, and "good", that is, high density (HDL), its level should not be lower than 1, 42 mmol/l;
• total cholesterol - should not exceed 5.2 mmol / l;
• triglycerides - should not exceed 2 mmol / l.

It also takes into account the coefficient of atherogenicity (CA), that is, the likelihood of developing atherosclerosis. It is calculated as follows: HDL is subtracted from total cholesterol, then the resulting amount is divided by HDL. Normally, CA should be less than 3. If CA is 3-4, then the patient has a small risk of developing atherosclerosis, if 5 or more, this is a high degree of probability of developing a heart attack, stroke.

If hyperlipidemia is detected in the blood, a complete examination of the patient is carried out: ECG, echography of the heart, encephalography, contrast angiography, ultrasound of the liver, kidneys, and endocrine system examination.

What is the treatment for hyperlipidemia?

The complex of hyperlipidemia treatment consists of 4 main components: diet therapy, taking statins (drugs that lower cholesterol), cleansing procedures and increasing physical activity.

diet therapy

Nutrition for hyperlipidemia should contain a minimum of fat - no more than 30%. It is recommended to replace animal fats with vegetable oils, and not refined, containing polyunsaturated fatty acids (sunflower, olive, linseed, sesame). They are recommended to be taken raw, that is, without heat treatment. You should also reduce the amount of carbohydrates - sweet dishes, flour and confectionery.

Food should contain a large amount of coarse fiber - at least a day, it is found in raw vegetables and fruits, cereals, legumes, greens, and they also contain many vitamins and microelements. Artichokes, pineapple, citrus fruits, celery are recommended as fat-burning products. Alcohol, which contains a large amount of carbohydrates, is contraindicated.

Statins

This is a whole group of drugs that block the enzyme HMG-CoA reductase, which is necessary for the synthesis of cholesterol. Practice has shown that regular use of statins reduces the number of heart attacks and strokes by 30-45%. The most popular are simvastatin, lovastatin, rosuvastatin, fluvastatin and others.

Cleansing the body

This refers to the cleansing of accumulated toxins, excess nutrients. Recommended periodic intake of sorbents, which are also in a large selection. These are activated carbon, sorbex, enterosgel, polysorb, atoxol and others. Chitosan, a preparation made from crustacean shell powder, has proven itself to be excellent, adsorbing well and removing fat molecules from the intestines.

In severe cases of hyperlipidemia in a hospital, extracorporeal blood purification is performed. The patient's venous system is connected to a device with many filter membranes, passes through them and returns back, already cleared of "bad" lipids.

Important: The intake of sorbents should be agreed with the doctor. Excessive passion for them can lead to the removal from the body, in addition to fat and toxins, of useful and necessary substances.

Increasing physical activity

Exercise therapy for hyperlipidemia is a prerequisite for improving blood circulation, removing lipids and reducing their sedimentation in blood vessels and organs. Also, any sports, games, hiking, cycling, swimming, just hygienic exercises in the morning - everyone can choose for themselves according to their taste and possibilities. The main thing is to eliminate hypodynamia.

Is prevention possible?

If only hyperlipidemia is not associated with organic pathology, heredity and hormonal disorders, then it is quite possible to prevent it. And this prevention is not the "discovery of America", but consists of the normalization of nutrition, the rejection of bad habits, feasts and physical inactivity, and increased physical activity.

Statistics show that in most cases hyperlipidemia is alimentary (food) and age-related. Therefore, its prevention in most cases is quite real. Even in the elderly and advanced age, pathology can be avoided.

Hyperlipidemia is a syndrome that occurs with many diseases, and also leads to the development of severe diseases. Regular examination and treatment, as well as preventive measures, will help to avoid serious consequences.

Dyslipidemia occupies a central place among metabolic disorders. Lipid imbalance is dangerous because it can lead to serious diseases of the cardiovascular system.

Currently, diseases of the cardiovascular system rank first in terms of prevalence and mortality ( mortality) in the population. If in 1900 cardiovascular diseases led to death in 10% of cases, by 2000 it had become the main cause of death.
Every year about 17.5 million people die from pathologies of the heart and blood vessels. Coronary heart disease accounts for 7.4 million deaths, stroke - 6.7 million. About 75% of deaths occur in low- and middle-income countries.

The reason for such a sharp increase in the number of diseases of the cardiovascular system is a sedentary lifestyle, smoking, unhealthy diet, unhealthy food, obesity, constant stress, and lack of medical control. The development of many diseases of the heart and blood vessels can be prevented by changes in lifestyle and nutrition.

The prevalence of diseases of the cardiovascular system and a high percentage of mortality are a global problem. This leads to a decrease in the working capacity of the population and large economic losses. Currently, a large number of recommendations and programs for the prevention and treatment of diseases of the cardiovascular system have been developed. The main goal of these programs is to educate the population about the basics of a healthy lifestyle and nutrition, as well as explaining the importance of periodic medical control ( especially those at risk).

What is dyslipidemia?

Dyslipidemia is an imbalance lipids ( fat) in blood. The reason may be a violation of the metabolism and excretion of fats, excessive intake of fats from food, genetic predisposition, and others. Dyslipidemia is not an independent disease. This is a laboratory indicator for assessing the risk of developing severe diseases of the cardiovascular system.

The body is made up of inorganic substances chemical compounds that do not contain carbon in the structure) and organic matter ( chemical compounds that contain carbon in their structure) that come from food. Inorganic substances include potassium, calcium, magnesium, phosphorus, sodium and others. To organic substances - proteins, carbohydrates, nucleic acids and fats ( lipids).

The major plasma lipids of clinical importance are:

• Cholesterol. This fat-like substance is a lipid. About 80% cholesterol produced in the body liver, kidneys, intestines, gonads), the remaining 20% ​​enter the body with food. Cholesterol is an important component of cell structure and ensures the stability of the cell membrane over a wide range of temperatures. The highest amount of cholesterol 24% ) forms the cell wall of erythrocytes ( red blood cells that carry oxygen). 17% of the amount of cholesterol is spent on the formation of membranes of liver cells, 15% - on the membranes of cells of the white matter of the brain, 5 - 7% of the gray matter of the brain. Also, this lipid is a precursor of bile acids. In the liver, cholesterol is converted into bile acids and their salts, which are transported from the gallbladder to the intestines and play an important role in the dissolution and absorption of dietary fats. Cholesterol forms the basis of steroid hormones - cortisol, progesterone, testosterone, aldosterone. In the skin, modified cholesterol forms vitamin D, which is necessary for the hormonal regulation of calcium and phosphorus, strengthening teeth and bones, increasing immunity, and others.
• Triglycerides. They are the main source of energy for cells. They consist of one molecule of glycerol and three molecules of fatty acids. Triglycerides are saturated, monounsaturated and polyunsaturated. Saturated fatty acids ( animal fats, coconut oil, etc.) are atherogenic ( contributing to the emergence atherosclerosis ). monounsaturated fats ( olive oil) and polyunsaturated fats ( sunflower oil and other vegetable oils) are not atherogenic. They are synthesized in the liver, adipose tissue, intestines, and also enter the body with food. Triglycerides are an alternative source of energy during fasting when glucose stores are depleted ( which is the main source of energy). With a lack of glucose, triglycerides located in adipocytes ( cells that make up adipose tissue), are cleaved by a special enzyme ( substance that speeds up chemical reactions) - lipases. This process is called lipolysis. Fatty acids released as a result of lipolysis are transported to other cells of the body, where they are oxidized ( are burned) with energy release. Glycerin ( lipolysis product) is converted to glucose in the liver.

Lipids do not dissolve in water. This prevents their transport into the blood plasma. For transport, lipids are “packed” into a protein shell, which consists of apoproteins ( apoproteins). A complex of proteins and lipids is called a lipoprotein, which is a spherical particle with an outer layer of proteins and a core of lipids ( cholesterol and triglycerides). There are four types of lipoproteins, differing in density, content of cholesterol, triglycerides and apoproteins. As the particle size decreases, their density increases. So the largest particles with the lowest density are chylomicrons, and the smallest in size with the highest density are high density lipoproteins.

The four main classes of lipoproteins are:

• Chylomicrons ( HM). Composition - triglycerides 90%, cholesterol 5%, apoproteins 2%, other lipids 3%. Synthesized in the wall of the small intestine from dietary fats. The main function of chylomicrons is to transport dietary triglycerides from the intestine to adipose tissue, where they are deposited ( postponed), and into the muscles, where they serve as a source of energy. After transportation of triglycerides, chylomicrons are converted into residual particles ( remnants) and tolerate exogenous ( coming from outside) cholesterol to the liver.
• Very low density lipoproteins ( VLDL). Composition - triglycerides 60%, cholesterol 15%, apoproteins 10%, other lipids 15%. Synthesized in the liver from endogenous domestic) sources. Their main function is to transport triglycerides from the liver to muscle cells and fat cells, as well as providing them with energy. After that, very low density lipoproteins are transformed into intermediate density lipoproteins ( LPPP) and transported to the liver. Very low density lipoproteins in the liver VLDL) are converted into low density lipoproteins ( LDL). An increase in very low density lipoprotein levels increases the risk of atherosclerosis. Atherosclerosis is a chronic disease in which cholesterol and other fats are deposited on the vessel wall in the form of plaques, which leads to a narrowing of the vessel lumen and impaired blood flow.
• Low density lipoproteins ( LDL, LDL - low density lipoprotein). Composition - cholesterol 55%, apoprotein 25%, triglycerides 10%, other lipids 10%. This is the main class containing a large amount of cholesterol - 70% of the plasma content. Formed in the liver from very low density lipoproteins. The main function is to transport non-nutritional cholesterol ( synthesized in the body) to all tissues. Low density lipoproteins ( LDL) are the main atherogenic ( contributing to the development of atherosclerosis) fraction of lipids and the main goal in the treatment of lipid-lowering agents. There are fractions of low density lipoproteins with different levels of atherogenicity. So "small dense" LDL have the highest degree of atherogenicity, "large floating" LDL are less atherogenic.
• High density lipoproteins ( HDL, HDL - high density lipoprotein). Composition - apoproteins 50%, cholesterol 20%, triglycerides 3%, other lipids 25%. Synthesized in the liver. When released into the bloodstream, high-density lipoproteins are primarily composed of apoproteins. They contain apolipoprotein A1, a blood plasma protein that is part of HDL and helps to remove cholesterol from the walls of blood vessels. As they circulate in the blood, they are enriched with cholesterol and transport its excess from extrahepatic cells to the liver for further excretion from the body. About 30% of blood cholesterol is part of high density lipoproteins. High-density lipoproteins are anti-atherogenic, that is, they prevent the formation of atherogenic plaques and the development of atherosclerosis. A high concentration of HDL significantly reduces the risk of developing coronary heart disease, atherosclerosis and other diseases of the cardiovascular system.

Classification of cholesterol, triglycerides, LDL, HDL

total cholesterol
< 5,2 ммоль/л (< 200 мг/дл ) 5.2 - 6.1 mmol/l ( 200 - 239 mg/dl) ≥ 6.2 mmol/l ( ≥ 240 mg/dl)	Normal level borderline high High level
LDL
< 2,6 ммоль/л (<100 мг/дл ) 2.6 - 3.3 mmol/l ( 100 - 129 mg/dl) 3.4 - 4.0 mmol/l ( 130 - 159 mg/dl) 4.1 - 4.8 mmol/l ( 160 - 189 mg/dl) ≥ 4.9 mmol/l ( ≥ 190 mg/dL)	Optimal Level Above optimal borderline high High level Very high level
HDL
< 1,0 ммоль/л (< 40 мг/дл для мужчин, < 50 мг/дл для женщин ) 1.0 - 1.59 mmol/l ( 40 - 59 mg/dl) ≥ 1.6 mmol/l ( > 60 mg/dl)	Low level ( increased risk of developing cardiovascular disease) Average level High level ( reduced risk of developing cardiovascular disease)
Triglycerides
< 1,7 ммоль/л (< 150 мг/дл ) 1.7 - 2.2 mmol/l ( 150 - 199 mg/dl) 2.3 - 4.4 mmol/l ( 200 - 499 mg/dl) > 4.5 mmol/l ( > 500 mg/dl)	Optimal Level borderline elevated High level Very high level

Normally, the level of triglycerides, cholesterol, low and high density lipoproteins are in a certain balance, performing their physiological functions. If this balance is disturbed, then the effect of these lipids on the body becomes negative. Such a condition in which the natural balance of lipids is disturbed and their amount goes beyond the normal range is called dyslipidemia. Dyslipidemias are manifested by an increase in the level of total cholesterol, triglycerides, low density lipoproteins, leading to the development of atherosclerosis or a decrease in the level of high density lipoproteins, which have an antiatherogenic effect.

Types of dyslipidemia

Dyslipidemias are classified depending on the mechanism of occurrence, laboratory manifestations, and many others. Therefore, several classifications of dyslipidemia have been developed. Each classification is an indication of the types of dyslipidemia and their causes.

According to the mechanism of occurrence, lipid imbalance is divided into:

• primary dyslipidemia. Primary dyslipidemias appear as a result of a metabolic disorder that is not a consequence of any disease. There are primary monogenic, primary polygenic, primary homozygous, primary heterozygous dyslipidemia. Primary monogenic dyslipidemia is an inherited lipid metabolism disorder that is associated with a disorder in genes ( carriers of hereditary information). Primary monogenic dyslipidemia is divided into familial combined hyperlipidemia, familial hypercholesterolemia, familial hypertriglyceridemia, familial hyperchylomicronemia, and others. Primary polygenic dyslipidemia appears as a result of hereditary genetic disorders and the influence of external factors ( nutrition, lifestyle and other). Primary homozygous dyslipidemia is an extremely rare form ( 1 in a million), in which the child receives defective genes from both parents. Primary heterozygous dyslipidemia is characterized by the inheritance of a defective gene from one of the parents. It occurs much more often - 1 case per 500 people.
• Secondary dyslipidaemias. Secondary dyslipidemias appear with various diseases, an unhealthy lifestyle, and when taking certain medications. Occur more often in the population of developed countries. Lipid metabolism disorder develops in obesity, diabetes mellitus, chronic renal failure, liver cirrhosis, malignant neoplasms, thyroid diseases and many other pathologies. Alcohol intake, a sedentary lifestyle, and malnutrition also lead to dyslipidemia. Drugs that disrupt fat metabolism include oral contraceptives ( contraceptive pills), beta-blockers, thiazide diuretics ( diuretics), corticosteroids.
• Alimentary dyslipidemia. Alimentary dyslipidemia develops with excessive consumption of animal fats. There are transient alimentary and permanent alimentary dyslipidemias. Transient nutritional dyslipidemias are characterized by a temporary increase in total cholesterol and low-density lipoprotein levels after a single meal rich in animal fats. Lipid imbalance develops the next day after eating. Permanent alimentary dyslipidemia is characterized by a persistent violation of lipid metabolism with regular consumption of fatty foods.

Depending on the type of lipids, the level of which is elevated, there are:

• isolated hypercholesterolemia- an increase in the level of cholesterol in the blood as part of lipoproteins ( complex of proteins and fats);
• combined hyperlipidemia- increased levels of cholesterol and triglycerides.

Donald Fredrickson ( American medical researcher) developed a classification of lipid disorders. This classification has been approved by the World Health Organization ( WHO) and is accepted as the international standard nomenclature for hyperlipidemias ( metabolic disorders of fats, characterized by their elevated levels in the blood). This classification does not indicate the causes of hyperlipidemia and does not take into account the level of high density lipoproteins ( HDL), which also play an important role in reducing the risk of atherosclerosis. Hyperlipidemia typing is carried out in a laboratory study of the content of various classes of lipoproteins in the blood.

Classification of hyperlipidemia according to Fredrickson

Type	Plasma cholesterol	LDL cholesterol	Lipoprotein triglycerides	Violations	Athero- geneity	Ras- pro- country-nen- ness	Clinical signs	Treatment
I	The level is elevated or within the normal range.	Increased or within normal limits.	Level up.	an excess of chylomicrons.	Not proven.	< 1%	- abdominalgia ( stomach ache); - xanthomas ( formations in the skin and other tissues in violation of lipid metabolism); - hepatomegaly ( enlargement of the liver); - lipemic retinopathy ( retinal damage in hyperlipidemia).	- diet.
IIa		Level up.	Fine.	LDL).	The risk of developing atherosclerosis, especially of the coronary arteries, is sharply increased ( blood supply to the heart).	10%	- xanthomas; - early atherosclerosis ( chronic vascular disease characterized by the deposition of cholesterol in the inner wall of the vessel).	- statins; - a nicotinic acid.
IIb	The level is elevated or normal.	Level up.	Level up.	An excess of low-density lipoproteins ( LDL) and very low density lipoproteins ( VLDL).	The risk of developing atherosclerosis is sharply increased.	40%	- xanthomas; - xanthelasma ( flat xanthomas); - early atherosclerosis.	- statins; - a nicotinic acid; - gemfibrozil.
III	Level up.	The level is low or within normal limits.	Level up.	Excess Remnants ( residual particles) chylomicrons and intermediate density lipoproteins ( LPPP).	The risk of atherosclerosis is significantly increased ( especially coronary and peripheral arteries).	< 1%	- obesity; - widespread atherosclerosis; - xanthomas.	predominantly gemfibrozil.
IV	The level is elevated or within the normal range.	Fine	Level up.	Excess very-low-density lipoprotein (VLDL) VLDL).	The risk of developing atherosclerosis of the coronary arteries is increased.	45%	- abdominalgia; - vascular atherosclerosis.	predominantly nicotinic acid.
V	Level up.	Within the normal range.	Level up.	Excess chylomicrons and very low density lipoproteins ( VLDL).	The risk of developing atherosclerosis.	5%	- abdominalgia; - pancreatic necrosis ( death of pancreatic tissue); - obesity; - xanthomas.	- diet; - a nicotinic acid; - gemfibrozil.

There is a classification based on phenotypes ( the totality of the biological properties of an organism that appeared in the process of its individual development) dyslipidemia, which indicates the cause of the development of the main types of lipid metabolism disorders.

Classification by etiology ( reason) phenotypes of hyperlipidemias

Type	Primary Causes	Secondary Causes
I	familial hyperchylomicronemia ( elevated levels of chylomicrons).	rarely - systemic lupus erythematosus ( a serious disease in which the immune system perceives the body's own cells as foreign and begins to destroy them).
IIa	familial hypercholesterolemia ( high cholesterol); polygenic hypercholesterolemia.	hypothyroidism ( a condition characterized by a long-term deficiency of thyroid hormones).
IIb	Familial combined hypercholesterolemia.	diabetes ( endocrine disease associated with impaired glucose uptake); anorexia nervosa ( the patient's constant desire to lose weight); nephrotic syndrome ( manifested by the presence of generalized edema, an increased content of proteins in the urine, a violation of protein metabolism).
III	familial dysbetalipoproteinemia ( remnant hyperlipidemia).	hypothyroidism; obesity; diabetes.
IV	familial combined hyperlipidemia ( elevated lipid levels); familial hypertriglyceridemia ( elevated triglycerides).	diabetes; chronic kidney disease.
V	familial hyperchylomicronemia; familial hypertriglyceridemia.	excessive alcohol consumption; taking diuretics ( diuretic drugs), oral contraceptives ( oral contraceptives).

Causes of dyslipidemia

The causes leading to lipid metabolism disorders are congenital and acquired.

There are the following groups of causes of dyslipidemia:

• causes of primary dyslipidaemias- inheritance from parents from one of the parents or very rarely from both) an abnormal gene responsible for the synthesis of cholesterol;
• causes of secondary dyslipidemias- an increase in the level of cholesterol, triglycerides, lipoproteins, caused by a violation of fat metabolism in various diseases ( diabetes mellitus, hypothyroidism and others), wrong way of life ( sedentary lifestyle, smoking, drinking alcohol) and certain medications ( beta-blockers, immunosuppressants, diuretics and others).
• causes of nutritional dyslipidemia- regular excessive consumption of animal fats.

The main causes of secondary hypertriglyceridemia are:

• genetic predisposition;
• obesity;
• kidney disease;
• hypothyroidism ( );
• autoimmune diseases ( diseases in which body cells are recognized by the immune system as foreign and destroyed) - systemic lupus erythematosus;
• drugs - estrogen tableted), thiazide diuretics, corticosteroids and others;
• type 2 diabetes;
• eating large amounts of simple carbohydrates confectionery, milk, sweet fruits and vegetables).

The main causes of secondary hypercholesterolemia are:

• hypothyroidism ( persistent deficiency of thyroid hormones);
• nephrotic syndrome ( a condition in which generalized edema is observed, a decrease in the level of proteins in the blood, an increase in the level of proteins in the urine);
• anorexia ( eating disorder with severe weight loss);
• therapy with corticosteroids and immunosuppressants ( drugs that suppress the immune system).

Allocate factors contributing to the development and progression of dyslipidemia. They also refer to factors in the development and progression of atherosclerosis. Factors are divided into modifiable ( that can be fixed or corrected) and unmodifiable ( that cannot be removed or changed).

Modifiable factors include:

• Lifestyle- hypodynamia ( sedentary lifestyle), excessive alcohol consumption, smoking, eating fatty foods, stress;
• arterial hypertension- persistent increase in blood pressure;
• diabetes- violation of the absorption of glucose with an increase in its level in the blood of more than 6 mmol / l on an empty stomach ( norm 3.5 - 5.5 mmol / l);
• abdominal obesity- waist circumference of more than 94 centimeters for men and more than 80 centimeters for women.

Non-modifiable factors include:

• male;
• age- men over 45;
• burdened family history- the presence of close relatives of cases of early atherosclerosis, familial dyslipidemia, myocardial infarction ( death of a part of the heart muscle due to a violation of its blood supply), stroke ( ) and others.

In the treatment of dyslipidemias and complications, and in the prevention of complications, doctors try to achieve target levels of risk factors. Targeted risk factors are the optimal indicators at which the risk of developing cardiovascular diseases and mortality is significantly reduced.

The target levels of the main risk factors are:

• arterial pressure ( HELL) < 140/90 мм.рт.ст., при почечной недостаточности - АД < 125/75 мм.рт.ст.;
• total cholesterol levels for patients with risk factors< 5 ммоль/л;
• total cholesterol levels for patients with cardiovascular disease< 4,5 ммоль/л;
• LDL-C level ( low density lipoprotein cholesterol) for patients with risk factors< 3 ммоль/л;
• LDL-C level for patients with cardiovascular diseases< 2,5 ммоль/л;
• the level of HDL cholesterol men/women> 1/1.2 mmol/l;
• triglyceride levels ( TG) < 1,7 ммоль/л;
• atherogenic index ( ratio of total cholesterol to high-density lipoprotein) < 3;
• body mass index ( the ratio of body weight in kg to the square of height in m) < 25 кг/м 2 ;
• waist circumference men/women< 94/80 сантиметров;
• fasting glucose level< 6 ммоль/л.

How does dyslipidemia manifest itself?

Dyslipidemia is a purely laboratory indicator. Patients with high levels of cholesterol, LDL, triglycerides do not develop specific symptoms. Usually, lipid metabolism disorders are detected incidentally during laboratory examination of patients during routine medical monitoring or diagnosis of cardiovascular diseases.

Violation of lipid metabolism can be manifested by external symptoms. External symptoms usually do not cause discomfort to the patient, so they are usually ignored and do not go to the doctor.

External symptoms of dyslipidemia include:

• xanthomas. Xanthomas are pathological formations on the skin or other tissues, consisting of an accumulation of phagocytes ( cells of the immune system that absorb particles foreign to the body) containing cholesterol and/or triglycerides. Skin lesions occur in all 5 types of dyslipidemia. Xanthomas are divided into eruptive, tuberous, tendon, flat. Eruptive xanthomas ( occur in I, III, IV, V types of hyperlipidemia) are composed of soft yellow papules ( dense red nodules) of small size with localization in the buttocks and thighs. tuberous xanthomas ( with II, III, IV types of hyperlipidemia) are large tumors or plaques with localization in the elbows, knees, buttocks and fingers. tendon xanthomas ( with II, III types of hyperlipidemia) are more often located in the region of the Achilles tendon ( calcaneal tendon) and extensor tendons of the fingers. flat xanthomas ( with I, II, III types of hyperlipidemia) are located in the area of ​​skin folds.
• Xanthelasma ( flat xanthomas of the eyelids). Xanthelasmas are slightly raised, flat, yellow-colored masses in the region of the eyelids. Occurs in type II and III hyperlipidemia. Xanthelasma is more often located on the upper eyelid at the inner corner of the eye. It can be single, multiple, or one of the manifestations of xanthomatosis ( multiple lesions of the skin xanthomas). It is more common in the elderly and especially in women. The appearance of xanthelasma and xanthoma in children indicates hereditary hypercholesterolemic xanthomatosis. The appearance of xanthelasma may indicate the presence of severe atherosclerosis and an increased risk of myocardial infarction.
• Lipoid corneal arch. The lipid arch of the cornea is a circular infiltration of the corneal stroma with lipids. As a result of the deposition of fats, the cornea loses its luster, and a white or yellowish ring forms on the periphery of the cornea. There is also a narrowing of the pupils, deformation of their shape is possible. Diagnosis of the lipoid arc is not difficult. It is performed by an ophthalmologist using special devices.

If xanthomatosis is detected in a patient, it is necessary to examine his lipid profile ( laboratory study of blood lipids). When diagnosing a violation of fat metabolism, treatment is prescribed. There is no specific treatment for xanthomatosis. The patient must follow a diet low in animal fats, take lipid-lowering drugs, and lead a healthy lifestyle.

Perhaps surgical treatment of xanthomatosis for cosmetic reasons. For this, excision with a scalpel or laser, electrocoagulation ( cauterization by electric current), cryotherapy ( exposure to low destructive temperatures) and the radio wave method ( destruction and excision of tissues under the influence of radio waves). Surgical treatment is performed under local anesthesia on an outpatient basis. After the procedure, a bandage is applied, and the patient goes home. Healing occurs within 1 - 1.5 weeks.

Dyslipidemias are dangerous complications. Violation of fat metabolism leads to the development of atherosclerosis, which is the cause of many cardiovascular diseases and death.

Why is high cholesterol dangerous?

Violation of lipid metabolism leads to an increase in blood total cholesterol, low density lipoproteins ( LDL - "bad" cholesterolVLDL). Dyslipidemia has no clinical symptoms, except for xanthomatosis. In general, hyperlipidemia does not cause discomfort to the patient. The main danger is the complications and consequences of impaired fat metabolism.

The main dangerous complication of dyslipidemia is atherosclerosis. Atherosclerosis is a chronic disease characterized by the deposition of cholesterol and other fats on the vessel wall, causing the vessels to thicken and lose their elasticity. More often, atherosclerosis affects middle-aged and elderly people. Also, atherosclerotic changes can occur in children with hereditary dyslipidemia.

Normally, the inner wall of blood vessels provides an anti-atherogenic effect ( preventing the deposition of atherosclerotic plaques), antithrombotic action ( preventing thrombosis) and the barrier function. Under the influence of various adverse factors ( smoking, sedentary lifestyle, malnutrition), as well as comorbidities ( diabetes mellitus, arterial hypertension) inner wall ( endothelium) arteries lose their integrity and protective functions. Increased permeability and adhesiveness ( adhesion) of the vascular wall. With dyslipidemia, total cholesterol, low-density lipoproteins accumulate in the cells of the inner layer of blood vessels ( "bad" cholesterol). Lipid deposits occur in the form of atherosclerotic plaques. Atherosclerotic plaque is an accumulation of fat ( cholesterol) and calcium. Further, platelets are attached to this site ( blood cells that provide thrombus formation and stop bleeding), proteins and other particles. This leads to the formation of a thrombus and narrowing of the lumen of the vessel. Over time, the lumen of the artery narrows significantly, which leads to poor blood circulation and nutrition of the internal organs and their necrosis ( tissue necrosis). A dangerous complication can cause a detachment of a part of a blood clot and its migration through the blood vessels. This can lead to thromboembolism - an acute blockage of the lumen of the vessel by a thrombus that has broken away from the original site of formation.

Depending on the atherosclerotic vascular lesion, there are:

• atherosclerosis of the aorta the largest blood vessel that carries blood from the heart to the internal organs). Atherosclerotic damage to the aorta leads to a persistent increase in blood pressure, to aortic valve insufficiency ( inability to prevent the backflow of blood from the aorta to the heart), circulatory disorders of the brain and other organs.
• Atherosclerosis of the heart vessels. The narrowing of the lumen of the vessels of the heart and the violation of its blood circulation leads to coronary heart disease ( ischemic heart disease). Ischemic heart disease is a disease that develops when there is insufficient supply of oxygen and nutrients to the heart muscle. The main manifestations are angina ( pain in the center of the chest), myocardial infarction ( necrosis of the muscle layer of the heart), cardiac arrhythmias ( abnormal heart rhythm), sudden cardiac death.
• Atherosclerosis of cerebral vessels. Violation of the blood circulation of the brain leads to a decrease in mental activity. When the vessel is completely closed by an atherosclerotic plaque, the blood circulation of a part of the brain is disturbed, followed by the death of brain tissue in this area. This pathology is called ischemic stroke and is extremely dangerous. Complications may include paralysis complete absence of voluntary movements in the limbs), speech disorder, cerebral edema, coma. Often, ischemic stroke leads to the death of the patient.
• Atherosclerosis of the intestinal vessels. The narrowing of the lumen of the vessels and the violation of the blood supply to the intestine leads to intestinal infarction ( death of its site due to insufficient supply of oxygen to the tissues).
• Atherosclerosis of the renal vessels. It is characterized by impaired blood supply to the kidney. Complications are kidney infarction, persistent increase in blood pressure and others.
• Atherosclerosis of the vessels of the lower extremities. Circulatory disorders of the lower extremities are characterized by the appearance of intermittent claudication, characterized by the appearance of pain in the legs while walking and lameness.

Complications of atherosclerosis(regardless of its location)divided into:

• Acute complications. They arise suddenly due to the separation of a blood clot from its original site of attachment. Broken thrombus ( embolus) migrates through the body with the blood stream and can cause blockage of any vessel. consequences of thromboembolism blockage of the vessel lumen by a detached thrombus) can become myocardial infarction ( death of a section of the muscular layer of the heart), stroke ( death of a part of the brain due to a violation of its blood supply) and other complications that can lead to the death of the patient.
• chronic complications. Atherosclerosis is a slowly progressive vascular disease. Narrowing of the vessel lumen results in chronic ischemia ( insufficient supply of oxygen and nutrients due to reduced blood flow) of the organ it nourishes.

Total cardiovascular risk

To assess the risk of developing cardiovascular diseases and mortality within 10 years, special formulas and scales were developed. With dyslipidemia, cardiovascular risk refers to the likelihood of developing cardiovascular diseases against the background of atherosclerosis over a certain period.

All patients are classified according to the level of risk according to the combination of risk factors and comorbidities. These scales help doctors assess the prognosis of a patient's life. Recommendations for examination, treatment and monitoring have also been developed for each level of risk ( observation) of the patient. The most well-known are the Framingham risk assessment scale, the SCORE scale ( Systemic assessment of coronary risk), ASSIGN ( Scottish risk assessment model) and others. The most commonly used and recommended by the European Society of Cardiology is the SCORE scale.

The SCORE scale helps to estimate the 10-year risk of developing deaths from cardiovascular diseases caused by atherosclerotic vascular disease. The scale is a table with risk factors. To calculate the total risk, 2 non-modifiable factors are taken into account ( gender, age) and 3 modifiable ( smoking, arterial hypertension, blood cholesterol).

According to the points collected, they distinguish:

• Very high risk risk SCORE ≥ 10%). This risk group includes patients with type 2 diabetes mellitus, myocardial infarction, stroke, chronic kidney disease, obesity and other severe pathologies. These patients have high levels of cholesterol, low density lipoproteins ( LDL).
• high risk ( risk SCORE ≥ 5% and< 10% ). The high-risk group includes patients with hereditary hyperlipidemia, arterial hypertension ( high blood pressure) and other pathologies.
• moderate risk ( risk SCORE ≥ 1% and< 5% ). This category of patients with moderate risk includes most middle-aged people. The risk is increased in the presence of premature coronary artery disease ( blood supply to the heart), obesity, increased levels of cholesterol and low-density lipoproteins, and others.
• Low risk ( risk score< 1% ). Patients at low risk are advised to change their lifestyle, diet, and regular medical monitoring to avoid the risk of developing serious complications.

Patients with cardiovascular disease, diabetes mellitus, chronic kidney disease, or very high levels of certain risk factors are automatically classified as very high risk and high risk. For the rest, the risk SCORE is calculated.

Also, to assess the risk of cardiovascular diseases, the calculation of the index is used ( coefficient) atherogenicity. For the calculation, a special formula and lipidogram indicators are used ( cholesterol, low-density lipoprotein, high-density lipoprotein).

Atherogenic coefficient ( KA) is calculated by the formula - KA = ( OH - HSLVP) / HSLVP.

You can apply another formula - KA = ( HSLNP + HSLPONP) / HSLVP.

Taking into account the level of triglycerides, the formula is used - KA = ( CHSLNP + TG / 2.2) / HSLVP.

Indicators of the coefficient of atherogenicity and their interpretation are:

• 2 - 3 (without units) - indicator of the norm;
• 3 - 4 - indicates a moderate risk of developing atherosclerosis and cardiovascular diseases, which can be prevented with diet and lifestyle modification;
• above 4 - indicates a high risk of developing vascular atherosclerosis and cardiovascular disease, which requires treatment with lipid-lowering drugs.

Life prognosis in dyslipidemia

The prognosis of life in dyslipidemia is individual for each patient. It depends on many factors and actions of the patient.

Factors affecting the prognosis of patients' life are:

• age;
• accompanying illnesses ( diabetes, obesity);
• blood lipid levels;
• vascular atherosclerosis ( localization, prevalence, rate of development of atherosclerotic changes);
• etiology of dyslipidaemia hereditary, acquired);
• early or late diagnosis;
• timely started and correctly selected treatment;
• cardiovascular risk ( according to the SCORE scale);
• the presence of complications of dyslipidemia ( atherosclerosis);
• the patient's lifestyle, nutrition, physical activity;
• patient compliance with all doctor's recommendations;
• periodic medical monitoring with a lipid profile study ( ).

In the case of early diagnosis of dyslipidemia and timely lifestyle changes, rejection of bad habits, timely initiated lipid-lowering drug treatment, the patient's risk of developing cardiovascular diseases and mortality is significantly reduced. Since the imbalance of lipids does not manifest itself in any way, it can only be detected during medical preventive examinations. The local doctor should explain to patients the need for periodic lipid profile studies ( laboratory study of lipid levels) in the presence of risk factors ( obesity, smoking, sedentary lifestyle, malnutrition, middle and old age). Serious diseases such as myocardial infarction and stroke can be avoided with constant monitoring of blood lipid levels.

If dyslipidemia was diagnosed already in the presence of complications ( atherosclerosis), then you should immediately begin treatment with lipid-lowering drugs ( lowering blood lipids). The prognosis of life in such patients is favorable if the patient responds well to treatment and the doctor has managed to achieve target blood lipid levels. In this case, the risk of cardiovascular disease and mortality is significantly reduced. The patient must strictly follow the doctor's instructions and undergo medical supervision.

With a significant increase in the level of lipids in the blood, severe concomitant diseases ( chronic kidney disease, diabetes mellitus), with complications of atherosclerosis ( myocardial infarction, stroke) the prognosis of the patient's life is disappointing. Despite lipid-lowering therapy, lifestyle changes, and even the achievement of target levels of lipids in the blood, pathological changes in the body and their consequences are already irreversible. These patients are at very high risk with high mortality.

Dyslipidemia is a non-innocuous increase in the level of lipids in the blood. Mortality from cardiovascular diseases ranks first worldwide. Therefore, local doctors, cardiologists, therapists and other specialists have a great responsibility for the timely diagnosis of hyperlipidemia, the prevention of the development of heart and vascular diseases and the reduction in the mortality rate from these diseases.

Diagnosis of dyslipidemia

Dyslipidemias are exclusively a laboratory indicator. Usually, a violation of fat metabolism does not have clinical symptoms. More often, dyslipidemia is diagnosed by chance during a routine medical examination or during the diagnosis of other diseases. The occurrence of hyperlipidemia is influenced by many factors, therefore, all complaints, lifestyle features, the patient's heredity and others should be carefully analyzed.

As a result of large studies, it has been demonstrated that a lipid profile should definitely be done (regardless of complaints):

• patients with type 2 diabetes ( appears predominantly in adulthood and old age);
• smoking patients;
• obese patients;
• patients with aggravated heredity ( with cases of cardiovascular diseases in the next of kin);
• patients with high blood pressure ( above 140/80 mm. Hg);
• patients with instrumentally confirmed cardiovascular diseases ( Ultrasound of the heart, ECG).

Diagnosis of dyslipidemias includes taking an anamnesis ( history of present illness and patient's life), examination and laboratory blood tests.

First of all, the doctor will take a detailed medical history of the patient.

History includes:

• history of complaints and present illness- what worries the patient at the moment when xanthomas appeared ( dense nodules of cholesterol over the surface of the tendons), xanthelasma ( deposits of cholesterol nodules under the skin of the eyelids), lipoid corneal arch ( deposition of cholesterol at the edges of the cornea of ​​the eye);
• anamnesis of life What comorbidities does the patient have? diabetes mellitus, thyroid disease), what diseases he suffered ( myocardial infarction, stroke and others), what lifestyle he leads, what kind of food he prefers, bad habits ( smoking, alcohol, sedentary lifestyle);
• family history- what diseases the next of kin of the patient had - myocardial infarction, stroke, atherosclerosis and other pathologies.

After collecting an anamnesis, the doctor will conduct an external examination. On examination, xanthoma, xanthelasma, lipoid corneal arch can be detected. There are no special external manifestations in dyslipidemia.

Laboratory research methods include:

• blood chemistry- determine the level of sugar in the blood, the level of proteins, creatinine ( protein breakdown product) to identify comorbidities;
• general analysis of blood and urine- reveals inflammatory processes and accompanying pathologies;
• immunological blood test- determine the content of antibodies ( proteins produced by the body against foreign substances or its own diseased cells) to cytomegalovirus and chlamydia ( microorganisms that may lead to the development of atherosclerosis), as well as the level of C-reactive protein, which is an indicator of inflammatory processes in the body;
• genetic analysis- identification of defective genes responsible for the development of hereditary dyslipidemias.

A specific laboratory analysis that reveals a lipid imbalance is a lipidogram - an analysis of the level of lipids in the blood. To obtain reliable results, the patient must strictly follow the recommendations of the doctor before conducting the study. Improper diet, alcohol consumption, smoking, inflammatory processes, infectious diseases can change the level of lipids in the blood.

The main requirements before conducting a lipid profile are:

• patient compliance with a strict diet for 2 to 3 weeks;
• determination of the concentration of triglycerides is carried out strictly on an empty stomach ( after 12 - 14 - hour night fasting), which is not related to the determination of cholesterol levels;
• analysis 3 months after severe illness ( stroke, myocardial infarction) or extensive surgical interventions;
• conducting a study 2 to 3 weeks after the illness of moderate severity;
• analysis, provided that the patient is rested, and before the procedure it is necessary to sit for 10 - 15 minutes;
• the application of a tourniquet before taking blood should not exceed 1 minute, if possible, avoid the application of a tourniquet.

About 5 milliliters of blood is collected for analysis. Determination of lipid levels is carried out in blood serum or blood plasma. If lipids are determined in the blood serum, then the blood is collected in empty test tubes. If in blood plasma, then anticoagulants are added to the test tube ( drugs that prevent blood clotting).

The laboratory determines:

• serum/plasma total cholesterol ( cholesterol, which is part of LDL, HDL, VLDL);
• serum/plasma HDL cholesterol concentration;
• serum/plasma triglycerides ( included in LDL, VLDL, HDL). Especially high levels of triglycerides are observed in patients with diabetes mellitus.

The level of low density lipoproteins ( LDL) is technically difficult to determine, so in most laboratories it is calculated using special formulas.

When interpreting the results, the following terms are used:

• hyperlipidemia- increased concentration of lipids in the blood ( cholesterol > 5.0 mmol/l and/or triglycerides > 1.8 mmol/l);
• hypercholesterolemia- increased levels of total cholesterol in the blood > 5.0 mmol/l);
• hypertriglyceridemia- increased concentration of triglycerides in the blood ( > 1.8 mmol/l).

Treatment of dyslipidemia, correction of lipid metabolism for each type of dyslipidemia

After diagnosing a lipid metabolism disorder, it is necessary to start treatment in a timely manner to prevent the development of complications.

Treatment of dyslipidemia is divided into:

• non-drug treatment;
• drug treatment;
• extracorporeal ( out of body) methods of treatment;
• genetic engineering methods.

Non-drug treatment

Non-drug treatment consists in a complete change in lifestyle, the rejection of bad habits ( smoking, excessive alcohol consumption), diet therapy. If a patient is diagnosed with dyslipidemia, he will first be advised to reconsider his lifestyle, diet, and exercise. Non-pharmacological treatment is prescribed for patients with low, moderate and even high total cardiovascular risk, depending on the level of cholesterol in the blood. If the values ​​of lipids in the blood are reduced, then non-drug treatment is continued. If diet, physical activity do not affect lipid levels, then lipid-lowering agents are prescribed ( lowering blood lipids).

• eating healthy food, taking into account the energy needs of the body to avoid the development of obesity;
• eating fruits, vegetables, legumes, nuts, fish, whole grain cereals in sufficient quantities;
• saturated fat replacement meat, eggs, chocolate, butter) into monounsaturated fats ( almonds, peanuts, avocado, sunflower, olive, nut oils) and polyunsaturated fats ( salmon, walnuts, soybean oil, corn oil, flax, sesame seeds);
• limiting the intake of table salt to 5 grams per day;
• reducing alcohol consumption to 10 - 20 grams per day for women and 20 - 30 grams per day for men;
• physical activity at least 30 minutes daily;
• to give up smoking.

The impact of lifestyle on blood lipid levels

Lifestyle and lowering total cholesterol ( OH) and low-density lipoprotein cholesterol ( cholesterol - LDL)	The intensity of the effect
Decreased intake of saturated fats ( eggs, coconut oil, chocolate, dairy products) in food	+++
Reduced consumption of trans fats ( margarine, fried products) in food	+++
Increase in the diet of foods rich in dietary fiber	++
Reducing the amount of cholesterol in the food you eat	++
Eating foods rich in phytosterols ( sunflower oil, buckwheat porridge, sesame seeds, corn oil, almonds, soybeans)	+++
Weight loss	+
	+
Lifestyle and lower triglyceride levels ( TG)
Weight loss	+++
Decrease in alcohol consumption	+++
Limiting the intake of monosaccharides and disaccharides ( honey, sweet fruits and vegetables - melon, tomatoes, grapes, bananas, cherries, beets and others)	+++
Regular physical activity	++
Use of supplements with n-3 polyunsaturated fats ( vitrum cardio omega-3)	++
Reducing the amount of carbohydrates ( bakery products, sweets, chocolate, dried fruits) in food consumed	++
Lifestyle and high-density lipoprotein cholesterol (HDL) cholesterol - HDL)
Limiting dietary intake of trans fats ( fast food, mayonnaise, semi-finished products)	+++
Regular physical activity	+++
Weight loss	++
Reducing alcohol consumption	++
Reducing the intake of carbohydrates from food and replacing them with unsaturated fats ( fish, nuts, vegetable oils)	++
Eating foods rich in dietary fiber cellulose) - carrots, oats, bran, apples	+

* +++ - very effective
++ - efficient
+ - less effective

The main attention should be paid to lowering the level of total cholesterol and low-density lipoproteins, since these lipids are atherogenic, that is, they contribute to the development of atherosclerosis and severe diseases of the cardiovascular system.

Products	Recommended for eating	Restriction of use	Complete exclusion from the diet or significant restriction of consumption
Flour products, cereals	Whole grain products	Rice, pasta, muesli, biscuit	Cakes, muffins, croissants, sweet pies
Vegetables	Any fresh and cooked		Vegetables cooked in butter or cream
Fruit	Any fresh or frozen	Dried or canned fruit, jam, sherbet, jelly, popsicles
Legumes	Any
Sweets	low calorie	Honey, chocolate, candies, sweet fruits	Cake, ice cream
fish, meat	Fatty fish, poultry meat	Lean beef, lamb, veal, seafood	Any sausages, bacon, wings
Dairy products, eggs	Skim milk, egg white	Milk, low fat cheese	Cream, egg yolk, yogurt
Cooking fats and sauces	Natural ketchup, vinegar, mustard	Vegetable oil, salad dressings	Butter, margarine, egg yolk sauces
nuts		All types	Coconut
Cooking method	Grill, boil, steam	Frying food	deep-frying

Lifestyle changes, diet and physical activity usually bring good results in the correction of dyslipidemia. Non-pharmacological treatment may become the main and only treatment ( depends on blood lipid levels and cardiovascular risk). Lifestyle modification is not limited to a certain period of time before results improve. Since after returning to the usual way of life there will again be disturbances in the lipid balance. This should already become a habitual way of life for the patient.

Medical treatment

Drug treatment is prescribed after a thorough examination of the patient and determining his risk group for developing cardiovascular diseases. Since the increase in cholesterol and low-density lipoproteins play a major role in the development of cardiovascular diseases, hypolipidemic ( lowering blood lipids) therapy specifically targets these lipids.

After a general examination of the patient and a study of his lipid profile, the doctor determines further treatment tactics. In some cases, non-pharmacological treatment is prescribed ( lifestyle modification, nutrition), in others, drug treatment with lipid-lowering drugs with careful monitoring is necessary ( observation) of the patient. When choosing treatment tactics, the level of low density lipoproteins is taken into account ( LDL) and the risk group of the patient.

Tactics for the treatment of dyslipidemia, taking into account the risk group of the patient and the level of LDL

Risk ( SCORE) %	Low-density lipoprotein cholesterol levels ( LDL cholesterol)
	< 1,8 ммоль/л	1.8 - 2.4 mmol/l	2.5 - 3.9 mmol/l	4.0 - 4.8 mmol/l	> 4.9 mmol/l
< 1% низкий	No treatment required	No treatment required	Lifestyle Modification	Lifestyle Modification
> 1% and< 5% умеренный	Lifestyle Modification	Lifestyle Modification	Lifestyle modification. If the target LDL level is not reached, start treatment with lipid-lowering agents.	Lifestyle modification. If the target LDL level is not reached, start treatment with lipid-lowering agents.	Lifestyle modification. If the target LDL level is not reached, start treatment with lipid-lowering agents.
> 5% and< 10% tall	Lifestyle modification and treatment with lipid-lowering agents	Lifestyle modification and treatment with lipid-lowering agents		Lifestyle modification with immediate initiation of lipid-lowering therapy	Lifestyle modification with immediate initiation of lipid-lowering therapy
> 10% very high	Lifestyle modification with immediate initiation of lipid-lowering therapy	Lifestyle modification with immediate initiation of lipid-lowering therapy	Lifestyle modification with immediate initiation of lipid-lowering therapy	Lifestyle modification with immediate initiation of lipid-lowering therapy	Lifestyle modification with immediate initiation of lipid-lowering therapy

When treating lipid-lowering drugs, doctors try to achieve a certain level of lipids in the blood ( target value), which significantly reduces the risk of developing cardiovascular diseases.

Optimal target lipid levels depending on the risk group ( SCORE)

Lipids	Patients at low risk	Patients at moderate risk	High Risk Patients	Patients at very high risk
total cholesterol	≤ 5.5 mmol/l	< 5,0 ммоль/л	≤ 4.5 mmol/l	≤ 4.0 mmol/l
low density lipoproteins	≤ 3.5 mmol/l	≤ 3.0 mmol/l	≤ 2.5 mmol/l	≤ 1.8 mmol/l
high density lipoproteins	husband. > 1.0 mmol/l female > 1.2 mmol/l	husband. > 1.0 mmol/l female > 1.2 mmol/l	husband. > 1.0 mmol/l female > 1.2 mmol/l	husband. > 1.0 mmol/l female > 1.2 mmol/l
Triglycerides	≤ 1.7 mmol/l	< 1,7 ммоль/л	< 1,7 ммоль/л	< 1,7 ммоль/л

For the treatment of hyperlipidemia ( elevated levels of fats in the blood) use lipid-lowering drugs, that is, lowering the level of lipids in the blood. In the treatment, drugs from one group or in combination with drugs from another group can be used. Assign lipid-lowering agents only after ineffective non-drug therapy. During treatment, the patient should be under the supervision of a physician and periodically take the necessary laboratory tests to assess the effectiveness of treatment and the function of other internal organs to prevent complications. The duration of treatment and doses are selected individually for each patient, taking into account his lipid profile, concomitant diseases, risk groups, etc.

Lipid-lowering drugs

Drug group	Name of drugs	Mechanism of action	Doses	Indications	Contraindications
Statins	simvastatin ( vasilip, simvacard, simlo)	They inhibit the enzyme responsible for the formation of cholesterol. Lower the level of TG, LDL, VLDL, increase the level of HDL.	Inside from 10 to 80 milligrams 1 time / day. Dose selection is carried out with an interval of 4 weeks.	- primary hypercholesterolemia ( type IIa and IIb) with inefficiency diet therapy, physical activity; Combined hypercholesterolemia and triglyceridemia; Ischemic heart disease; prevention cardiovascular diseases.	- pregnancy; Women of childbearing age not using contraception; Hypersensitivity to the drug; Impaired liver function ( hepatitis, cirrhosis) in the active stage.
	fluvastatin ( leskol forte)		Inside, 20 - 40 milligrams per day.
	atorvastatin ( liptonorm, liprimar)		Inside from 10 to 80 milligrams per day.
	rosuvastatin ( mertenil, rosulip)		Inside from 10 to 40 milligrams per day.
Inhibitor of absorption (absorption) of cholesterol in the intestine	ezetimibe ( ezetrol)	They prevent the reabsorption of cholesterol from the intestines to the liver. Unlike bile acid sequestrants, they do not increase the secretion of bile acids, and unlike statins, it does not inhibit the synthesis of cholesterol in the liver.	Tablets of 10 milligrams are taken 1 time / day, regardless of food intake and time of day.	- primary hypercholesterolemia; Homozygous familial hypercholesterolemia.	- moderate or severe liver damage; Application simultaneously with fibrates; Pregnancy and lactation; Children and teenagers under 18; drug intolerance.
	INEGY is a combined preparation containing 10 mg of ezetimibe and 10, 20, 40 or 80 mg of simvastatin, which complement each other with their mechanism of pharmacological action.		Depending on the indications, take 1 tablet orally ( 10 milligrams ezetimibe + 10 to 80 milligrams simvastatin) 1 time / day. in the evening.
Sequestrants (isolators) of bile acids	cholestyramine	They bind cholesterol to bile acids synthesized from cholesterol in the liver. The bile acids in bile are excreted into the intestines, where approximately 97% are reabsorbed and returned to the liver through the bloodstream. By binding bile acids, the liver uses more cholesterol to synthesize new acids, thereby lowering cholesterol levels.	The powder is dissolved in 60 - 80 milliliters of water. Take 4 - 24 grams per day, divided into 2 - 3 doses before meals.	as a result, the features of not being absorbed into the blood are used for pregnant, breastfeeding women, children and adolescents in the treatment of familial hypercholesterolemia.	- familial hyperlipoproteinemia III and IV types; The defeat of the biliary tract - biliary cirrhosis of the liver, obstruction of the biliary tract; drug intolerance.
	colestipol		inside. The initial dose of 5 g / day, if necessary, increase by 5 g / day every 4 to 8 weeks.
	kolesevelam ( welchol)		Inside at a dose of 625 milligrams per day. If necessary, increase the dose.
Fibric acid derivatives - fibrates	bezafibrate ( bezamidin, bezifal, tsedur)	They increase the activity of the enzyme - lipoprotein lipase, which breaks down LDL, VLDL, increases the level of HDL.	Inside, 200 milligrams 2-3 times / day.	- hypertriglyceridemia ( increased levels of triglycerides in the blood); Familial combined dyslipidemia (hereditary lipid imbalance).	Liver diseases - liver failure, cirrhosis of the liver; kidney failure; Pregnancy, breastfeeding; Age up to 18 years.
	fenofibrate ( lipantil)		Inside, 100 milligrams 2 times / day. before or during meals.
	ciprofibrate ( lipanor)		Inside 100 - 200 milligrams 1 time / day.
Nicotinic acid - niacin	Nicotinic acid, niacin, vitamin PP, vitamin B 3	They normalize the level of lipoproteins in the blood, reduce the concentration of total cholesterol, LDL, increase the level of HDL.	For prophylaxis inside, 15-25 milligrams per day after meals. For treatment, take orally 2-4 grams per day after meals.	hyperlipidemia type IIa, IIb, III, IV, V.	- age up to 2 years; - peptic ulcer of the stomach and 12 duodenal ulcer ( acute stage).
Omega-3 unsaturated fatty acids	omakor	Suppress synthesis ( production) LDL, VLDL, improve their excretion and increase excretion ( selection) bile. Reduce the level of triglycerides, delay their synthesis in the liver.	Inside, 2 - 4 capsules per day during meals.	- prevention of lipid metabolism disorders ( dyslipidemia); Complex treatment of dyslipidemia ( in combination with diet therapy, with therapy with statins and other lipid-lowering drugs).	- age up to 18 years; Cholelithiasis; Exacerbation of chronic cholecystitis ( inflammation of the gallbladder) and pancreatitis ( ).
	vitrum cardio omega-3		For prevention - 1 capsule per day after meals. For treatment - 1 capsule 2-3 times a day after meals. The course of treatment is at least three months.

The main goal of the treatment of dyslipidemia is to prevent the development of cardiovascular diseases. This can be achieved not only by lowering the level of total cholesterol, low density lipoproteins ( "bad" cholesterol), but also an increase in the level of high-density lipoproteins ( "good" cholesterol). Most lipid-lowering drugs increase HDL levels.

Extracorporeal treatments

Extracorporeal treatment is a therapy that is carried out outside the human body. Extracorporeal methods of treatment in combination with other methods of treatment ( diet therapy, therapy with lipid-lowering drugs) give a good and long-lasting effect.

Extracorporeal methods of treatment include plasma sorption and hemosorption. Plasma sorption is a method of effective purification of blood plasma from various harmful products by contacting plasma with special sorbents ( substances that selectively absorb molecules or particles) outside the human body. During plasma sorption, the patient's blood is divided into blood cells and plasma. Plasma is the liquid part of the blood that does not contain any cells ( erythrocytes, lymphocytes, leukocytes and others), except for the solution of proteins in water. With plasma sorption, only plasma is passed through the filters, with hemosorption - blood.

According to the type of sorbent, there are:

• non-selective plasma sorption. As a sorbent, activated carbon is used, which is the most famous sorbent with a wide range of absorbable ( absorbed) substances.
• Semi-selective plasma sorption - cascade plasma filtration. It is a high-tech semi-selective purification method that allows selective removal of lipids from plasma ( cholesterol, low density lipoproteins and others). As a filter, ion-exchange resins are used, which have selectivity for certain substances. It is the most modern method of extracorporeal "purification" of blood. The course of treatment is 5 - 10 procedures with a frequency of 6 months to 1.5 years.
• Selective plasma sorption - immunosorption of lipoproteins. It is a high-tech selective ( electoral) a method that allows selective removal of molecules or particles from blood plasma ( low density lipoproteins). To purify plasma, special filters are used - immunosorbents containing antibodies to certain substances. The duration of one procedure is 3-6 hours. Frequency of the course - 1 procedure every 1 - 4 weeks.

Any manipulation with the collection of blood and its components is a serious intervention, therefore, before the procedure, the patient must undergo a complete medical examination and pass the necessary blood tests.

The procedure is carried out by specialists in a specialized office. The patient sits in a chair. A needle is inserted into the vein, connected to special tubes that are connected to the plasma sorption apparatus. Through these tubes, the blood enters the machine, where it is divided into blood cells and plasma. Then the plasma passes through special filters, where it is cleared of the "bad" fractions of cholesterol - low density lipoproteins ( LDL), very low density lipoproteins ( VLDL) and others. The plasma then recombines with blood cells and returns to the patient's body. After the procedure, a special compression ( squeezing) bandage for a period of 6 hours. With this bandage, the patient goes home.

There are no absolute contraindications to plasma sorption, with the exception of active bleeding. Relative contraindications include acute infectious diseases, low plasma protein levels ( hypoproteinemia), menstruation and others.

Genetic Engineering

Genetic engineering may be an effective treatment for hereditary dyslipidemias in the future. The essence of the method of such treatment is to change the hereditary material of cells ( DNA) responsible for the transmission of the defective gene.

Treatment for hypercholesterolemia and elevated low-density lipoprotein levels

With hypercholesterolemia, diet, exercise, smoking and alcohol cessation, and weight loss are recommended. You should eat more nuts, fruits, vegetables, legumes, oily fish and others.

In the medical treatment of hypercholesterolemia, statins are used at the maximum recommended or maximum tolerated dose. Do not forget that statins are hepatotoxic ( can disrupt the structure and function of the liver). Therefore, during treatment with statins, it is necessary to periodically monitor liver enzymes - ALAT, ASAT, which are released into the blood when liver cells are destroyed. Another serious complication of statin use is myopathy ( progressive muscle disease with metabolic disorders in muscle tissue), up to the development of rhabdomyolysis ( extreme myopathy with destruction of muscle cells). Myoglobin ( skeletal muscle oxygen-binding protein), released during the destruction of muscle cells, can significantly damage the kidneys with the development of kidney failure. main marker ( indicator) muscle breakdown is an increase in the level of creatine phosphokinase ( CPK - an enzyme in muscle fibers that is released when they are destroyed). In order to avoid the risk of developing myopathies, the combination of statins with gemfibrozil from the fibrate group should be avoided. The risk of developing unwanted complications increases with age, with hypothyroidism, with low body weight, in females, with impaired renal and hepatic functions.

Patients who are resistant to statin therapy may be given cholesterol absorption inhibitors ( alone or in combination with nicotinic acid), bile acid sequestrants, nicotinic acid. A combination of statins with cholesterol absorption inhibitors, a combination of statins with bile acid sequestrants, and others may also be used.

Treatment with statins is carried out under close medical supervision with periodic laboratory tests. Despite the complications, statins are called the "drug of immortality" because they affect the DNA enzyme ( telomerase), responsible for youth and longevity.

Treatment for hypertriglyceridemia

One of the serious complications of hypertriglyceridemia is the development of acute pancreatitis ( inflammation of the pancreas). The risk of developing pancreatitis increases with an increase in triglyceride levels above 10 mmol / l. With the development of the disease, the patient must be hospitalized, timely start drug therapy and careful monitoring.

In the treatment of hypertriglyceridemia, proper nutrition, weight loss and regular exercise are of no small importance. This helps to reduce triglycerides in the blood by 20 - 30%.

Of the medications for the treatment of hypertriglyceridemia, statins, fibrates, nicotinic acid and n-3 polyunsaturated fatty acids are used. If necessary, a combination of statins and nicotinic acid, statins and fibrates, statins and n-3 polyunsaturated fatty acids, and others can be prescribed.

Treatment to increase high-density lipoprotein levels

High-density lipoproteins are called "good" cholesterol, an anti-atherogenic factor. High density lipoproteins help remove excess cholesterol from the body. Therefore, in the treatment of dyslipidemia and the prevention of the development of diseases of the cardiovascular system, attention should be paid to increasing the level of high density lipoproteins ( HDL).

Nicotinic acid is currently the most effective high-density lipoprotein-raising drug. Statins and fibrates are also able to increase these lipid levels equally. In patients with type 2 diabetes, the ability of fibrates to increase HDL levels may be reduced.

Treatment of dyslipidemia in various clinical situations

In the treatment of dyslipidemia, it is necessary to take into account the etiology of hyperlipidemia, the age and gender of the patient, his comorbidities, and other factors. This will help make therapy more effective and significantly reduce the risk of complications.

Treatment of dyslipidemia in various clinical situations

Clinical situation	Features of therapy
Hereditary dyslipidemias	Early and accurate diagnosis is essential. If possible, DNA testing is required. When a patient has hereditary dyslipidemia, it is important to conduct a survey of his next of kin. In the treatment of familial dyslipidemia, statins are used in high doses. If necessary, a combination of statins and cholesterol absorption inhibitors and/or bile acid sequestrants is used. Children whose parents are sick with hereditary dyslipidemia should be carefully examined. When indicated, they are prescribed drug therapy.
Elderly age	The elderly are most susceptible to diseases of the heart and blood vessels. They are in the high and very high risk group. All elderly patients need to undergo medical monitoring and lipid profile studies. Elderly patients with cardiovascular diseases are treated according to the same algorithms as in ordinary patients. When prescribing lipid-lowering therapy, comorbidities should be taken into account.
Children	Dieting is the main treatment for dyslipidemia in childhood. An exception is familial hypercholesterolemia, in which lipid-lowering drugs may be prescribed. A thorough periodic examination of the patient is necessary and, if necessary, the appointment of lipid-lowering drug therapy.
Women	Women are not prescribed lipid-lowering drugs during pregnancy and lactation.
Metabolic syndrome and type 2 diabetes	Metabolic syndrome means the simultaneous presence of several risk factors in a patient - obesity, arterial hypertension, elevated triglyceride levels, low HDL levels, diabetes mellitus. In such patients, the risk of developing diseases of the cardiovascular system is 2 times higher and the risk of mortality is 1.5 times higher. The administration of drugs should be started with small doses, gradually increasing them until the target lipid levels are reached. It is also necessary to start lipid-lowering therapy in patients who do not suffer from diseases of the cardiovascular system, but who have 1 or more risk factors.
Heart failure and valvular disease	Lipid-lowering therapy is not indicated in patients with valvular heart disease without coronary disease ( blood supply to the heart). The use of statins is not indicated in patients with moderate or severe heart failure. Perhaps the appointment of n-3 polyunsaturated fatty acids as an adjunct to the treatment of heart failure.
Autoimmune diseases (autoimmune thyroiditis)	Autoimmune diseases ( diseases in which the immune system recognizes the body's own cells as foreign and destroys them) are characterized by progressive atherosclerosis. Since it is assumed that the immune system plays a role in the development of atherosclerosis. This significantly increases the risk of heart and vascular diseases, as well as patient mortality. However, there is no indication for prophylactic lipid-lowering treatment in patients with autoimmune diseases.
kidney disease	Chronic kidney disease is a serious factor in the development of cardiovascular disease. Therefore, the main goal of treatment of such patients is to reduce the level of cholesterol - LDL. The use of statins helps slow the progression of renal dysfunction and prevents the development of end-stage kidney disease.
Organ transplant	Organ transplant patients are forced to take lifelong immunosuppressive drugs to prevent rejection of the transplanted organ. These drugs negatively affect lipid metabolism, provoking the development of dyslipidemia. Strict control and correction of factors in the development of diseases of the heart and blood vessels is necessary. The use of statins is recommended, starting with low doses and gradually increasing the dose if necessary. With intolerance to statins, therapy with other groups of lipid-lowering drugs is possible.
Other conditions and pathologies	Patients who have had a stroke, heart attack, with concomitant vascular atherosclerosis, with a high and very high risk are recommended to start lipid-lowering therapy with periodic laboratory and instrumental monitoring.

Prevention of dyslipidemia

Dyslipidemias lead to life-threatening complications, so special attention should be paid to the prevention of these disorders.

Prevention of dyslipidemia is divided into:

• primary;
• secondary.

Primary prevention

Primary prevention of dyslipidemia is aimed at preventing lipid metabolism disorders.

The main principles of primary prevention of dyslipidemia are:

• normalization of body weight;
• healthy diet low in fat and salt up to 5 grams per day), the use of vegetables, fruits;
• quitting smoking and alcohol abuse;
• physical activity, individually selected for the patient, taking into account his state of health;
• avoidance of stress and emotional overload;
• maintaining glucose levels within normal limits 3.5 - 5.5 mmol/l);
• maintaining blood pressure within normal limits below 140/90 millimeters of mercury);
• regular medical check-ups with laboratory testing of blood lipids ( lipidogram), especially in patients with a positive family history ( whose close relatives had dyslipidemia, atherosclerosis, stroke, myocardial infarction);
• timely treatment of diseases that can lead to impaired lipid metabolism ( thyroid disease, liver disease).

Secondary prevention

Secondary prevention is carried out in patients with pre-existing dyslipidemia and is aimed at preventing the onset and progression of vascular atherosclerosis, as well as the occurrence of dangerous complications.

The main principles of secondary prevention of dyslipidemia are:

• non-drug effects on modifiable risk factors ( cessation of smoking, alcohol consumption, medical examinations with a lipid profile, diet and others);
• drug treatment of dyslipidaemia the use of statins, fibrates and other lipid-lowering drugs).

Is dyslipidemia treated with folk remedies?

In the treatment of dyslipidemia, folk remedies can be used. Before using folk remedies, you must consult your doctor and undergo the necessary studies. Treatment with folk remedies can be the main therapy ( monotherapy) or part of complex treatment by other methods. The choice of treatment tactics depends on the level of cholesterol, triglycerides, low-density lipoproteins, determined in a laboratory blood test. The choice of treatment is also influenced by the risk of developing cardiovascular diseases, determined by the doctor using specially designed scales. It is not worth giving preference only to alternative methods of treating hyperlipidemia, as this is fraught with dangerous complications. During treatment, be sure to periodically do a lipid profile.

In the treatment of hypercholesterolemia apply:

• A decoction of rose hips. Dried and crushed rose hips ( 20 grams) place in an enamel bowl and pour 200 - 300 milliliters of boiling water. Simmer in a water bath over low heat for about 15 minutes. Cool and strain. Take 100 - 150 milliliters 2 times a day.
• A decoction of immortelle. Ten grams of dried crushed immortelle leaves pour 200 milliliters of water. Heat in a water bath for 30 minutes, stirring frequently. Strain and refrigerate. Take 1 full dessert spoon ten minutes before meals 2 times a day. The course of treatment is 1 month. After a 10-day break, repeat the course of treatment.
• Milk thistle seed powder. Milk Thistle Seed Powder Take one teaspoon daily with meals.
• Ground turmeric root. Ground turmeric root should be consumed in the amount of 1-6 grams per day. Turmeric can be added to any dish. You can buy it at any grocery store.
• Drinks from rowan berries. To prepare a drink from mountain ash, it is necessary to wash the berries of mountain ash and pour boiling water for 2-3 minutes. Then strain and squeeze the juice with a juicer. To prepare the infusion of rowan berries, pour 400 milliliters of boiling water and let it brew for an hour. Then add honey or sugar to taste. Infusion to drink on the day of preparation.
• Linseed oil. Flaxseed oil take 20 grams in the morning on an empty stomach for 40 days. After a 20-day break, repeat the course of treatment. Treatment for hypercholesterolemia is long, but effective.

Are dyslipidemias a contraindication to joining the military?

Dyslipidemia is not a contraindication for military service. Violation of fat metabolism in young people is extremely rare. The exception is hereditary hyperlipidemia. This pathological condition in most cases can be easily corrected, starting with lifestyle changes, increased physical activity, smoking cessation and alcohol abuse, weight loss in obesity and proper nutrition. In some cases, after consulting a doctor, an additional intake of cholesterol-lowering drugs is required.

In the case of a combination of dyslipidemia with other pathological conditions ( diabetes mellitus, arterial hypertension, thyroid disease and others) or complications of dyslipidemia with atherosclerotic vascular lesions and cardiovascular diseases, military service is contraindicated. This is considered by a special commission on a case-by-case basis.

Which doctor treats dyslipidemia?

The primary diagnosis of dyslipidemia can be made by the local doctor in whom the patient is observed. The local doctor can give recommendations on lifestyle modification, and if necessary, prescribe lipid-lowering drugs. It is necessary to observe the patient in dynamics with the study of biochemical blood tests and lipidograms.

Since the etiology reasons for the appearance) dyslipidemia is diverse, as well as the complications and treatment of the disease affects many organs and systems, then several specialists can deal with the treatment of violations of the level of lipids in the blood.

Treatment and diagnosis of dyslipidemia is carried out:

• Cardiologist. With the initial diagnosis of dyslipidemia in a patient, the local doctor will refer him for a consultation with a cardiologist. A cardiologist examines the state of the patient's cardiovascular system using laboratory and instrumental studies ( ultrasound examination of the heart and blood vessels, ECG and others). This will help to start treatment in a timely manner and avoid fatal complications.
• Endocrinologist. Many diseases of the endocrine system exacerbate the patient's condition with dyslipidemia and increase the risk of cardiovascular disease. Diabetes mellitus has a particularly negative effect, since this disease also affects the vessels and may reduce the effect of some lipid-lowering agents.
• Nutritionist. The nutritionist will analyze the nutrition and select a diet individually for each patient, taking into account the level of lipids in the blood. The patient must adhere to the recommendations of a nutritionist for life.
• Geneticist. A consultation with a geneticist is necessary for familial hereditary types of dyslipidemia to confirm the diagnosis. In the future, correction of hereditary material is possible ( Genetic Engineering) to exclude the transmission of dyslipidemia by inheritance.
• Doctors of other specialties. When treating or diagnosing a patient, it may be necessary to consult doctors of different specialties. For example, liver disease may be a contraindication to the treatment of dyslipidemia with lipid-lowering drugs. In this case, the patient should consult a hepatologist. Chronic kidney disease is one of the risk factors, so a consultation with a nephrologist is necessary. The surgeon will help get rid of xanthomas, xanthelasma with the help of surgery.

Treatment of dyslipidemia should be complex with the involvement of doctors of various specialties. This will help to achieve good results, prevent the development of severe diseases of the cardiovascular system and reduce the mortality rate of patients.

Dyslipidemia is a pathological condition caused by a violation of the metabolism of fats in the body and leading to the development. The vascular walls thicken, the lumen of the vessels narrows, blood circulation in the internal organs is disturbed, which ends with or, hypertension, stroke or heart attack.

An abnormally elevated level of lipids in the blood is called hyperlipidemia or hyperlipoproteinemia. This condition is a direct consequence of a person's lifestyle. The appearance of hyperlipidemia depends on the nature of the patient's diet, the medications he takes, physical activity and bad habits.

Dyslipidemia is a laboratory indicator indicating an imbalance of fatty substances in the human body., which are low molecular weight compounds synthesized in the liver and transported to cells and tissues with the help of lipoproteins - complex lipid-protein complexes.

Active biosynthesis of fats in the body, impaired excretion and their abundant intake with food lead to hyperlipidemia, which does not manifest specific symptoms, but provokes the formation of various diseases.

Classification

Dyslipidemia is a metabolic pathology caused by an imbalance of lipid fractions in the blood and the gradual accumulation of fats in the body.

• The classification according to Fredrickson is based on the type of lipid, the level of which increases - chylomicrons, cholesterol, LDL, VLDL. According to this classification there are 6 types of hyperlipidemia, 5 of which are atherogenic- rapidly leading to atherosclerosis.

• According to the mechanism of occurrence, dyslipidemia is primary and secondary. The primary form is a hereditary disease, and the secondary is the result of some pathologies.
• In a separate group are nutritional dyslipidemia caused by excessive inclusion in the diet of foods containing animal fats. It is of two types: transient- developing after a single consumption of fatty foods, and constant- caused by its regular intake.

Etiology

It is almost impossible to single out one specific cause of dyslipidemia. A whole complex of etiological factors plays an important role in the development of pathology. These include:

1. Heredity,
2. nutritional features,
3. hypodynamia,
4. Alcoholism,
5. tobacco smoking,
6. Stress,
7. Endocrinopathy - obesity, hypothyroidism,
8. calculous cholecystitis,
9. Hypertension,
10. Taking medications - hormonal contraceptives, antihypertensive drugs,
11. Hormonal changes - pregnancy, menopause,
12. Gout,
13. Uremia,
14. Male,
15. Elderly age.

Dyslipidemia is the result of the active formation of fats, excessive intake from food, impaired breakdown and excretion from the body.

Persons with a family history of early atherosclerosis are most susceptible to the development of pathology. Also at risk are people who have had a myocardial infarction or ischemic stroke.

Symptoms

The basis of the clinical symptoms of dyslipidemia is the metabolic syndrome, which is a complex violation of fat metabolism and blood pressure regulation mechanisms. It is manifested not only by a change in the normal ratio of lipids in the blood, but also by hyperglycemia, persistent hypertension, and impaired hemostasis.

Symptoms of hyperlipoproteinemia may be absent for a long time. In this case, the disease can be detected only by the results of a laboratory blood test. But after a few months and even years, the pathology will manifest itself with characteristic symptoms and end with the development of serious ailments.

• Cholesterol, being deposited under the skin of the eyelids, forms flat yellow formations.
• Xanthomas are nodules located above the tendons of a person on the hands, feet, back, and abdomen.
• The lipoid corneal arch is a whitish band framing the outer contour of the cornea of ​​the eye. These are cholesterol deposits that usually appear in people over 50;

xanthomas and xantelisms are manifestations of dyslipidemia

Hyperlipoproteinemia is a clinical and laboratory diagnosis: only lipidogram data indicate the presence of pathology. Clinical signs are not significant and are not diagnostically significant. Despite this, experienced specialists may suspect dyslipidemia after the first communication with the patient.

Diagnostics

It is possible to detect dyslipidemia in a patient only with the help of laboratory diagnostics.

A complete diagnostic examination of the patient includes:

Treatment

Usually, dyslipidemia is a secondary pathology that occurs against the background of a disease or develops as a result of exposure to negative factors. To get rid of the pathology, it is necessary to identify and treat the underlying disease in a timely manner.

Treatment of dyslipidemia is individual, complex, including drug, non-drug, extracorporeal therapy, diet therapy. They normalize the metabolism of lipids in the body and reduce the level of cholesterol in the blood.

Patients are shown drug correction of dyslipidemia, compliance with the recommendations of a nutritionist, modification of lifestyle.

Non-drug treatment

For patients with dyslipidemia, specialists give the following recommendations:

• Normalize body weight by switching to a fractional, balanced and fortified diet,
• Dose physical activity,
• Adjust the mode of work and rest,
• Limit alcohol intake or completely stop it,
• fight smoking,
• Avoid stressful and conflict situations.

diet therapy

Treatment of dyslipidemia is a long and complex process that requires discipline, patience and strength from the patient. Timely and complete therapy, as well as the elimination of risk factors, significantly prolong and improve the life of patients.

Prevention

To avoid the development of dyslipidemia, the following rules must be followed:

1. Normalize the weight
2. To live an active lifestyle,
3. avoid stress,
4. Get regular check-ups,
5. Healthy food,
6. Fight smoking and alcoholism
7. Timely and correctly treat diseases leading to dyslipidemia.

Dyslipidemia and atherosclerotic changes in the body develop over the years and require the same long and persistent treatment. You can prevent the development of pathology by following the recommendations of specialists: monitor weight, move more and quit bad habits. This will help the vessels to remain elastic and healthy for many years. If dyslipidemia is timely prevented, diagnosed and treated, it is possible to prolong and save the life of the patient.

Video: lecture on dyslipidemia and atherosclerosis

In the case when a person has an excess of lipids, there may be a risk of developing hyperlipidemia. This disease is characterized by the fact that the blood is saturated with cholesterol and triglycerides, which are lipids.

The term "hyperlipidemia" shows the level of lipids in the blood, in other words, characterizes the presence of an excess of the most common fats in the blood.

Who is affected by the syndrome and why is it dangerous

The main factors in the development of the disease is gender. As a rule, in representatives of the strong half of humanity, this disease occurs much more often than in women. Hyperlipidemia is most predisposed to the elderly, as well as those who have a burdened heredity. The development of the disease is also affected by modifiable mechanisms, in other words, long-term consumption of foods high in fat, overweight, lack of physical activity, some drugs can lead to hyperlipidemia.

It is very difficult to determine the onset of the disease, since there are simply no specific manifestations of a clinical nature. The first symptoms may appear only when a person has already developed atherosclerotic disease. It can be detected only by a laboratory method, which is called a lipidogram. This test is performed on an empty stomach.

Hyperlipidemia is dangerous because it can cause the development of atherosclerosis. The disease leads to the appearance of plaques on the surface of the arteries, which consist of cholesterol, fibrous tissue and calcium. Due to the fact that these plaques begin to grow, the lumen of the arteries narrows and the general blood flow is disturbed. All this can lead to various diseases of the cardiovascular system. In particular, a patient with hyperlipidemia is at risk of developing coronary disease, myocardial infarction, aortic aneurysm, cerebral circulatory disorders, and many others.

Types of hyperlipidemia

The disease is divided by doctors into several different types, depending on the etiopathogenetic factors and the principles of its occurrence. The first type of the disease is quite rare. This pathology is based on a deficiency of lipase activity and is characterized by an increase in chylomicrons and triglycerides in the blood. It does not affect the development of atherosclerotic changes, but to a greater extent affects the functioning of the pancreas and can lead to pancreatitis.

The second type of disease is characterized by the activity of the formation of beta-lipoproteins or a decrease in the function of their destruction. This leads to the fact that low density lipoproteins begin to accumulate in the body. Such hyperlipidemia usually begins to develop at an early age. The consequence of this pathology may be the development of circulatory disorders in various arterial vessels and, as a consequence, the occurrence of heart attacks.

The disease of the third type is quite rare, and its occurrence is characterized by the presence of an abnormal lipoprotein in the human blood. This form of hyperlipidemia can provoke the formation of atherosclerotic plaques on the arteries. Such patients are prone to obesity and diabetes. They may eventually develop gout and atherosclerosis.

The fourth type of hyperlipidemia can be characterized by an elevated plasma triglyceride content. This form of the disease affects middle-aged people who have been diagnosed with pancreatic dysfunction, and chronic changes in some vessels have also been observed. Patients may be prone to obesity and pancreatitis.

Violation of some processes of destruction and excretion of triglycerides, which enter the body in excess with food, leads to the occurrence of hyperlipidemia of the fifth type. Quite often, this pathology is observed in adolescents and can lead to disorders in the pancreas and, as a result, the development of pancreatitis.

Therapy for hyperlipidemia is based on the stabilization of cholesterol levels in the body. The course of treatment is prescribed depending on the type of disease and the general condition of the patient. A certain diet is recommended, in which fatty foods are excluded from the menu, in addition, the patient must completely stop smoking and drinking alcoholic beverages. In general, the prognosis for a cure for hyperlipidemia is favorable if therapy was started on time and the patient's atherosclerosis process did not go too far.

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Hyperlipidemia classification

Hyperlipidemia (hyperlipoproteinemia, dyslipidemia) is an abnormally elevated level of lipids and / or lipoproteins in human blood. Violation of lipid and lipoprotein metabolism is quite common in the general population. Hyperlipidemia is an important risk factor for the development of cardiovascular diseases, mainly due to the significant influence of cholesterol on the development of atherosclerosis. In addition, some hyperlipidemias affect the development of acute pancreatitis.

The classification of lipid disorders, based on the change in the profile of plasma lipoproteins during their electrophoretic separation or ultracentrifugation, was developed by Donald Fredrickson in 1965. The Fredrickson classification is accepted by the World Health Organization as the international standard nomenclature for hyperlipidemias. However, it does not take into account the level of HDL, which is an important factor in reducing the risk of atherosclerosis, as well as the role of genes that cause lipid disorders. This system remains the most common classification.

Type I hyperlipoproteinemia

A rare type of hyperlipidemia that develops in LPL deficiency or a defect in the LPL activator protein, apoC2. Manifested in an increased level of chylomicrons, a class of lipoproteins that carry lipids from the intestines to the liver. The frequency of occurrence in the general population is 0.1%.

Hyperlipoproteinemia type II

The most common hyperlipidemia. It is characterized by an increase in LDL cholesterol. It is subdivided into types IIa and IIb depending on the absence or presence of high triglycerides.

Type IIa

This hyperlipidemia can be sporadic (due to malnutrition), polygenic, or hereditary. Hereditary hyperlipoproteinemia type IIa develops as a result of a mutation in the LDL receptor gene (0.2% of the population) or the apoB gene (0.2% of the population). The familial or hereditary form is manifested by xanthomas and the early development of cardiovascular diseases.

Type IIb

This subtype of hyperlipidemia is accompanied by an increased concentration of triglycerides in the blood as part of VLDL. A high level of VLDL occurs due to the increased formation of the main component of VLDL - triglycerides, as well as acetyl-coenzyme A and apoB-100. A more rare cause of this disorder may be delayed clearance (removal) of LDL. The frequency of occurrence of this type in the population is 10%. This subtype also includes hereditary combined hyperlipoproteinemia and secondary combined hyperlipoproteinemia (usually in metabolic syndrome).

Treatment for this hyperlipidemia includes dietary modification as a major component of therapy. Many patients require the appointment of statins to reduce the risk of cardiovascular disease. In the case of a strong rise in triglycerides, fibrates are often prescribed. The combined use of statins and fibrates is highly effective but has side effects such as the risk of myopathy and should be under constant medical supervision. Other drugs (nicotinic acid, etc.) and vegetable fats (ω 3 fatty acids) are also used.

Hyperlipoproteinemia type III

This form of hyperlipidemia is manifested by an increase in chylomicrons and LPP, therefore it is also called dis-beta-lipoproteinenia. The most common cause is homozygosity for one of the apoE isoforms, E2/E2, which is characterized by impaired binding to the LDL receptor. The occurrence in the general population is 0.02%.

Type IV hyperlipoproteinemia

This subtype of hyperlipidemia is characterized by an elevated concentration of triglycerides and is therefore also called hypertriglyceridemia. The frequency of occurrence in the general population is 1%.

Type V hyperlipoproteinemia

This type of hyperlipidemia is in many ways similar to type I, but is manifested not only by high chylomicrons, but also by VLDL.

Other rare forms dyslipidemia not included in the accepted classification:

• Hypo-alpha-lipoproteinemia
• Hypo-beta-lipoproteinemia (0.01-0.1%)

The hyperlipidemia phenotype. WHO classification of hyperlipidemias

The phenotype of hyperlipidemia is determined according to the WHO classification (see table).

WHO classification of hyperlipidemias

Decreased or normal

Elevated or normal

Decreased or normal

The WHO classification does not take into account the selective reduction of HDL-cholesterol, which is more often observed in men and is accompanied by damage to the coronary and cerebral vessels. This classification does not make it possible to diagnose the disease that caused hyperlipidemia, however, it allows you to establish the degree of its atherogenicity.

The most significant in connection with the prevalence and atherogenicity are II a, II b and IV types of hyperlipidemia due to the increased content of LDL and VLDL in the blood and, accordingly, an increase in the levels of total cholesterol, LDL cholesterol and triglycerides.

In patients with coronary heart disease, the concentration of total cholesterol and LDL-cholesterol is usually elevated (phenotypes IIa and IIb).

Patients with metabolic syndrome and type 2 diabetes mellitus are more likely to have lipid disorders, with increased triglyceride levels and a decrease in HDL-cholesterol, however, cases of elevated LDL-cholesterol and triglycerides are not uncommon (IIb and / or IV phenotypes).

Diagnosis and correction of lipid metabolism disorders in order to prevent and treat atherosclerosis. Russian recommendations. Developed by the VNOK Expert Committee. M., 2004.

Diagnosis and correction of lipid metabolism disorders for the prevention and treatment of atherosclerosis // Brief Russian recommendations. Developed by a group of VNOK experts. M., 2005.

Rehabilitation in diseases of the cardiovascular system / Ed. I.N. Makarova. M., 2010.

Handbook of dietetics / Ed. V.A. Tutelyan, M.A. Samsonov. M., 2002.

Thompson G.R. A guide to hyperlipidemia. - MSD, 1991.

Pogozheva A.V. The use of plant and animal sources of omega-3 PUFAs in the diet therapy of cardiovascular patients. Guidelines. M., 1999.

Pogozheva A.V. Cardiovascular disease, diet and omega-3 PUFAs. M, 2000.

What are the reasons for the development of hyperlipidemia and where to start treatment?

Fats found in the body of any person have a scientific name - lipids. These compounds perform a number of important functions, but in a situation where their concentration exceeds the permissible norm for any reason, there is a risk of serious health problems.

What is hyperlipidemia and hypolipidemia?

The term "hyperlipidemia" refers to an abnormal increase in the concentration of lipids or lipoproteins in the blood, and the most common increase in the level of triglycerides and cholesterol. The opposite condition, in which there is a decrease in triglycerides, cholesterol and lipoproteins, is called "hypolipidemia". Hyperlipidemia and hypolipidemia are the result of metabolic disorders.

Elevated lipid levels can lead to atherosclerosis. In this case, plaques are formed on the inner walls of blood vessels and arteries, consisting directly of lipids, as a result of which their lumen decreases, and this, in turn, disrupts blood circulation. Sometimes almost complete blockage of the vessel can occur. Atherosclerosis greatly increases the possibility of manifestation of pathologies associated with the cardiovascular system, including strokes and heart attacks.

Important! By itself, hyperlipidemia does not give pronounced symptoms. It is the diseases that appear as a result of hyperlipidemia, for example, acute pancreatitis or atherosclerosis, that have characteristic symptoms. An increase in the concentration of lipids can be detected by conducting analyzes for their content.

Classification of hyperlipidemias

In 1965, Donald Fredrickson created a classification of lipid metabolism disorders. It was later adopted by the World Health Organization and remains the most used international standard classification to this day.

There are the following types of the disease "hyperlipidemia":

1. The first type (I) is the rarest. It is characterized by a deficiency of lipoprotein lipase (LPL) or a violation in the activator protein against the background of an increased content of chylomicrons. This type of pathology is not associated with atherosclerotic diseases, but leads to pancreatic dysfunction. It is treated with a diet based on a sharp restriction of the amount of fat consumed.
2. Hyperlipidemia type II (II) is the most common form of the disease. The main difference lies in the increase in LDL cholesterol. At the same time, this pathology is divided into 2 types: IIa and IIb. Hyperlipidemia subtype IIa is hereditary or occurs as a result of malnutrition. In the case of a hereditary factor, the occurrence of pathology is due to a mutation in the LDL receptor gene or apoB. Disease subtype IIb includes hereditary mixed hyperlipidemia and mixed secondary hyperlipidemia. In this case, an increased content of triglycerides in the composition of VLDL is observed.
3. The third form of the disease (III) is less common, but no less dangerous. The concentration of LPPP in the blood plasma increases, the occurrence of atherosclerotic plaques is provoked. Often people suffering from this type of disease are prone to developing gout and obesity.
4. The fourth type of hyperlipidemia (IV) is characterized by a high content of triglycerides in the blood. In the process of research, an increase in VLDL was found. The risk group for this pathology includes middle-aged people suffering from obesity, diabetes and pancreatic dysfunction.
5. The fifth type of pathology (V) is similar to the first, as it is characterized by a high chylomicron count, but this case is accompanied by an increase in the concentration of VLDL. It is possible to develop a severe form of pancreatic dysfunction.

Causes of the disease

The causes of hyperlipidemia have a genetic basis or lie in the wrong lifestyle and poor nutrition. The mechanism of the onset of the disease is often associated with a hereditary predisposition, so the pathology can manifest itself even at a young age. An unhealthy diet with a high level of fat causes the development of the disease much less often, although this option is not excluded.

There are two groups of factors predisposing to the development of the disease. The first one is uncontrollable:

• heredity;
• age (older people are more susceptible to pathology);
• male (statistically, men are more likely to have this disease).

The second is factors that can be controlled. Most often they are associated with lifestyle and the presence of bad habits in humans:

• hypodynamia;
• the use of certain drugs;
• constant overeating, eating high-calorie foods;
• diabetes mellitus and hormonal disorders.

Hyperlipidemia can be found in women during pregnancy. This is explained by physiological changes in the female body in the process of bearing a child, and over time, the indicator normalizes. A significant contribution to the development of the disease is made by bad habits: alcohol abuse and smoking. Therefore, it is important to lead a healthy lifestyle and try to follow the rules of a balanced diet.

Treatment and prevention

In hyperlipidemia, the main and most effective strategy for treatment and prevention is lifestyle adjustment. Increasing physical activity, adhering to the principles of a healthy diet and giving up bad habits are the keys to success in the fight against the disease.

As for the diet, the complete exclusion of fast food and fast food becomes a prerequisite. Such food is supersaturated with carbohydrates and does not bring any benefit to the body. In no case does a diet imply a complete exclusion of fats from the menu, because they are necessary for the full functioning of all internal systems and organs. But it is important to minimize your intake of foods high in saturated fat and cholesterol.

In cases where correcting lifestyle and nutrition is not enough, specialists resort to the help of medications. Fibrates and statins are mainly used. Nicotinic acid is used, sometimes the treatment of hyperlipidemia is supplemented with vitamin B5. In exceptionally severe cases, a blood purification procedure and laser irradiation may be necessary.

Advice! In the presence of relatives suffering from diseases associated with the cardiovascular system, to exclude hyperlipidemia, experts recommend making it a rule to periodically undergo an examination for the concentration of lipids in the blood plasma.

Hyperlipidemia

Hyperlipidemia is a diagnostic syndrome that is characterized by abnormally high levels of lipids or lipoproteins in the blood. The syndrome itself is a fairly common phenomenon and is mostly asymptomatic. Nevertheless, hyperlipidemia is a risk factor for the development of cardiovascular diseases, especially atherosclerosis, and needs to be controlled, corrected and treated.

Types of hyperlipidemias

The classification of types of hyperlipidemias was developed by Donald Fredikson in 1965 and has been adopted by the World Health Organization as an international standard. It is still in use today. According to Fredikson's classification, there are five types of hyperlipidemias.

Type I. This is a rare type of hyperlipidemia that occurs when lipoprotein lipase is deficient or there is a defect in the lipoprotein lipase activator protein. In this type of disease, levels of chylomicrons (lipoproteins that carry lipids from the intestines to the liver) are elevated. Hyperlipidemia worsens after fatty foods and decreases after fat restriction, so diet is the main treatment.

Type II. A common type of hyperlipidemia in which low-density lipoprotein levels are elevated. It is subdivided into two subtypes depending on the presence of high triglycerides, which require the additional administration of gemfibrozil during treatment. Hyperlipidemia of this type leads to the development of atherosclerosis after years and can cause a heart attack in older men and women.

Type III. A type of hyperlipidemia also called dys-beta lipoproteinemia. The disease is characterized by hereditary causes, and is associated with a defect in Apolipoprotein E, and is also characterized by an increase in the level of high density lipoproteins. Carriers of hyperlipidemia are prone to obesity, gout, mild diabetes mellitus and are at risk for atherosclerosis.

Type IV. A type of hyperlipidemia characterized by elevated levels of triglycerides. Their levels rise after taking carbohydrates and alcohol. Against the background of this syndrome, atherosclerosis, obesity, diabetes mellitus and pancreatitis can develop.

Type V. A type of hyperlipidemia, similar to the first, but in contrast to it, not only the level of chylomicrons, but also very low density lipoproteins increases. Therefore, as in the case of the first type, the fat content in the blood jumps after eating fatty and carbohydrate foods. Hyperlipidemia of this type is fraught with the development of severe pancreatitis, which develops against the background of eating too fatty foods.

In addition to this classification, there are two more types of hyperlipidemia - hypo-alpha-lipoproteinemia and hypo-beta-lipoproteinemia.

Symptoms

Hyperlipidemia is mostly asymptomatic and is most often detected during a general biochemical blood test. Preventive analysis for cholesterol levels should be carried out from the age of 20 at least once every five years. Sometimes, with hyperlipidemia, fatty bodies are formed in the tendons and skin of the patient, which are called xanthomas. An enlarged liver and spleen, as well as signs of pancreatitis, can serve as a pathological symptom.

Causes of the disease

The level of blood lipids depends on a number of factors, which include the presence of saturated fatty acids and cholesterol in the daily diet, body weight, level of physical activity, age, diabetes, heredity, medication, blood pressure disorders, kidney and thyroid disease, smoking and drinking alcoholic beverages.

Treatment of hyperlipidemia

Depending on the type of hyperlipidemia, either a diet with increased physical activity alone or a specific combination of drugs can be prescribed, the choice of which can only be made by the attending physician. Treatment of hyperlipidemia is almost always accompanied by a low-fat diet and control of blood lipids. To reduce the level of cholesterol and triglycerides, a course of exercise therapy is prescribed, aimed at weight loss. The well-being of the patient is well affected by the elimination of bad habits, as well as therapeutic cleansing procedures.

Treatment for hyperlipidemia may include statins, which lower blood cholesterol levels and keep cholesterol from being deposited in the liver. Additionally, fibrates and choleretic drugs may be prescribed. In the treatment of hyperlipidemia, vitamin B5 has proven itself well.

This article is posted for educational purposes only and does not constitute scientific material or professional medical advice.

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Classification of hyperlipidemias

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Ischemic heart disease - therapy of dyslipidemia

Roza Ismailovna Yagudina, Ph.D. n., prof., head. Department of Organization of Drug Supply and Pharmacoeconomics and Head. Laboratory of Pharmacoeconomic Research of the First Moscow State Medical University named after A.I. I. M. Sechenov.

Evgenia Evgenievna Arinina, Candidate of Medical Sciences, Leading Researcher, Laboratory of Pharmacoeconomic Research, First Moscow State Medical University. I. M. Sechenova

Cardiovascular disease (CVD) is the leading cause of death worldwide. WHO estimates that 17.3 million people died of CVD in 2008, accounting for 30% of all deaths worldwide. 7.3 million of this number died from coronary heart disease. According to WHO forecasts, by 2030, about 23.3 million people will die from CVD every year.

The group of cardiovascular diseases combines several nosological units:

• coronary heart disease - a disease of the blood vessels that supply blood to the heart muscle;
• disease of the cerebral vessels that supply it with blood;
• disease of the peripheral arteries supplying blood to the arms and legs;
• rheumatic heart disease - damage to the heart muscle and heart valves as a result of a rheumatic attack caused by streptococcal bacteria;
• congenital heart disease - deformations of the structure of the heart existing from birth;
• deep vein thrombosis and pulmonary embolism - the formation of blood clots in the leg veins that can displace and move to the heart and lungs.

One of the most common pathologies in the structure of CVD is coronary heart disease (CHD), which we will devote a number of articles to. IHD, according to WHO, is an acute or chronic dysfunction of the heart resulting from an absolute or relative decrease in the supply of myocardium with arterial blood.

In more than 90% of cases, the anatomical basis for the development of coronary artery disease is damage to the coronary arteries of the heart, leading to a decrease in coronary blood flow and an imbalance between the need of the heart muscle for oxygen and nutrients and the possibilities of blood supply to the heart. Often this effect is caused by dyslipidemia, leading to the development of atherosclerosis, therefore, in the first article on the problem of pharmacotherapy of coronary artery disease, we will dwell on dyslipidemia (hyperlipidemia) in detail.

Currently, the following forms of IHD are distinguished:

• Sudden cardiac arrest
• angina pectoris
• Painless cardiac ischemia
• Syndrome X (microvascular angina)
• myocardial infarction
• Cardiosclerosis (atherosclerosis)
• Heart failure
• Heart rhythm disorders

Types of dyslipidemia

What is it and how to treat? Dyslipidemia (hyperlipidemia) is an increase in lipid and lipoprotein levels relative to optimal values ​​and / or a possible decrease in high-density lipoprotein or alpha-lipoprotein levels. In the group of dyslipidemias, the focus is on hypercholesterolemia, since elevated levels of cholesterol (low-density lipoprotein) are directly related to an increased risk of coronary artery disease.

In plasma, the two major lipid fractions are cholesterol and triglycerides. Cholesterol (Cholesterol) is the most important component of cell membranes; it forms the “skeleton” of steroid hormones (cortisol, aldosterone, estrogens and androgens) and bile acids. Cholesterol synthesized in the liver enters the organs and tissues and is utilized by the liver itself. Most of the cholesterol in the composition of bile acids is in the small intestine, from the distal parts of which approximately 97% of the acids are absorbed with subsequent return to the liver (the so-called enterohepatic circulation of cholesterol). Triglycerides (TG) play an important role in the process of energy transfer of nutrients into cells. Cholesterol and TG are transported in plasma only as part of protein-lipid complexes - lipoproteins (complexes include a simple protein - protein).

Currently, there are several classifications of dyslipidemia. One of them divides dyslipidemia into types according to the factors of occurrence into primary and secondary.

Primary dyslipidemias are disorders of lipid metabolism, most often associated with genetic abnormalities. These include: conventional (polygenic) and familial (monogenic) dyslipidemia, familial hypercholesterolemia, familial endogenous hypertriglyceridemia, familial chylomicronemia, familial combined dyslipidemia.

Lipoproteins differ in size, density, amount of cholesterol and TG, and the composition of apoproteins (proteins localized on the surface of lipoproteins - lipoprotein receptor ligand, enzyme cofactors):

• chylomicrons (XM) - saturated TG and poor cholesterol, are formed in the wall of the small intestine from alimentary fats;
• very low density lipoproteins (VLDL) - synthesized in the liver from endogenous sources and contain a lot of TG and little cholesterol. An increase in VLDL levels is associated with an increased risk of atherogenesis;
• low-density lipoproteins (LDL) - cholesterol-containing class. They are synthesized in the liver, transferring cholesterol to its "consumers" - the adrenal glands, liver, etc. Today, LDL is considered the main atherogenic fraction of lipoproteins and the main "target" for lipid-lowering drugs;
• high-density lipoproteins (HDL) are an anti-atherogenic class of lipoproteins that ensure the elimination of excess cholesterol from the walls of arteries and tissues. HDL have a positive effect on the state of the endothelium and prevent the oxidation of LDL.

The classification of primary lipid disorders was developed back in 1965 by the American researcher Donald Fredrickson. It has been adopted by the WHO as the international standard nomenclature for dyslipidemias/hyperlipidemias and remains the most common classification (see Table 1).

Occurrence in the general population, %

Primary hyperlipoproteinemia, hereditary hyperchylomicronemia

Decreased lipoprotein lipase (LPL) or impaired LPL activator - apoC2

Increased level of HM

Polygenic hypercholesterolemia, hereditary hypercholesterolemia

Elevated LDL (TG is normal)

Decreased LDL receptor and elevated apoB

Elevated LDL, VLDL and TG

ApoE defect (homozygotes apoE 2/2)

Elevated DLPP, increased HM levels

Increased formation of VLDL and their slow decay

Increased formation of VLDL and reduced lipoprotein lipase

Elevated VLDL and HM

Secondary dyslipidemias are lipid metabolism disorders that develop against the background of the following diseases:

• obesity (increased TG levels, decreased HDL-C);
• sedentary lifestyle (decreased levels of HDL-C);
• diabetes mellitus (increased levels of TG, total cholesterol);
• alcohol consumption (increased levels of TG, HDL-C);
• hypothyroidism (increased levels of total cholesterol);
• hyperthyroidism (decrease in the level of total cholesterol);
• nephrotic syndrome (increased levels of total cholesterol);
• chronic renal failure (increased levels of total cholesterol, TG, decreased HDL);
• cirrhosis of the liver (decrease in the level of total cholesterol);
• obstructive liver disease (increased levels of total cholesterol);
• malignant neoplasms (decrease in the level of total cholesterol);
• Cushing's syndrome (increased levels of total cholesterol);
• iatrogenic lesions while taking: oral contraceptives (increased levels of TG, total cholesterol), thiazide diuretics (increased levels of total cholesterol, TG), b-blockers (increased levels of total cholesterol, decreased HDL), corticosteroids (increased levels of TG, increased total cholesterol ). See table 2 for cholesterol levels.

below 5.2 (200 mg/dl)

below 3.0 (115 mg/dl)

Borderline (mild) hypercholesterolemia

above 6.2 (250 mg/dl)

Target level for patients with coronary artery disease, with clinical manifestations of CVD, and patients with diabetes mellitus

less than 4.5 (175 mg/dl)

less than 2.5 (100 mg/dl)

Treatment of dyslipidemias (hyperlipidemias)

If the patient suffers from coronary artery disease and has dyslipidemia, it is advisable to avoid smoking, control blood pressure, take aspirin, and, if possible, conduct hormone replacement therapy in postmenopausal women. The decision on the need for drug therapy is made based on the level of LDL-C and an assessment of other risk factors for developing coronary artery disease (including HDL values). For people with low HDL levels without an increase in LDL levels, pharmacotherapy is not indicated.

The key to successful correction of secondary hyperlipoproteinemia is the detection and treatment of the underlying disease. For example, rational hormone replacement therapy often normalizes lipid levels in patients with diabetes mellitus and hypothyroidism. With ethanol-induced hypertriglyceridemia, a similar result is achieved by avoiding alcohol.

Currently, several groups of drugs are used to treat lipid profile disorders. Their hypolipidemic effect is based on the ability to reduce the content of atherogenic lipoproteins (LP) in the blood plasma: VLDL, LDL and their lipids - cholesterol and TG. Classes of lipid-lowering drugs and the main indications for their use, see table 3.

At the present stage of development of medicine, the main class of lipid-lowering drugs used in the treatment of coronary heart disease are statins, which have the largest evidence base. Statins are structural inhibitors of the enzyme hydroxy-methylglutaryl-coenzyme-A-reductase (HMG-CoA), which regulates cholesterol biosynthesis in hepatocytes. As a result of a decrease in the intracellular content of cholesterol, the hepatocyte increases the number of membrane receptors for LDL on its surface. Receptors bind and remove atherogenic LDL particles from the bloodstream and, thus, reduce the concentration of cholesterol in the blood.

Statins also have vascular and pleiotropic effects. At the level of the vascular wall, by reducing the formation of cholesterol and LDL, they increase the ratio of HDL / LDL, reduce the inclusion of cholesterol in the subintima of the vessels, help stabilize existing atherosclerotic plaques by reducing the lipid core, and therefore reduce the risk of plaque rupture and thrombosis.

The classification of HMG-CoA reductase inhibitors is based on differences in statins both in chemical structure (drugs obtained by fermentation of mushrooms and synthetic statins) and in terms of the time they started to be used in clinical practice (statins of the I-IV generation). The first statins (simvastatin, pravastatin and lovastatin) were isolated from a culture of penicillin fungi and Aspergillus terrens fungi; fluvastatin (II generation), atorvastatin (III generation) and rosuvastatin (IV generation) are synthetic drugs. Statins also differ in their physicochemical and pharmacological properties: simvastatin and lovastatin are more lipophilic; atorvastatin, rosuvastatin and pravastatin are more hydrophilic; fluvastatin is relatively lipophilic. These properties provide different permeability of drugs through cell membranes, in particular liver cells. The half-life of statins does not exceed 2-3 hours, with the exception of atorvastatin and rosuvastatin, the half-life of which exceeds 12 hours, which probably explains their higher efficiency in lowering cholesterol and LDL-C.

Side effect: increased levels of liver enzymes, less often - hepatitis, myopathy and myositis, extremely rarely - rhabdomyolysis. These substances can cause headache, abdominal pain, flatulence, constipation, diarrhoea, nausea and vomiting. Methods for monitoring the safety of treatment is the assessment of the activity of transaminases and creatine phosphokinase, which must be carried out before treatment, repeated after 2–3 weeks, 2–3 months. and then every 6-12 months. or more often. Statins should be discontinued if there is a persistent increase in alanine aminotransferase and / or aspartate aminotransferase more than 3 times, with creatine phosphokinase activity more than 5 times normal, or with severe symptoms of muscle damage.

Fibrates are derivatives of fibric acid. Fibrates are lipid-lowering drugs that mainly affect the metabolism of triglyceride-rich lipoprotein particles (HM, VLDL, and DILI). They also moderately lower LDL-C levels by decreasing small, dense LDL particles and increasing large, less dense LDL, which increases their recognition by liver receptors and improves catabolism. Fibric acid derivatives are able to increase the synthesis of "good cholesterol" apoproteins - apo A-I, apo A-II. These drugs improve the lipolysis of TG-rich lipoproteins by activating lipoprotein and hepatic lipases. The pleiotropic and hypolipidemic effects of fibrates are realized through the activation of nuclear α-receptors that activate peroxisome proliferation (PPARα). The use of fibrates leads to a decrease in TG levels by 20–50% from the initial level and an increase in HDL-C by 10–20%.

Side effects: digestive disorders, headache, dizziness, skin rashes, sometimes atrial fibrillation, rarely - hematopoietic depression, myositis, visual impairment.

NB! The combined administration of statins and fibrates is highly effective, but has side effects (for example, the risk of myopathy) and should be under constant medical supervision.

Ezetimibe is a selective inhibitor of cholesterol absorption in the small intestine by inhibiting the activity of the corresponding NPC1L1 transporter. It is a prodrug. After absorption, it is metabolized to the pharmacologically active ezetimibe-glucuronide. In plasma, most (90%) of the drug and its metabolite bind to proteins. Excretion occurs mainly through the intestines.

Side effects: dyspepsia, headache, weakness, myalgia, depression. Less often - hypersensitivity reactions, toxic hepatitis, toxic pancreatitis. Thrombocytopenia, myopathy, and rhabdomyolysis are very rare.

Bile acid sequestrants

The mechanism of action of these drugs (water-insoluble anion-exchange resins that are not absorbed in the intestine) is to bind bile acids in the intestine, which prevents their enterohepatic circulation, as a result of which the liver increases the production of bile acids using cholesterol from its own reserves. The activity of hepatic receptors for LDL increases, and the level of total cholesterol and cholesterol-LDL in plasma decreases (by 6–9 and 15–25%, respectively) with a slight increase in HDL. In some patients, the concentration of TG (compensatory synthesis of VLDL) sometimes increases, which requires caution in the use of these drugs in the presence of initial hypertriglyceridemia. At TG levels above 400–500 mg/dL, sequestrants should be discontinued.

Side effects: can cause constipation, less often diarrhea, also nausea, vomiting. Sometimes hypertriglyceridemia and a lack of vitamins A, D and K are noted.

When used in the full therapeutic dose (3.5-4 g per day), nicotinic acid reduces the production of VLDL with a secondary decrease in LDL levels (by 15-25%) and an increase in HDL (by 25-35%). Nicotinic acid also nearly halved TG and lipoprotein levels. Unfortunately, 50-60% of patients cannot tolerate the full dose. Prostaglandin-mediated flushing of the skin is described by patients as a feeling of "rush", heat, often with skin itching. This problem is partially solved by prescribing 81-325 g of aspirin per day (or another antiprostaglandin agent) and starting therapy in small doses (50-100 mg at dinner), which are doubled every week to 1.5 g per day. After reassessment of the lipid spectrum, the dose is divided into parts and brought up to 3–4.5 g per day.

It is recommended to use short-acting nicotinic acid preparations. Long-acting forms (enduracin) are expensive and reduce LDL-C to a lesser extent. Nicotinic acid can enhance the effect of antihypertensive drugs with a sudden sharp drop in blood pressure.

Side effects: often - redness of the face, dizziness, increased transaminases, dry skin, itching, dyspeptic disorders (loss of appetite, diarrhea, nausea, vomiting, abdominal pain, flatulence). Rarely - insomnia, tachycardia, peripheral edema, increased uric acid levels and the development of exacerbation of gout, gynecomastia and severe liver damage. Very rarely - prolongation of prothrombin time and a decrease in the number of platelets.

Omega-3-polyunsaturated fatty acids

The relevance of the use of omega-3-polyunsaturated fatty acids (omega-3-PUFAs) is associated with the identification of an association between an extremely low level of cardiovascular diseases (atherosclerosis, coronary heart disease, hypertension) in the inhabitants of Greenland and their consumption of a large amount of seafood with a high content omega-3‑PUFA. In the blood plasma of the inhabitants of Greenland, high concentrations of eicosapentaenoic and docosahexaenoic acids were noted, with a low content of linoleic and arachidonic acids. The lipid-lowering effect of fish oil is to suppress the synthesis of VLDL and LDL, to improve their clearance and increase bile excretion.

When using drugs containing eicosapentaenoic and docosahexaenoic acids, the most significant positive effect is observed in patients with dyslipidemia types IIb and V: the content of TG, VLDL and LDL decreases, the level of HDL increases. Metabolites of eicosapentaenoic acid also have antispasmodic and platelet aggregation inhibiting properties. Omega-3-PUFAs have a profibrinolytic effect, reducing the activity of an inhibitor of tissue plasminogen activator, and also reduce the content of fibrinogen.

Side effects: most often - digestive disorders, less often - taste perversion, dizziness, headache, liver damage, hypersensitivity reactions, hyperglycemia, very rarely - arterial hypotension, leukocytosis.

Classes of lipid-lowering drugs

The main indications for the appointment

Suppressing the synthesis of cholesterol - inhibitors of HMG-CoA reductase (simvastatin, pravastatin, lovastatin, fluvastatin, atorvastatin, rosuvastatin, cerivastatin *)

IIa and IIb types of hyperlipoproteinemia (at the level of TG< 400 мг/дл (4,5 ммоль/л))

Reduces the production of LDL and VLDL - nicotinic acid derivatives and preparations based on omega-3 polyunsaturated fatty acids

All types of hyperlipoproteinemia, especially with an increase in both cholesterol and TG

Interfering with the absorption of lipids in the intestine - bile acid sequestrants (anion exchange resins cholestyramine *, colestipol *; non-specific enterosorbents, specific cholesterol enterosorbents)

IIa type of hyperlipoproteinemia (less than 10% of patients; TG< 200 мг/дл – 2,3 ммоль/л).

Catabolism-enhancing TGs – fibrates (bezafibrate*, gemfibrozil*, ciprofibrate, fenofibrate)

Type IIa hyperlipoproteinemia and type III dysbetalipoproteinemia. Use in selective hypertriglyceridemia (type IV) is only necessary for very high triglycerides (> 1000 mg/dL - 11.3 mmol/L) to reduce the risk of acute pancreatitis, not to treat CAD

Selective inhibition of cholesterol absorption in the small intestine due to inhibition of the activity of the corresponding NPC1L1 transporter (ezetimibe)

coated tablets

long-acting film-coated tablets, capsules

film-coated tablets, tablets

film-coated tablets

"Enduracin", "Nicotinic acid", "Nicotinic acid-Vial"

long-acting tablets, tablets, solution for injection

Laropiprant + nicotinic acid

modified release tablets

Omega-3 triglycerides + garlic bulb extract

Omega-3 triglycerides [EPA/DHA=1.5/1 - 50%]

Omega-3 triglycerides [EPA/DHA=1.2/1 – 90%]

Fish oil tissue

Exlip ® , Lipantil ® 200 M, Traykor

modified release capsules

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Fats found in the body of any person have a scientific name - lipids. These compounds perform a number of important functions, but in a situation where their concentration exceeds the permissible norm for any reason, there is a risk of serious health problems.

What is hyperlipidemia and hypolipidemia?

The term "hyperlipidemia" refers to an abnormal increase in the concentration of lipids or lipoproteins in the blood, and the most common increase in the level of triglycerides and cholesterol. The opposite condition, in which there is a decrease in triglycerides, cholesterol and lipoproteins, is called "hypolipidemia". Hyperlipidemia and hypolipidemia are the result of metabolic disorders.

Elevated lipid levels can lead to atherosclerosis. In this case, plaques are formed on the inner walls of blood vessels and arteries, consisting directly of lipids, as a result of which their lumen decreases, and this, in turn, disrupts blood circulation. Sometimes almost complete blockage of the vessel can occur. Atherosclerosis greatly increases the possibility of manifestation of pathologies associated with the cardiovascular system, including strokes and heart attacks.

Formation of atherosclerotic plaques in blood vessels

Important! By itself, hyperlipidemia does not give pronounced symptoms. It is the diseases that appear as a result of hyperlipidemia, for example, acute pancreatitis or atherosclerosis, that have characteristic symptoms. An increase in the concentration of lipids can be detected by conducting analyzes for their content.

Classification of hyperlipidemias

In 1965, Donald Fredrickson created a classification of lipid metabolism disorders. It was later adopted by the World Health Organization and remains the most used international standard classification to this day.

Fredrickson's classification of hyperlipidemia

There are the following types of the disease "hyperlipidemia":

1. The first type (I) is the rarest. It is characterized by a deficiency of lipoprotein lipase (LPL) or a violation in the activator protein against the background of an increased content of chylomicrons. This type of pathology is not associated with atherosclerotic diseases, but leads to pancreatic dysfunction. It is treated with a diet based on a sharp restriction of the amount of fat consumed.
2. Hyperlipidemia type II (II) is the most common form of the disease. The main difference lies in the increase in LDL cholesterol. At the same time, this pathology is divided into 2 types: IIa and IIb. Hyperlipidemia subtype IIa is hereditary or occurs as a result of malnutrition. In the case of a hereditary factor, the occurrence of pathology is due to a mutation in the LDL receptor gene or apoB. Disease subtype IIb includes hereditary mixed hyperlipidemia and mixed secondary hyperlipidemia. In this case, an increased content of triglycerides in the composition of VLDL is observed.
3. The third form of the disease (III) is less common, but no less dangerous. The concentration of LPPP in the blood plasma increases, the occurrence of atherosclerotic plaques is provoked. Often people suffering from this type of disease are prone to developing gout and obesity.
4. The fourth type of hyperlipidemia (IV) is characterized by a high content of triglycerides in the blood. In the process of research, an increase in VLDL was found. The risk group for this pathology includes middle-aged people suffering from obesity, diabetes and pancreatic dysfunction.
5. The fifth type of pathology (V) is similar to the first, as it is characterized by a high chylomicron count, but this case is accompanied by an increase in the concentration of VLDL. It is possible to develop a severe form of pancreatic dysfunction.

Lipoproteins, their functions and decoding of abbreviations

Causes of the disease

The causes of hyperlipidemia have a genetic basis or lie in the wrong lifestyle and poor nutrition. The mechanism of the onset of the disease is often associated with a hereditary predisposition, so the pathology can manifest itself even at a young age. An unhealthy diet with a high level of fat causes the development of the disease much less often, although this option is not excluded.

There are two groups of factors predisposing to the development of the disease. The first one is uncontrollable:

• heredity;
• age (older people are more susceptible to pathology);
• male (statistically, men are more likely to have this disease).

The second is factors that can be controlled. Most often they are associated with lifestyle and the presence of bad habits in humans:

• hypodynamia;
• the use of certain drugs;
• constant overeating, eating high-calorie foods;
• diabetes mellitus and hormonal disorders.

Hyperlipidemia can be found in women during pregnancy. This is explained by physiological changes in the female body in the process of bearing a child, and over time, the indicator normalizes. A significant contribution to the development of the disease is made by bad habits: alcohol abuse and smoking. Therefore, it is important to lead a healthy lifestyle and try to follow the rules of a balanced diet.

Factors that reduce the risk of pathology

Treatment and prevention

In hyperlipidemia, the main and most effective strategy for treatment and prevention is lifestyle adjustment. Increasing physical activity, adhering to the principles of a healthy diet and giving up bad habits are the keys to success in the fight against the disease.

As for the diet, the complete exclusion of fast food and fast food becomes a prerequisite. Such food is supersaturated with carbohydrates and does not bring any benefit to the body. In no case does a diet imply a complete exclusion of fats from the menu, because they are necessary for the full functioning of all internal systems and organs. But it is important to minimize your intake of foods high in saturated fat and cholesterol.

Balanced diet

In cases where correcting lifestyle and nutrition is not enough, specialists resort to the help of medications. Fibrates and statins are mainly used. Nicotinic acid is used, sometimes the treatment of hyperlipidemia is supplemented with vitamin B5. In exceptionally severe cases, a blood purification procedure and laser irradiation may be necessary.

Advice! In the presence of relatives suffering from diseases associated with the cardiovascular system, to exclude hyperlipidemia, experts recommend making it a rule to periodically undergo an examination for the concentration of lipids in the blood plasma.

Yet:

The importance of lipids in the life of the human body and their functions