Dyslipidemia clinical guidelines. Reasons for the development of the disease. Non-pharmacological treatment usually consists of

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 the high mortality rate are 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?

The body is made up of inorganic substances chemical compounds that do not contain carbon in the structure) and organic matter ( chemical compounds, the structure of which contains carbon) 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 important component structure of cells and ensures the stability of the cell membrane to a wide range of temperatures. The largest number 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 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.

The four main classes of lipoproteins are:

• Chylomicrons ( HM). Composition - triglycerides 90%, cholesterol 5%, apoproteins 2%, other lipids 3%. synthesized in the wall 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 internal) 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

Types of dyslipidemia

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 dyslipidemia occurs when various diseases, wrong way of life, when taking certain medicines. Occur more often in the population of developed countries. Violation of lipid metabolism develops with obesity, diabetes mellitus, chronic renal failure, cirrhosis of the liver, 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.

• 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.

Classification of hyperlipidemia according to Fredrickson

Classification by etiology ( reason) phenotypes of hyperlipidemias

Causes of dyslipidemia

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.

• 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).

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.

• male gender;
• 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.

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?

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.

To external symptoms dyslipidaemias include:

• xanthomas. Xanthomas are pathological formations on the skin or other tissues, consisting of accumulations 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 on the periphery of the cornea a white or yellowish color. 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.

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 radio wave method (destruction and excision of tissues under the influence of radio waves). Surgical treatment is carried out under local anesthesia in outpatient settings. 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?

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 dyslipidemias.

Fine inner wall vessels provides 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 lesion of the aorta leads to a persistent increase 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 ( a disease characterized by pain in the center 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 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.

• 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

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. Most used and recommended European Society cardiologists - 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 lifestyle, nutrition, regular medical monitoring to avoid the risk of developing serious complications.

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 disease, 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

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 ( ).

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 achievement of target blood lipid levels 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

• 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).

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 this 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.

To laboratory methods studies 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 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 nutrition, 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 strict diet within 2 - 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;
• testing 2-3 weeks after past illnesses moderate;
• 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.

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.

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

Treatment of dyslipidemia is divided into:

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

Non-drug treatment

• use healthy food taking into account the energy needs of the body to avoid the development of obesity;
• eating fruits, vegetables, legumes, nuts, fish, cereals from whole grain in sufficient quantity;
• saturated fat replacement meat, eggs, chocolate, butter) on the monounsaturated fats (almonds, peanuts, avocado, sunflower, olive, nut oils) and polyunsaturated fats ( salmon, walnuts, soybean oil, corn oil, flax, sesame seeds);
• restriction of use table salt up 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

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.

Medical treatment

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

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

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 must be under the supervision of a doctor and periodically take the necessary laboratory tests to assess the effectiveness of treatment and the function of other internal organs for the prevention of 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

Extracorporeal treatments

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.

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

Treatment for hypercholesterolemia and elevated low-density lipoprotein levels

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

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.

Treatment to increase high-density lipoprotein levels

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

Treatment of dyslipidemia in various clinical situations

Prevention of dyslipidemia

• primary;
• secondary.

Primary prevention

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;
• smoking cessation and abuse alcoholic drinks;
• 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 examinations with a laboratory study of the level of lipids in the blood ( 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

Basic Principles secondary prevention dyslipidemias 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 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 root turmeric. 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?

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?

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 endocrine system exacerbate the patient's condition with dyslipidemia and increase the risk of cardiovascular disease. Especially Negative influence has diabetes mellitus, 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.

A disease that is characterized by a violation of lipid metabolism in the human body. It is manifested by an increase in the level of cholesterol in the blood.

What is cholesterol?

Cholesterol is a fat-like substance found in all tissues and organs. Thanks to this compound, many hormones are produced. Without cholesterol, the coordinated work of the digestive and central nervous systems is impossible. Cholesterol is vital for the human body. Most of it is formed in the liver, but the substance enters the body and along with food. In the blood, cholesterol binds to protein and forms lipoprotein compounds, which are different both in density (low and high) and in properties.

Low-density lipoproteins ("bad" cholesterol) settle on the walls of blood vessels and form which impedes blood flow. High-density lipoproteins (“good” cholesterol) are able to remove “bad” cholesterol from tissues and transport it to the liver for processing. The determining factor for the occurrence of atherosclerosis is the balance of these two types of cholesterol.

Causes of the disease

The main factors provoking dyslipidemia syndrome are:

1. genetic predisposition. Violation of lipid metabolism can provoke mutations in genes that are responsible for the production of protein compounds that combine with cholesterol, the production of cell receptors and lipid metabolism enzymes.
2. Lifestyle. Improper diet, lack of physical activity, bad habits and excess weight have the most negative impact on lipid metabolism.
3. Stress. With psycho-emotional overstrain, the activity of the nervous system increases, which leads to

Types of dyslipidemia

The disease is classified according to the increase in the size of lipoproteins and lipids (Fredrickson classification). There are primary and secondary dyslipidemia. Depending on the increase in one type of cholesterol, isolated or pure hyperlipidemia may occur. If both cholesterol and triglycerides are elevated, hyperlipidemia may be mixed or combined.

Dyslipidemia: what is it and what are the symptoms of the disease?

With this disease, there are no specific signs, but symptoms of the underlying disease may appear. Signs indicating possible presence dyslipidemia, may be the following:

• type 2 diabetes mellitus;
• body mass index above 30;
• early heart failure in parents;
• arterial hypertension;
• the level of high density lipoproteins is less than 0.9 mol/l for men and less than 1 mol/l for women.

Dyslipidemia: what is this disease and what is its treatment?

Therapy of the disease consists in the correction of lifestyle. If lipid metabolism is disturbed, then the patient must adhere to a strict diet with limited intake of animal fats. With such a diagnosis, physical activity should be limited, avoided stressful situations, get enough sleep.

If the above methods do not give the desired result, then drug therapy is prescribed. Anion exchange resins, fibrates, hyparins, fish oil, nicotinic acid and other drugs are used for treatment.

In this article, you learned about a condition such as dyslipidemia: what kind of disease it is, its causes, symptoms and treatment principles.

If the level of "bad" cholesterol in the blood is increased, the balance between HDL and LDL is disturbed, they speak of dyslipidemia. This condition is fraught with the development of atherosclerosis and its complications: heart attack, stroke.

Dyslipidemia is not a diagnosis or a disease, but such a condition requires heightened attention. Unfortunately, it occurs quite often. Dyslipidemia is understood as a violation of fat metabolism, in which dangerous fractions accumulate in the blood, leading to atherosclerosis (atherogenic).

A person learns about dyslipidemia by receiving the result of a blood test. In most cases, the patient does not even suspect what it is, since the pathological condition does not manifest itself in any way.

for the human body normal functioning need fats and fat-like substances. One of them is cholesterol. The main share of this compound is formed in the liver and only a fifth part comes from food. Cholesterol is essential for all cells. It is involved in the construction of membranes, but cannot get into the tissues with the blood flow, since it is insoluble in plasma. Carrier proteins are needed to deliver cholesterol to cells. When combined with lipid, they form lipoprotein complexes of the following types:

• VLDL (very low density);
• LDL (low density);
• LPPP (intermediate density);
• HDL (high density).

The lower the density of the lipoprotein, the easier it breaks down, releasing cholesterol. VLDL and LDL deliver lipid from the liver to the cells, and the higher the concentration of these fractions, the higher the probability of “losing” cholesterol “on the way”. He, in turn, settles on the walls of blood vessels, restricting blood flow and forming an atherosclerotic plaque.

More stable HDL. They provide reverse transport of cholesterol to the liver, where bile is formed from it. All excess of this lipid should normally be excreted, but this is not always the case. When low-density lipoproteins increase in the blood, and the concentration of HDL decreases, this is one of the signs of dyslipidemia.

Doctors operate with such an indicator as the coefficient of atherogenicity. This is the ratio of total cholesterol to HDL content, reduced by one. If the value of the atherogenic index is greater than 3, then they speak of dyslipidemia.

In addition, this pathological condition is accompanied by excessive plasma concentrations of triglycerides and chylomicrons. The former are esters of glycerol and fatty acids. Splitting, they give energy to cells - this is one of their most important functions. An increase in the concentration of triglycerides (TG) in the blood plasma is another sign of dyslipidemia. Like cholesterol, these compounds “travel” around the body in combination with proteins. But an excess of free TG is fraught with a high risk of atherosclerosis.

However, elevated concentrations of another transport form - chylomicrons - are also observed in some forms of dyslipidemia.

Symptoms

An increase in the concentration of "bad" cholesterol (LDL and VLDL) threatens the risk of atherosclerosis. However, this disease does not manifest itself in any way or gives an erased symptomatology until there is a complete blockage of any large vessel and the associated ischemic tissue damage (necrosis, heart attack, stroke).

However, dyslipidemia can be seen in some cases. Its striking features are characteristic deposits of cholesterol: xanthoma and xanthellism, lipoid arch of the cornea.

Xanthomas usually form over tendons. These are dense nodules, and their favorite areas of growth are the areas of the feet, palms, hands, less often the back.

Xanthelasmas are easy to spot on the face. These are yellowish formations filled with cholesterol. They are located on the eyelids and are cosmetic defects. It makes no sense to treat them until the balance of lipids in the blood is normalized.

In patients over 50 years of age, a lipoid arch around the cornea can sometimes be observed. It is grayish or white in color. Lipoid arc is nothing but excess cholesterol.

Reasons and forms

There are many reasons for the violation of the lipid profile, and in accordance with them there is such a classification of dyslipidemia:

• primary;
• secondary;
• alimentary.

The primary form is an independent pathology. It is not associated with any disease or other factors. Primary dyslipidemia is determined by mutations in one or more genes responsible for the formation of cholesterol:

• heterozygous form (only 1 parent passed on the defective gene);
• homozygous form (both parents passed on to offspring 1 gene with a mutation).

Homozygous familial dyslipidemia occurs 2 times less frequently than heterozygous: on average, 1 person in a million. But this condition is more difficult.

However, often defects in the genetic material are superimposed on environmental factors that provoke metabolic disorders. In this case, they speak of polygenic dyslipidemia. This is the most common form of the pathological condition. If lipid metabolism disorders caused only gene mutations, dyslipidemia is considered monogenic.

Unlike the primary, the secondary form develops against the background of any disease:

• diabetes;
• hypothyroidism;
• liver pathology;
• estrogen deficiency (women);
• gout;
• obesity;
• stones in the gallbladder.

Some drugs can also provoke secondary dyslipidemia:

• hormonal (contraceptive) means;
• pressure medications.

The physiological secondary form of dyslipidemia is acceptable during pregnancy. After childbirth, fat metabolism returns to normal.

It is impossible to completely defeat the primary form of pathology, since the defective genetic material can be changed modern medicine not under power. It will be possible to get rid of secondary dyslipedemia only by taking control of the underlying disease. But the alimentary form is the easiest to treat. Such violations are caused by excessive intake of cholesterol in the body with food. If you adjust the diet, the lipid profile is normalized, and drug treatment is not required.

Fredrickson classification

AT medical practice allocate types of dyslipidemia depending on which lipid fractions in the blood predominate. According to this principle, the Fredrickson classification was compiled. According to it, there are 5 main groups.

Type 1 dyslipidemias are hereditary. They are associated with excessive accumulation chylomicrons in the blood, but are not considered atherogenic.

Dyslipidemia 2a, unlike the first, is more dangerous and is polygenic. At the same time, LDL is contained in excess in the blood plasma. If, in addition, the content of VLDL and / or triglycerides is increased, they speak of type 2b.

The risk of atherosclerosis is even greater in dyslipidemia 3. In this case, the concentration of VLDL increases. The same fractions accumulate in type 4 dyslipidemia, but unlike the 3rd type, it is not hereditary, but is provoked by internal causes. The fifth type of disorders is determined genetically and is manifested by excessive accumulation of VLDL, triglycerides and chylomicrons.

Dyslipidemia type 2a and all subsequent ones lead to atherosclerosis. These conditions should not be ignored!

Development of atherogenic dyslipidemia

Atherogenic dyslipidemia is registered if the balance between LDL and HDL is disturbed, that is, the concentration of “bad” cholesterol increases and “good” cholesterol decreases. Quantitatively, this is expressed by an increase in the atherogenic index up to 3 units or more.

Additional risk factors are lifestyle features:

• hypodynamia;
• regular alcohol consumption;
• smoking;
• stress;
• love for fast food.

All of these points can trigger pathological changes encoded genetically, or aggravate the course of an already developed condition. Against the background of these factors, astheno-vegetative syndrome is formed. It manifests itself in disorders of the autonomic nervous system that can negatively affect any organ.

Often, asthenovegetative disorders develop with hypertension, diabetes mellitus, and atherosclerosis. And in such cases it is extremely difficult to figure out what exactly was the trigger.

Dyslipidemia in children

Lipid metabolism disorders are registered not only in adults. They affect children and teenagers. They most often have primary dyslipidemia, that is, hereditary. In 42% of cases, form 2b is diagnosed. At the same time, xanthomas, signs of heart damage and vegetative-asthenic disorders appear in a child by the age of five.

Secondary dyslipidemia in children is most often observed in pathologies of the gastrointestinal tract. Diseases of the duodenum and stomach, diseases of the liver and pancreas can disrupt the balance of lipids in children's body. A decrease in the formation of bile acids is naturally accompanied by an increase in the concentration of LDL.

In addition, dyslipidemia is always observed in obesity, diabetes mellitus. There are also carbohydrate-associated forms. Improper nutrition with a predominance of fast food, sweets, muffins, fatty and fried foods in the children's diet, especially if the child does not play sports, likes to sit in front of the TV or spends a lot of time at the computer, is a direct path to excess weight.

Treatment

If an adult or child is diagnosed with dyslipidaemia, treatment will not necessarily be medical. The tactics of therapy is determined by the neglect of the process, the presence and degree of atherosclerotic changes, and comorbidities. Approaches to reduce "bad" cholesterol in the blood can be as follows:

• lifestyle changes;
• diet;
• drug treatment;
• extracorporeal therapy.

Non-drug approach

Minor changes in the lipid profile usually do not require drug therapy. Diet and lifestyle changes help to cope with them. With high cholesterol, you will have to give up such products:

• fast food;
• sausages, pates, semi-finished products;
• fat meat;
• butter and dairy products with high fat content;
• fast carbohydrates (shop confectionery);
• alcohol.

All food containing animal fats is prohibited, but vegetable oil and seafood are allowed, with the exception of shrimp. Seafood is rich in unsaturated omega fatty acids capable of lowering the level of "bad" cholesterol. They have the same property vegetable fats contained in nuts, flax seeds. These products can be consumed without fear - they do not increase cholesterol.

In addition, with dyslipidemia, it is important to include fresh or stewed, baked, boiled vegetables in the diet. The fiber contained in bran effectively binds cholesterol. Fish is a good source of protein lean varieties meat:

• turkey;
• chicken (breast);
• rabbit.

However, you should not limit yourself to diet alone. It is important to reconsider the lifestyle, give up nicotine (smoking), alcohol, snacks. If there is overweight, you have to fight it. With hereditary and secondary dyslipidemia, moderate exercise is necessary, it is important to exercise regularly, but not to exhaust the body. A destructive genetic program can be triggered by non-compliance with the regime of work and rest, increased nervous tension, and regular stress. It is important to pay special attention to this.

Traditional medicine methods

When a non-drug approach is not enough - the patient has significantly increased "bad" cholesterol, atherosclerosis develops, there visible signs hypercholesterolemia - you can not do without medicines. For this purpose, drugs of the following groups are usually prescribed:

• statins;
• fibrates;
• bile acid sequestrants;
• cholesterol absorption inhibitors;
• omega-3 PUFAs (polyunsaturated fatty acids);
• a nicotinic acid.

The most commonly prescribed are statins and bile acid sequestrants. The first increase the destruction of lipids, inhibit their synthesis in the liver, and in addition, improve the condition of the inner lining (intima) of blood vessels, give an anti-inflammatory effect. The most effective are Atorvastatin, Rosuvastatin, Simvastatin, Lovastatin.

If the drugs of the first group do not cause a decrease in “bad” cholesterol, bile acid sequestrants are added to them. This therapy is very effective, but has serious side effects. Bile acid sequestrants do not have a direct effect on fat metabolism and cholesterol formation. They bind bile acids in the intestinal lumen and force them out. The liver, in response to this, begins to actively synthesize new bile, for which it consumes cholesterol. So the level of this lipid goes down. The following bile acid sequestrants are used:

• Cholestyramine;
• Colestipol.

If the level of triglycerides in the blood is high, fibrates are prescribed. These drugs increase the level of HDL, which has an anti-atherogenic effect. The group includes Clofibrate, Cyclofibrate, Fenofibrate.

Effectively lower "bad" cholesterol and omega-3 PUFAs, as well as nicotinic acid (niacin) and other B vitamins. Fish oil is rich in unsaturated omega acids. You can get them in large quantities by eating sea fish.

Other drugs of choice for dyslipidaemia are cholesterol absorption inhibitors. They have limited effectiveness, since they do not affect the synthesis of cholesterol by the body, but only bind and remove fats from food. The only authorized member of the group is ezitimibe.

However, not everyone is helped by the drugs of the listed groups, and for some patients (children, pregnant women) they are completely contraindicated. Then extracorporeal therapy is required to combat dyslipidemia. It is carried out by the following methods:

• UV blood;
• hemosorption;
• cryoprecipitation;
• plasmapheresis;
• ultrafiltration.

All these methods are hardware. They involve the "processing" of blood outside the patient's body, aimed at filtering, breaking down or binding and removing cholesterol and other lipid fractions.

Whatever the nature of the occurrence of dyslipidemia, it is always important to remember about prevention. It will help prevent or delay and alleviate the course of this pathological condition. It is important to properly compose a diet, avoid bad habits and stress, and do not forget about physical education.

Dyslipidemia is an increase in plasma cholesterol levels and/or a decrease in triglycerides or HDL levels, which contributes to the development of atherosclerosis. Dyslipidemia can be primary (genetically determined) or secondary. The diagnosis is established by measuring the levels of total cholesterol, triglycerides and lipoproteins in the blood plasma. Dyslipidemia is treated based on a specific diet, exercise, and lipid-lowering medications.

ICD-10 code

E78 Disorders of lipoprotein metabolism and other lipidemias

Causes of dyslipidemia

Dyslipidemia has primary causes of development - single or multiple genetic mutations, as a result, patients experience hyperproduction or defects in the release of triglycerides and LDL cholesterol, or hypoproduction or excessive excretion of HDL. Primary lipid disorders are suspected in patients when there are clinical signs of a condition such as dyslipidaemia, early onset of systemic atherosclerosis and CAD (before age 60 years), a family history of CAD, or an established serum cholesterol level > 240 mg/dL (> 6.2 mmol/l). Primary disorders are the most common cause of development in childhood and in a small percentage of cases in adults. Many of the names still reflect the old nomenclature, according to which lipoproteins were subdivided into a and chains by gel electrophoretic separation.

Dyslipidemia in adults most often develops due to secondary causes. The most important factors in its development in developed countries are sedentary image life, overeating, especially the abuse of fatty foods containing saturated fats, cholesterol and trans fatty acids (TFA). TFAs are polyunsaturated fatty acids to which hydrogen atoms have been added; they are most widely used in food processing and are atherogenic, saturated fat. Other common secondary causes include diabetes mellitus, alcohol abuse, chronic kidney failure or complete loss of kidney function, hypothyroidism, primary biliary cirrhosis and other cholestatic liver diseases, drug-induced pathology (drugs such as thiazides, blockers, retinoids, highly active antiretroviral drugs, estrogen and progesterone, and glucocorticoids).

Dyslipidemia often develops against the background of diabetes mellitus, since patients with diabetes have a tendency to atherogenesis in combination with hypertriglyceridemia and high levels of LDL, while low levels of HDL fractions (diabetic dyslipidemia, hypertriglyceridemia, hyperapo B). Patients with type 2 diabetes have a particularly high risk of developing a condition such as dyslipidemia. Clinical combinations may include marked obesity and/or poor control of diabetes, which may result in increased circulation of FFA in the blood, leading to increased production of VLDL in the liver. VLDL-rich triglycerides then transfer these TGs and cholesterol to LDL and HDL, helping to form TG-rich, small, low-density LDL and excrete TG-rich HDL. Diabetic dyslipidemia is often exacerbated by a significant excess of the patient's daily calorie intake and a decrease in physical activity, which are characteristic features of the lifestyle in patients with type 2 diabetes. Women with type 2 diabetes may have a specific risk of developing cardiovascular disease.

Pathogenesis

There is no natural division into normal and abnormal lipid levels because lipid measurement itself is a lengthy process. There is a linear relationship between blood lipid levels and risk of developing cardiovascular disease, so many people who have "normal" cholesterol levels make efforts to get even lower. Therefore, there is no specific range of numerical values ​​for levels indicative of a condition such as dyslipidemia; this term is applied to those levels of blood lipids that are amenable to further therapeutic correction.

Evidence for the benefit of such a correction is strong enough for slightly elevated LDL levels and less strong for the task of lowering elevated triglyceride levels and increasing low HDL levels; in part because elevated triglyceride levels and low HDL levels are stronger risk factors for cardiovascular disease in women than in men.

Symptoms of dyslipidemia

Dyslipidemia itself has no symptoms of its own, but it can lead to clinical symptoms cardiovascular pathology, including ischemic heart disease and obliterating atherosclerosis of the vessels of the lower extremities. High triglyceride levels [> 1000 mg/dL (> 11.3 mmol/L)] may be a cause of acute pancreatitis.

High levels of LDL can lead to eyelid xanthomatosis, corneal opacities, and tendon xanthomas found at the Achilles, elbow, and knee tendons and around the metacarpophalangeal joints. In homozygous patients with the development of familial hypercholesterolemia, additional clinical signs may occur in the form of plantar or cutaneous xanthomas. Patients with severe triglyceride elevations may have xanthomatous lesions on the trunk, back, elbows, buttocks, knees, forearms, and feet. Patients with rare dysbetalipoproteinemia may have palmar and plantar xanthomas.

Severe hypertriglyceridemia [> 2000 mg/dL (> 22.6 mmol/L)] can lead to white, creamy deposits (lipemia retinalis) on the retinal arteries and veins. A sudden rise in the level of lipids in the blood is also clinically manifested by the appearance of white, "milky" inclusions in the blood plasma.

Forms

Dyslipidemia has traditionally been classified according to the model of enlargement of lipids and lipoproteins (Fredrickson classification). Dyslipidemia is divided into primary and secondary and is subdivided according to an increase in cholesterol alone (pure or isolated hypercholesterolemia) or depending on an increase in both cholesterol and triglycerides (mixed or combined hyperlipidemia). The above classification system does not address specific lipoprotein abnormalities (eg, decreased HDL or increased LDL), which can lead to nosological disease despite normal plasma cholesterol and triglyceride levels.

Diagnosis of dyslipidemia

Dyslipidemia is established based on the measurement of serum lipids, although such a study may not be required due to the presence of a characteristic clinical picture in patients. Routine measurements (lipid spectrum) include the determination of total cholesterol (TC), triglycerides, HDL and LDL.

A direct measurement of total cholesterol, triglycerides and HDL in plasma is carried out; quantitative values ​​of total cholesterol and triglyceride levels reflect the content of cholesterol and TG in all circulating lipoproteins, including chylomicrons, VLDL, HDL, LDL and HDL. The level of fluctuations in TC values ​​is about 10%, and TG is up to 25% with daily measurement, even in the absence of a nosological form of the disease. TC and HDL can be measured without fasting, but in most patients, to obtain the most correct results, the study must be carried out strictly on an empty stomach.

All measurements should be taken in healthy patients (outside of acute inflammatory diseases), as in acute inflammation triglyceride levels increase and cholesterol levels fall. The lipid spectrum remains valid during the first 24 hours after the development of acute MI, and then changes occur.

The most commonly calculated LDL count reflects the amount of cholesterol not found in HDL and VLDL; the level of VLDL is calculated from the content of triglycerides (TG / 5), i.e. LDL = OH [HDL + (TG / 5)] (Friedland's formula). The cholesterol contained in VLDL is calculated from the level of triglycerides (TG / 5), because the concentration of cholesterol in VLDL particles is usually 1/5 of the total lipid content in this particle. This calculation is correct only when the triglyceride level

LDL can also be directly measured in the blood using the plasma ultracentrifugation method, which separates the chylomicron and VLDL fractions from HDL and LDL, as well as through the method enzyme immunoassay. Direct measurement in plasma may be useful in some patients with elevated triglyceride levels to determine if LDL is also elevated, but such a direct study is not routine in clinical practice. The role of apo B determination is under investigation, as its levels reflect all non-HDL-cholesterol (i.e., cholesterol found in VLDL, VLDL residues, LDLR, and LDL) and may be a better predictor of the risk of CHD than only one LDL.

Fasting lipid spectrum should be measured in all adults > 20 years of age and repeated every 5 years thereafter. Measurement of lipid levels should be supplemented by determining the presence of other cardiovascular risk factors, such as diabetes mellitus, tobacco smoking, arterial hypertension, and the presence of a family history of coronary artery disease in men of the 1st degree of relatives up to 55 years of age or in women of the 1st degree of relatives up to 65 years of age.

There is no specific age beyond which patients would not need further screening, but it is clear that screening is no longer necessary once patients reach the age of 80, especially if they develop coronary artery disease.

Screening is indicated in patients under 20 years of age who have risk factors for atherosclerosis such as diabetes, hypertension, smoking, and obesity, hereditary forms of CAD in close relatives, grandparents, or siblings, or if cholesterol levels increase by more than 240 mg/dL ( > 6.2 mmol/l), or dyslipidemia in relatives. In cases where relationship information is not available, as is the case with adoptions, screening is at the discretion of the attending physician.

In patients with hereditary forms of CAD and normal (or nearly normal) lipid levels, in patients with a strong family history of cardiovascular disease, or high LDL levels refractory to drug therapy, apolipoprotein levels [Lp (a)] should still be measured. Plasma levels of Lp(a) can also be directly measured in patients with borderline high LDL levels to decide on drug correction. In these same patients, C-reactive protein and homocysteine ​​levels can be determined.

Laboratory methods for studying secondary causes that provoke such a condition as dyslipidemia, including the determination of fasting blood glucose, liver enzymes, creatinine, TSH levels and urine proteins, should be implemented in most patients with newly diagnosed dyslipidemia and in the case of unexplained negative dynamics of individual components lipidograms.

Treatment of dyslipidemia

Dyslipidemia is treated by prescribing all patients with coronary artery disease(secondary prevention) and in some cases in patients without CAD (primary prevention). The guidelines developed by the Commission on the Treatment of Atherosclerosis in Adults (ATP III), operating within the framework of the National Education Program (NCEP), are the most authoritative scientific and practical publication, which directly defines the indications for prescribing therapy to adult patients. The guidelines focus on reducing elevated LDL levels and implementing secondary prevention to address high TG levels, low HDL levels, and metabolic syndrome. An alternative treatment guideline (Sheffield table) uses the TC:HDL ratio in combination with the verification of CHD risk factors for the prevention of cardiovascular risk, but this approach does not lead to the desired effect of preventive treatment.

Therapeutic tactics in children has not been developed. Strict adherence to a specific diet in childhood is a difficult task, and besides, there is no reliable scientific evidence that lowering lipid levels in childhood is effective method prevention of cardiovascular disease in these same patients in the future. In addition, the issue of prescribing lipid-lowering therapy and its effectiveness for a long time (years) is quite debatable. However, the American Academy of Pediatrics (AAP) recommends this therapy in some children with elevated LDL levels.

The specific treatment regimen depends on the established anomaly of lipid metabolism, although there is often a mixed pattern of lipid metabolism disorders. And in some patients, single abnormalities of lipid metabolism may require a complex therapeutic approach, including the use of several types of treatment; in other cases, the use of the same therapeutic method for several types of lipid metabolism disorders can be quite effective. Therapeutic measures should always include treatment of hypertension and diabetes mellitus, smoking cessation, and in those patients who have a risk of MI or cardiovascular death over the next 10 years of 10% or more (as assessed by the Framingham Table, Table 1596 and 1597), the mandatory prescription of small doses of aspirin.

In general, therapeutic regimens for both sexes are the same.

Elevated LDL levels

The clinical conditions, on the basis of which the patient is classified as at risk of developing cardiac events in the future, are similar to the criteria for the risk of developing CHD itself (CHD equivalents, such as diabetes mellitus, abdominal aortic aneurysm, obliterating atherosclerosis of peripheral vessels and atherosclerosis carotid arteries manifested by clinical symptoms); or the presence of 2 risk factors for coronary artery disease. The ATP III guidelines recommend that such patients have an LDL level of less than 100 mg/dl, but it is clear that in practice the goal of therapy is even more stringent - to keep the LDL level below 70 mg/dl, these are the numbers that are optimal for patients. with a very high risk (for example, with an established diagnosis of coronary artery disease and diabetes and other poorly controlled risk factors, in the presence of metabolic syndrome or acute coronary syndrome). When prescribing drug therapy, it is desirable that the dose of drugs provided a reduction in LDL levels by at least 30-40%.

The AAP recommends dietary therapy for children with LDL levels above 110 mg/dL. Medical therapy is recommended for children over 10 years of age who have a poor therapeutic response to dietary therapy and persistent LDL levels of 190 mg/dL or more and who do not have a family history of hereditary cardiovascular disease. Drug therapy is also recommended for children over 10 years of age with an LDL level of 160 mg / dL and above and a simultaneous family history of cardiovascular pathology or having 2 or more risk factors for the development of this pathology. Risk factors in childhood other than family history and diabetes include smoking, arterial hypertension, low HDL levels (

The therapeutic approach includes lifestyle changes (taking into account the peculiarities of the diet and the need for physical activity), taking medications, nutritional supplements, physiotherapy and other procedures, and experimental methods treatment. Much of the above is also effective for the treatment of other lipid disorders. Sufficient physical activity has a direct direct impact to reduce LDL levels in some patients, which is also useful for ideal weight control.

Changing the habitual mode and nature of nutrition and physical activity should in any case be considered the initial elements of therapy, whenever it is carried out.

Therapeutic diet includes reducing the dietary content of saturated fat and cholesterol; increasing the content of monounsaturated fats, dietary fiber and total carbohydrates and achieving ideal body weight. For this purpose, consultation with a nutritionist is often very helpful, especially in elderly patients who have dyslipidemia.

The length of the lifestyle change period used prior to initiation of lipid-lowering therapy is controversial. In patients with moderate or low cardiovascular risk, it is prudent to allow 3 to 6 months for this. Usually, 2-3 visits of the patient to the doctor within 2-3 months are enough to assess the motivation and determine the degree of adherence of the patient to the established dietary framework.

Medical therapy is the next step, which is used when changing only one lifestyle is ineffective. However, for patients with significantly elevated LDL-C [> 200 mg/dL (> 5.2 mmol/L)] and high CV risk, drug therapy should be combined with diet and exercise from the start of treatment.

Statins are the drugs of choice for correcting LDL levels and have been shown to reduce the risk of cardiovascular mortality. Statins inhibit hydroxymethylglutaryl CoAreductase, a key enzyme in cholesterol synthesis, by regulating LDL receptors and increasing LDL clearance. The drugs in this group reduce LDL levels by a maximum of 60% and cause a slight increase in HDL and a moderate decrease in TG levels. Statins also help to reduce intra-arterial and (or) systemic inflammation by stimulating the production of endothelial nitric oxide; they can also reduce the deposition of LDL in endothelial macrophages and the content of cholesterol in cell membranes during the development of systemic chronic inflammation processes. This anti-inflammatory effect appears to be atherogenic even in the absence of lipid elevation. Side effects are non-specific, but manifest as an increase in liver enzymes and the development of myositis or rhabdomyolysis.

Described the development of muscle intoxication and without an increase in enzymes. The development of side effects is more typical for elderly and senile people with combined multiple organ pathology and receiving multidrug therapy. In some patients, switching from one statin to another during treatment or reducing the dose of the prescribed statin eliminates all problems associated with the side effects of the drug. Muscle toxicity is most pronounced when some of the statins are used with drugs that inhibit cytochrome P3A4 (eg, with macrolide antibiotics, azole antifungals, cyclosporins) and with fibrates, especially gemfibrozil. The properties of statins are common to all drugs in the group and differ little for each specific drug, so its choice depends on the patient's condition, LDL levels and the experience of the medical staff.

Bile acid sequestrants (FFAs) block the reabsorption of bile acids in the small intestine, have a strong inverse regulatory effect on hepatic LDL receptors, promoting the capture of circulating cholesterol for bile synthesis. Drugs in this group contribute to the reduction of cardiovascular mortality. To activate the reduction of LDL levels, bile acid sequestrants are usually used in conjunction with statins or nicotinic acid preparations and are the drugs of choice for prescribing children and women planning pregnancy. These medicines are enough effective group lipid-lowering drugs, but their use is limited due to the side effects they cause in the form of flatulence, nausea, convulsions and constipation. In addition, they can also increase TG levels, so their use is contraindicated in patients with hypertriglyceridemia. Cholestyramine and colestipol, but not colosevelam, are incompatible (impede absorption) with simultaneous reception other drugs - all known thiazides, β-blockers, warfarin, digoxin and thyroxin - their effect can be smoothed out by prescribing FFA 4 hours before or 1 hour after taking them.

Ezetimibe (Ezetimibe) inhibits intestinal absorption of cholesterol, phytosterol. It usually reduces LDL by only 15-20% and causes a slight increase in HDL and a moderate decrease in TG. Ezetimibe can be used as monotherapy in patients with intolerance to statin drugs or can be prescribed in combination with statins in patients on maximum doses drugs of this group and having a persistent increase in LDL. Side effects rarely develop.

Complementing treatment with a lipid-lowering diet includes dietary fiber and affordable margarine containing vegetable fats (sitosterol and campesterol) or stanols. In the latter case, LDL reduction of up to 10% can be achieved without any effect on HDL and TG levels through competitive replacement of cholesterol on the villous epithelium of the small intestine. Adding garlic to the diet walnuts as an LDL-lowering food ingredient is not recommended due to the apparent minimal effectiveness of such supplements.

Additional methods of treatment are included in complex therapy in patients with severe hyperlipidemia (LDL

Among the new methods currently being developed for lowering LDL levels, in the near future, it is possible to use peroxisome proliferator-activated receptor (PPAR) agonists with thiazolidinedione-like and fibrate-like properties, LDL receptor activators, an LPL activator, and apo E recombinants. -LDL antibodies and acceleration of LDL clearance from serum) and transgenic engineering (gene transplantation) are conceptual areas of research that are currently under study, but the clinical implementation of which is possible in a few years.

Elevated triglyceride levels

It is still unclear whether elevated triglyceride levels have an independent effect on the development of cardiovascular disease, since an increase in triglycerides is associated with numerous metabolic abnormalities, as a result of which CHD develops (eg, diabetes, metabolic syndrome). The consensus is that lowering high triglyceride levels is clinically warranted. There are no specific therapeutic targets for correcting hypertriglyceridemia, but triglyceride levels

Initial therapy includes lifestyle changes (measured exercise, weight loss, and avoidance of refined sugar and alcohol). Supplementing the diet (2 to 4 times per week) with 3-fatty acid-rich fish dishes can be clinically effective, but 3-fatty acid levels in fish are often low, so supplementation may be needed. In patients with diabetes and who have dyslipidemia, blood glucose levels should be strictly monitored. With the ineffectiveness of the above measures, it should be considered appropriate to prescribe lipid-lowering drugs. Patients with very high triglyceride levels should be treated with medication from the time of diagnosis in order to reduce the risk of developing acute pancreatitis as quickly as possible.

Taking fibrates reduces triglyceride levels by approximately 50%. They begin to stimulate endothelial LPL, which leads to an increase in fatty acid oxidation in the liver and muscles and a decrease in intrahepatic VLDL synthesis. The drugs of this group also increase L-PVP by almost 20%. Fibrates can cause gastrointestinal side effects, including dyspepsia and abdominal pain. In some cases, they can cause cholelithiasis. Fibrates contribute to the development of muscle intoxication in cases where they are prescribed in conjunction with statins and potentiate the effects of warfarin.

The use of nicotinic acid preparations may also have a positive clinical effect.

Statins may be used in patients with triglyceride levels

Omega-3 fatty acids in high doses can positive effect to lower triglyceride levels. 3 fatty acids EPA and DHA are found as active ingredients in fish oil or capsules 3. Side effects include belching and diarrhea and can be reduced by dividing the daily dose of fish oil capsules into 2 or 3 times daily with meals. The administration of 3 fatty acids may be useful in the treatment of other diseases.

Low HDL

Therapeutic interventions aimed at increasing HDL levels may result in a reduction in the risk of death, but scientific publications on this topic are few. In the ATP III guidelines, low HDL is defined as the level

Therapeutic measures include increasing physical activity and adding to diet monounsaturated fats. Alcohol increases HDL levels, but its use is not recommended as a treatment due to many other side effects of its use. Medical therapy is recommended in cases where lifestyle changes alone are not sufficient to achieve your goals.

Nicotinic acid (niacin) is the most effective drug for increasing HDL levels. Its mechanism of action is unknown, but it has an effect on both raising HDL and inhibiting HDL clearance and may promote the mobilization of cholesterol from macrophages. Niacin also lowers TG levels and, at doses of 1500 to 2000 mg/day, lowers LDL. Niacin causes flushing (and associated redness of the skin), pruritus and nausea; pre-administration of small doses of aspirin can prevent these side effects, and the slow effect of small doses of the drug divided into several doses per day is often the cause of a significant reduction in the severity of side effects. Niacin can cause an increase in liver enzymes and rarely liver failure, insulin resistance, hyperuricemia and gout. It may also increase homocysteine ​​levels. In patients with moderate LDL and below average HDL levels, treatment with niacin in combination with statins can be very effective in preventing cardiovascular disease.

Fibrates increase HDL content. Recombinant HDL infusions (eg, apolipoprotein A1 Milano, a specific HDL variant in which the amino acid cysteine ​​is replaced by arginine at position 173 to form a dimer) are currently a promising treatment for atherosclerosis but require further development. Torcetrapib, a CETP inhibitor, markedly increases HDL and lowers LDL, but its effectiveness in atherosclerosis has not been proven, and this drug also needs further study.

Elevated lipoprotein levels (a)

The upper limit of normal for lipoprotein (a) is about 30 mg/dL (0.8 mmol/L), but individual values ​​rise higher in African and American populations. To date, there are very few medications that can act on elevated levels of lipoprotein (a) or prove the clinical effectiveness of such an effect. Niacin is the only drug that directly lowers lipoprotein(a) levels; when administered in high doses, it can reduce lipoprotein(a) by about 20%. The usual treatment strategy in patients with elevated lipoprotein(a) levels is to actively lower LDL levels.

How is secondary dyslipidemia treated?

Diabetic dyslipidemia is treated with lifestyle changes combined with statins to lower LDL and/or fibrates to lower TG levels. Metformin reduces TG levels, which may be the reason for the preferred choice of this drug among all antihyperglycemic agents when prescribing treatment for a patient with diabetes. Some thiazolidinediones (TZD) increase both HDL and LDL (probably to a lesser extent those that have an atherogenic effect). Some TZDs also lower TG. These drugs should not be chosen as the main lipid-lowering agents in the treatment of lipid disorders in diabetic patients, but they may be useful as adjunctive therapy. Patients with very high TG levels and less than optimal diabetes control may have a better response to insulin therapy than to oral hypoglycemic agents.

Dyslipidemia in patients with hypothyroidism, kidney disease, and/or obstructive liver disease first includes therapy for underlying causes, and then for lipid abnormalities. Altered levels of the lipid spectrum in patients with slightly reduced thyroid function (TSH level at the upper limit of normal) are normalized with the appointment of hormonal replacement therapy. It should be considered reasonable to reduce the dose or complete cessation taking a drug that caused a violation of lipid metabolism.

Dyslipidemia Monitoring

Lipid levels after initiation of therapy should be checked periodically. There are no data to support specific monitoring intervals, but measuring lipid levels 2-3 months after starting or changing treatment and then 1 or 2 times a year after lipid levels have stabilized is common practice.

Despite rare cases of hepatotoxicity and accumulation of toxins in the muscles during statin use (0.5-2% of all cases), a popular recommendation for a condition such as dyslipidemia is the baseline measurement of liver and muscle enzyme levels at the beginning of treatment. Many specialists use at least one additional study of liver enzymes 4-12 weeks after the start of treatment and thereafter annually during therapy. Statin therapy may be continued until liver enzymes are more than 3 times the upper limit of normal. Muscle enzyme levels do not need to be monitored regularly until patients develop myalgias or other symptoms of muscle damage.

Forecast

Dyslipidemia has a variable prognosis, depending on the dynamics of the lipid spectrum and the presence of other risk factors for cardiovascular disease.

Dyslipidemia: essence, causes, manifestations, diagnosis, how to treat, prevention

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 is disturbed during internal organs that 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 gender,
15. Elderly age.

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

AT most susceptible to the development of pathology of the person, in the family history of which there are cases of early atherosclerosis. 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 for a long time may be missing. 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.

Complete diagnostic examination 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. Eat properly,
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