Dyslipidemia treatment with folk remedies. Elevated LDL levels. Development of atherogenic dyslipidemia

Dyslipidaemia is a major and possibly even predisposing risk factor for atherosclerotic cardiovascular disease (ASCVD) that occurs before others important factors risks are starting to show up. Epidemiological evidence also suggests that hypercholesterolemia and possibly coronary atherosclerosis are themselves risk factors for ischemic stroke. Between 2009 and 2012, more than 100 million American adults aged ≥20 years are estimated to have general level cholesterol (CH) ≥200 mg/dl and nearly 31 million people have levels ≥240 mg/dl.

There is growing evidence of the presence of such a risk factor for the occurrence of peripheral vascular diseases, ischemic stroke, as well as ASBP, as insulin resistance, an increase in the severity of which leads to an increase in the level of triglycerides (TG), low-density lipoprotein (LDL) and a decrease in the concentration of high-density lipoprotein (HDL). ) in blood plasma.

In this regard, on April 23, 2017, the journal Endocrine Practice published medical guidelines for practitioners developed by the Board of Directors of the American Association of Clinical Endocrinologists (AACE) Board of Directors and the Board of Trustees of the American College of Endocrinology (American College of Endocrinology (ACE) Board of Trustees) that conform to previously published AACE protocols for standardized delivery of clinical practice guidelines.

According to the authors, another reason for developing this guideline was the controversial 2013 American Heart Association/American College of Cardiology guidelines, which eliminated LDL-lowering goals and instead recommended varying the intensity of statin therapy.

In essence, this guideline is a systematically developed message designed to help healthcare professionals make medical solutions for specific clinical cases, but, as the authors state, they are in no way a substitute for the independent judgment of a healthcare professional and should not be considered as guidance.

The developers clarify that most of the content of these recommendations is based on literature reviews, and in questionable aspects, the authors used professional judgment. These guidelines are a working document that reflects the state of the art at the time of publication, but as rapid changes are expected in this area, periodic revisions are inevitable. Medical workers it is recommended to use this information in conjunction with the best clinical assessment not a substitute, and the recommendations provided may not be appropriate in all situations. Any decision by practitioners to apply these guidelines should be made in the light of local possibilities and individual circumstances.

The summary of this document contains 87 recommendations, of which 45 (51.7%) are classified as A, 18 (20.7%) - B, 15 (17.2%) - C and 9 (10.3%) - to grade D. These detailed, evidence-based guidelines enable nuanced clinical decision making that spans many aspects. medical care in real conditions. This update contains 695 sources, of which 203 (29.2%) are high-quality evidence, 137 (19.7%) are moderate-quality evidence, 119 (17.1%) are weak, and 236 (34.0%) ) cases, there is no clinical evidence.

The authors indicated risk factors for the development of ASBP following states. The main ones include: increasing age, high levels of serum cholesterol and LDL; an increase in the level of cholesterol that is not associated with HDL (non-HDL cholesterol); lowering HDL levels; the presence of diabetes mellitus, arterial hypertension, chronic kidney disease; smoking; burdened family history of ASBP. How additional factors risk noted: obesity; burdened family history of hyperlipidemia; increased LDL levels; hypertriglyceridemia on an empty stomach and after meals; polycystic ovary syndrome; dyslipidemic (lipid) triad (combination of hypertriglyceridemia, high LDL-C and low HDL-C). The authors also identified non-traditional risk factors such as increased levels of lipoprotein (a), increased activity of blood coagulation factors, concentrations of inflammatory markers, homocysteine ​​levels, uric acid, TG.

The authors clarified that recommendations for screening for dyslipidemia vary according to age groups. According to them, the results of a number of studies have shown that atherosclerotic changes can be present at an early stage of life, long before the onset of symptoms. Although the risk of ASBP in young adults is low, adults over 20 years of age should be assessed for dyslipidemia every 5 years. More frequent assessments are warranted for young adults with a positive family history of premature ASBP (established myocardial infarction or sudden death under the age of 55 for the father or other first-degree male relative, or up to the age of 65 for the mother or other first-degree female relative).

All young people with diabetes should have their lipid profile screened at the time of diagnosis. If the LDL is in the range acceptable level risk (<100 мг/дл), то установление липидного профиля, повторяемое каждые 3–5 лет, также является обоснованным, но может проводиться и чаще на основе индивидуальных клинических соображений.

Given the high prevalence of ASPD among middle-aged individuals (men ≥45 years, women ≥55 years), even in the absence of risk factors, it is recommended that this category of people be screened for dyslipidemia at least every 1–2 years. More frequent lipid testing is recommended when multiple risk factors for ASBP are present. The frequency of testing should be based on individual clinical circumstances and physician judgment. All patients with diabetes should be screened at the time of diagnosis and annually thereafter.

The AACE advocates screening for dyslipidemia in all adults aged 65–75 years, regardless of risk status for ASPD, and in adults over 75 years of age who have multiple risk factors for ASPD. Although the association between high LDL-C and ASBP weakens with age, elevated serum cholesterol levels in the elderly (males ≥65 years old, females ≥75 years old) are associated with a greater absolute number of acute coronary events than in middle-aged and young people. The Prospective Study of Pravastatin in the Elderly at Risk (PROSPER), with a sample of 5804 participants over the age of 70 years, demonstrated a secondary, but not primary, benefit of prevention of ASBP for the group treated with this drug.

There is evidence that atherosclerosis begins early in life and elevated lipid levels during adolescence predispose to their increase in adulthood. In addition, studies show that the presence and severity of atherosclerotic lesions in children and young people are associated with serum lipid levels and are associated with the development of atherosclerosis and ASBP in the future. Despite the consensus that early intervention is warranted even in very young patients, the most effective diagnostic and treatment approaches for dyslipidemia in pediatric practice remain far from clear.

The original guidelines for the management of cholesterol in children and adolescents were published by the National Cholesterol Education Program (NCEP) in 1992 and focused primarily on identifying children with elevated LDL levels. Since then, in line with the fact that patterns of dyslipidemia in children and adolescents have evolved to include categories of combined dyslipidemia with associated features of obesity, moderately severe elevated triglycerides, elevated LDL, and decreased HDL, more recent recommendations have emerged that reflect these changes.

Although the NCEP guidelines continue to be updated, the Expert Panel on Blood Cholesterol Levels in Children and Adolescents was published as early as 1992, so the American Academy of Pediatrics (AAP) presented a clinical report on lipid screening and cardiovascular disease in children to replace his previous position statements regarding cholesterol in the pediatric population.

The AAP and the National Heart, Lung, and Blood Institute (NHLBI) currently recommend universal screening of children for elevated cholesterol levels at 9–11 years of age and again after puberty (17–21 of the year). As a general rule, regular screening is not recommended between 12 and 16 years of age, as new data on risk factors in this age group have not been studied. Children aged 2–3 years and older who have risk factors for ASBP, intermediate or high risk other associated diseases, a burdened family history of premature development of ASBP or dyslipidemia.

AACE also supports the recommendations of other organizations to screen children and adolescents for the following risk factors for ASPD: obesity (or elevated body mass index), insulin resistance, diabetes, arterial hypertension, smoking, health conditions with moderate or high risk of complications (eg, chronic or end-stage kidney disease, kidney transplantation, postorthotopic heart transplantation, Kawasaki disease with regressed or recurrent aneurysms, chronic inflammatory disease, HIV, or nephrotic syndrome), a positive family history of premature development of ASBP or dyslipidemia.

Moreover, according to the American Heart Association (AHA), children who are overweight or obese should be promptly screened for other elements of the insulin resistance syndrome, and the presence of such factors may change aspects of treatment.

This guideline also highlights screening features in women, indicating that the diagnosis of ASPD can be particularly problematic, as approximately half of the female population with symptoms suggestive of ischemia has angiographically normal or near-normal coronary arteries. In addition, symptoms in women are often less obvious and/or atypical compared to those in men. These differences can lead to delays in evaluation and diagnostic testing, the use of smaller amounts of the prescribed drug for the treatment and prevention of dyslipidaemia, cardiovascular disease, or endocrinological pathology. In addition, traditional diagnostic methods such as imaging, electrocardiography, and tests with exercise, may be less accurate in women, taking into account anatomical and hormonal features, which should also be taken into account by practitioners.

The authors have established a list of the main recommended screening methods to identify risk factors for the development of cardiovascular pathology. vascular system. These methods include: fasting lipid profile, LDL, HDL, non-HDL cholesterol, apolipoproteins, triglycerides. It is also recommended to exclude secondary causes of dyslipidemia by testing for a possible underlying pathology. thyroid gland, liver and kidneys, as well as to exclude diabetes mellitus. Additional tests have been proposed, such as a highly sensitive method for determining C-reactive protein, determining the level of lipoprotein-associated phospholipase A2, homocysteine, as well as some methods of functional diagnostics and genetic screening.

The authors point out that the treatment of dyslipidemia requires a comprehensive strategy for lipid control, as well as the elimination of associated metabolic disorders and modifiable risk factors such as arterial hypertension, diabetes mellitus, obesity and smoking. Insulin resistance, which is often, but not necessarily, associated with obesity and underlies most cases of type 2 diabetes mellitus, also has an established relationship with dyslipidemia.

The primary approach to prevention in people with lipid disorders involves lifestyle changes, including physical activity, and drug therapy. Treatment may also include pharmacotherapy combined with educational programs to further reduce risk through smoking cessation and weight loss. In addition, the use of insulin in people with poorly controlled both types of diabetes mellitus to lower blood glucose levels often reduces circulating TG levels.

In conclusion, the authors noted that this guideline is a practical tool that endocrinologists, as well as other healthcare professionals, healthcare-related organizations, and regulators, can use to reduce the risk and reverse the consequences of developing dyslipidemia. It provides guidance on screening, risk assessment, and treatment recommendations for a range of individuals with various lipid disorders.

The guidelines highlight the importance of treating abnormal LDL-C in some people to achieve lower LDL levels than previously stated, as well as measuring indicators of calcification. coronary arteries and markers of inflammation to facilitate risk stratification. Particular attention is paid to persons with diabetes mellitus, familial hypercholesterolemia, women and young people with dyslipidemia. Both clinical and cost-effectiveness data are provided to help guide treatment decisions.

• Jellinger P.S., Handelsman Y., Rosenblit P.D. et al.(2017) American Association of Clinical Endocrinologists and American College of Endocrinology Guidelines for Management of Dyslipidemia and Prevention of Cardiovascular Disease. Endocr Practice. (Suppl 2): ​​1–87.

Oleg Martyshin

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

The prevalence of diseases of the cardiovascular system and a high percentage of mortality are a global problem. This leads to a decrease in the working capacity of the population and large economic losses. Currently, a large number of recommendations and programs for the prevention and treatment of diseases of the cardiovascular system have been developed. The main goal of these programs is to educate the population on the basics of a healthy lifestyle and nutrition, as well as explain 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 that contain carbon in their structure) that come from food. Inorganic substances include potassium, calcium, magnesium, phosphorus, sodium and others. To organic substances - proteins, carbohydrates, nucleic acids and fats ( lipids).

The major plasma lipids of clinical importance are:

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

The four main classes of lipoproteins are:

• Chylomicrons ( HM). Composition - triglycerides 90%, cholesterol 5%, apoproteins 2%, other lipids 3%. Synthesized in the wall of the small intestine from dietary fats. The main function of chylomicrons is to transport dietary triglycerides from the intestine to adipose tissue, where they are deposited ( postponed), and into the muscles, where they serve as a source of energy. After transportation of triglycerides, chylomicrons are converted into residual particles ( remnants) and tolerate exogenous ( coming from outside) cholesterol to the liver.
• Very low density lipoproteins ( VLDL). Composition - triglycerides 60%, cholesterol 15%, apoproteins 10%, other lipids 15%. Synthesized in the liver from endogenous 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 extremely rare form (1 in a million), in which the child receives defective genes from both parents. Primary heterozygous dyslipidemia is characterized by the inheritance of a defective gene from one of the parents. It occurs much more often - 1 case per 500 people.
• Secondary dyslipidaemias. Secondary dyslipidemias appear with various diseases, an unhealthy lifestyle, and when taking certain medications. Occur more often in the population of developed countries. Lipid metabolism disorders develop with obesity, diabetes mellitus, chronic renal failure, liver cirrhosis, malignant neoplasms, thyroid diseases and many other pathologies. Alcohol intake, a sedentary lifestyle, and malnutrition also lead to dyslipidemia. Drugs that disrupt fat metabolism include oral contraceptives ( contraceptive pills), beta-blockers, thiazide diuretics ( diuretics), corticosteroids.
• Alimentary dyslipidemia. Alimentary dyslipidemia develops with excessive consumption of animal fats. There are transient alimentary and permanent alimentary dyslipidemias. Transient nutritional dyslipidemias are characterized by a temporary increase in total cholesterol and low-density lipoprotein levels after a single meal rich in animal fats. Lipid imbalance develops the next day after eating. Permanent alimentary dyslipidemia is characterized by a persistent violation of lipid metabolism with regular consumption of fatty foods.

• 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 dyslipidemias, 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). Xanthelasma are slightly raised flat formations yellow color 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 increased risk development of myocardial infarction.
• Lipoid corneal arch. The lipid arch of the cornea is a circular infiltration of the corneal stroma with lipids. As a result of the deposition of fats, the cornea loses its luster, and a white or yellowish ring forms on the periphery of the cornea. There is also a narrowing of the pupils, deformation of their shape is possible. Diagnosis of the lipoid arc is not difficult. It is performed by an ophthalmologist using special devices.

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

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

Why is high cholesterol dangerous?

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

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

Depending on the atherosclerotic vascular lesion, there are:

• atherosclerosis of the aorta the largest blood vessel that carries blood from the heart to the internal organs). Atherosclerotic damage to the aorta leads to a persistent increase in blood pressure, to aortic valve insufficiency ( inability to prevent the backflow of blood from the aorta to the heart), circulatory disorders of the brain and other organs.
• Atherosclerosis of the heart vessels. The narrowing of the lumen of the vessels of the heart and the violation of its blood circulation leads to coronary heart disease ( ischemic heart disease). Ischemic disease heart disease is a disease that develops when there is insufficient oxygen supply 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. When the lumen of the vessel is narrowed, 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, suffered a heart attack myocardial infarction, stroke, chronic kidney disease, obesity and other severe pathologies. These patients have high levels of cholesterol, low density lipoproteins ( LDL).
• high risk ( risk SCORE ≥ 5% and< 10% ). The high-risk group includes patients with hereditary hyperlipidemia, arterial hypertension ( high blood pressure) and other pathologies.
• moderate risk ( risk SCORE ≥ 1% and< 5% ). This category of patients with moderate risk includes most middle-aged people. The risk is increased in the presence of premature coronary artery disease ( blood supply to the heart), obesity, increased levels of cholesterol and low-density lipoproteins, and others.
• Low risk ( risk score< 1% ). Patients at low risk are advised to change their lifestyle, diet, and regular medical monitoring to avoid the risk of developing serious complications.

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

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

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

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

Indicators of the coefficient of atherogenicity and their interpretation are:

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

Life prognosis in dyslipidemia

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 the achievement of target levels of lipids in the blood, pathological changes in the body and their consequences are already irreversible. These patients are at very high risk with high mortality.

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

Laboratory research methods include:

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

specific laboratory analysis, revealing a lipid imbalance is a lipidogram - an analysis of the level of lipids in the blood. To obtain reliable results, the patient must strictly follow the recommendations of the doctor before conducting the study. Improper diet, alcohol consumption, smoking, inflammatory processes, infectious diseases able to 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;
• conducting a study 2 to 3 weeks after the illness of moderate severity;
• analysis, provided that the patient is rested, and before the procedure it is necessary to sit for 10 - 15 minutes;
• the application of a tourniquet before taking blood should not exceed 1 minute, if possible, avoid the application of a tourniquet.

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) into monounsaturated fats ( almonds, peanuts, avocado, sunflower, olive, nut oils) and polyunsaturated fats ( salmon, walnuts, soybean and 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 reducing 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 should 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 to prevent complications. The duration of treatment and doses are selected individually for each patient, taking into account his lipid profile, concomitant diseases, risk groups, etc.

Lipid-lowering drugs

Extracorporeal treatments

Extracorporeal methods of treatment include plasma sorption and hemosorption. Plasmosorption is a method of effective purification of blood plasma from various harmful products by contacting the 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. Used as a sorbent Activated carbon, which is the best known 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. To relative contraindications include - acute infectious diseases, low levels of protein in the blood plasma ( 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 can be prescribed.

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

Basic Principles primary prevention dyslipidemias 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 the normal range ( below 140/90 millimeters of mercury);
• regular medical check-ups with laboratory testing of blood lipids ( lipidogram), especially in patients with a positive family history ( whose close relatives had dyslipidemia, atherosclerosis, stroke, myocardial infarction);
• timely treatment 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 research (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. Diabetes mellitus has a particularly negative effect, since this disease also affects the vessels and it is possible to reduce the effect of some lipid-lowering drugs.
• 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.

Dyslipidemia (hyperlipidemia, hyperlipoproteinemia) is not a disease - it is just a sign indicating a violation of fat metabolism. The condition is characterized by a change in the ratio of lipoproteins and fats in the blood. The main danger of this disorder is its ability to lead to atherosclerosis, which, in turn, causes the development of severe pathologies of the heart and blood vessels - myocardial infarction, hypertension, stroke. Therefore, the treatment of this disorder should be timely.

In most cases, we are talking about an abnormally elevated level of lipids in the blood - this pathological condition is called hyperlipidemia. Hyperlipidemia depends on a person's lifestyle - an insufficient level of mobility, bad eating habits, taking certain medications, drinking alcohol and smoking can lead to the development of this condition. According to ICD-10, this pathological condition has the code E78, and it can be congenital or acquired.

The mechanism of development of such a pathological condition as dyslipidemia is the peculiarity of the transport of fats through the blood. This function is performed by three types of lipoproteins (complex lipid-protein complexes): LDL (low density lipoprotein), VLDL (very low density lipoprotein) and HDL (high density lipoprotein). The problem is that LDL is not a reliable vehicle, so when they transport cholesterol from the liver to the cells, some of it is lost and settles on the walls of blood vessels, thereby causing the formation of cholesterol plaques. This is what is called "bad" cholesterol.

As for HDL, it is an excellent vehicle for fat cells, and therefore when lipids are removed from cells with the help of HDL, they do not settle anywhere and are not “lost” - such cholesterol is commonly called “good”. In fact, cholesterol is not good and bad, the difference is only in the lipid-protein complexes in which it is transported. Thus, dyslipidemia develops if LDL loses a large amount of lipids that settle on the walls of blood vessels. And this happens when they enter the body in excess, so they say that wrong image life is the trigger for the development of this disorder, leading to.

The reasons

It is impossible to unequivocally name the reasons for this violation. At the same time, depending on the mechanism of development, experts talk about the primary, secondary and alimentary form of the pathological condition. Primary is also called hereditary, and it is associated with gene mutations, so its causes are defects that can be contained in the genes of one or both parents and are inherited.

Secondary occurs as a result of pathological conditions of various organs and systems of the body. In particular, the causes of this form of violation are: liver disease.

Alimentary dyslipidemia develops when too much fat is ingested in a person's food. In addition, they talk about this form if it developed while taking certain medications. The reasons may also lie in the presence of predisposing factors in a person, such as:

• bad habits;
• malnutrition;
• abdominal obesity;
• age above 50 years.

People with a burdened family history, that is, those who have or had patients with or who have suffered in the family, have a higher risk of developing a disorder such as hyperlipidemia than people whose relatives have never suffered from pathologies of the cardiovascular system.

Classification

To date, the classification of such a pathological condition has several directions. The main classification is considered according to Fredrickson, according to which the following types of hyperlipidemia are distinguished:

The first type (1) is quite rare and the reason for the development of such dyslipidemia is an enzymatic deficiency in the body. The second type (2a) is the most common type of disorder, and it occurs due to mutations in genes. It is to this type that hereditary dyslipidemia belongs. The third type (2b) is also common and both hereditary hyperlipidemia and combined hyperlipidemia develop according to this type, that is, resulting from a combination of hereditary factors and environmental factors (nutrition, diseases of internal organs).

Dyslipidemia type 3 is characterized by an increase in blood LDL and triglycerides. Hyperlipidemia type 4 is of endogenous origin, characterized by an increase in the level of VLDL. And, finally, type 5 dyslipidemia also refers to hereditary disorders that occur with an increase in the level of choline microns in the blood.

Modern medical classification This violation also distinguishes several forms according to the mechanism of development, among which are the aforementioned primary, secondary and alimentary dyslipidemia. But the classification of hereditary hyperlipidemia depends on which parent passed the defective gene to the child. And in this case, hyperlipidemias are monogenic, heterozygous and homozygous.

There is also a classification of this disorder, depending on which lipids are contained in the blood. According to this classification, isolated and combined dyslipidemia are distinguished. ICD code 10 of an isolated form, in which the level of cholesterol in the blood is elevated - E78.0. ICD code 10 of the combined form, in which not only the level of cholesterol increases, but also the level of triglycerides - E78.2.

Symptoms

It is impossible to unambiguously name the symptoms of such a disorder of fat metabolism as dyslipidemia, because, as mentioned above, this is not a disease, but its symptom. In most cases, when hyperlipidemia is already noted in the blood, a person complains of symptoms of heart and vascular diseases.

These are symptoms such as:

• dyspnea;
• increase in blood pressure.

Symptoms characteristic of a metabolic disorder are:

• xanthomas;
• xanthelasma;
• lipoid corneal arch.

Xanthomas are small subcutaneous nodules that can be localized on the back, feet, hands, abdomen. Xanthelasma are flat formations containing cholesterol inside and are mainly located on the eyelids. If we talk about the lipoid arch of the cornea, then we mean the deposition of cholesterol along the outer contour of the cornea, which looks like a whitish stripe.
These symptoms can clearly indicate that a person has developed hyperlipidemia, which means that if treatment is not prescribed, there is a high probability that he will soon develop atherosclerosis with all the ensuing consequences.

Note that the symptoms of such a disorder as hyperlipidemia do not have an important diagnostic value, since they are characteristic of many diseases. And since hyperlipidemia is only a laboratory indicator of a violation of fat metabolism, the main diagnostic criterion is a lipid profile.

Treatment

In order for the treatment of such a pathological condition as hyperlipidemia to be effective, it must be individual and complex. Patients are shown a change in lifestyle:

• increase in physical activity;
• normalization of sleep and wakefulness;
• limiting alcohol intake and smoking cessation;
• avoidance of stressful and conflict situations.

Diet plays an important role in treatment. First of all, a diet with such pathological disorder, like dyslipidemia, requires the division of food into small portions, which should be taken at least 6 times a day. In addition, the diet involves the rejection of the intake of animal fats, as well as foods rich in cholesterol.

Proper nutrition for people with such a disorder should become permanent, that is, become their way of life.

If we talk about drug treatment, then it consists in taking drugs such as:

• cholesterol adsorption inhibitors;
• statins;
• ion exchange resins;
• fibrates;
• Omega-3 polyunsaturated fatty acids.

Also, patients with this diagnosis are shown extracorporeal treatment. In particular, such treatment is used in cases where a person has a severe form of the disorder - atherogenic dyslipidemia.

Is everything correct in the article from a medical point of view?

Answer only if you have proven medical knowledge

Diseases with similar symptoms:

Obesity is a state of the body in which fat deposits begin to accumulate in excess in its fiber, tissues and organs. Obesity, the symptoms of which are weight gain of 20% or more when compared with the average values, is not only a cause of general discomfort. It also leads to the appearance of psycho-physical problems against this background, problems with the joints and spine, problems associated with sex life, as well as problems associated with the development of other conditions associated with such changes in the body.

Dyslipidemia is pathological process occurring in violation of the lipid balance of the blood. This type of pathology is not a disease, but only one of the factors of development Atherosclerosis is a chronic disease, with the manifestation of seals in the vascular walls of the arteries and a significant narrowing of the lumen, accompanied by impaired blood supply to the internal organs.
The total content of lipid complexes in bloodstream with dyslipidemia, it increases significantly due to an increase in their formation and production in the human body, as well as a violation of their normal excretion.

Pathology in most cases occurs in the process of a long and persistent increase in cholesterol in the bloodstream.

Dyslipidemia is not a rare type of deviation and medical statistics in this regard says that pathology occurs in almost every second inhabitant of the planet.

Symptoms of dyslipidemia

Violation of lipid metabolism and the content of the lipids themselves in the bloodstream can only be detected during laboratory diagnostic methods. Symptoms of the disease manifest themselves as:

• Xanthoma - nodular dense formations, with a high content of cholesterol inside, located in the areas of the tendon ligaments. In rare cases, xanthomas can be on the soles of the feet, palms of a person, on the skin and part of the back;
• Xanthelasma - remnants and deposits of cholesterol under the skin, localized in the eyelids. They resemble the structure of yellowish nodules, not very different from the skin;
• Corneal arch of lipoid type - white or gray color a rim characteristic of cholesterol deposits under the edge of the cornea. The presence of a similar sign is typical for people after 50 years. The formation of a lipoid arch earlier means that dyslipidemia has a genetic inheritance.

Disease classification

This type of pathological changes is usually classified according to the following points:

• According to Fredrickson;
• development mechanism;
• By lipid type.

According to Fredrikson, the classification does not have sufficient popularity among medical professionals. But in some cases, this classification is used, as it is adopted by the World Health Organization. The basic factor that is taken into account is the type of lipid, the level of which exceeds the norm as much as possible. Pathology has 6 types, but only 5 of them have an atherogenic ability (leading to the maximum rapid development atherosclerosis).

1. Primary type - pathological changes of the genetic hereditary type (an increase in chylomicrons is found in the patient's bloodstream). This is the only type of pathology that does not lead to the development of atherosclerosis.
2. Type secondary - pathological changes of a genetic nature, in which hypercholesterolemia and combined lipidemia are formed.
3. Type three - characteristic of this type of pathology, is a significant increase in the content of triglycerides and lipoproteins with low density.
4. The fourth type is lipidemia, which has an endogenous origin. In this type, there is an increase in low density lipoproteins.
5. Type five - characterized by an increase in chylomicrons in the bloodstream.

According to the mechanism of development, dyslipidemia is classified as follows:

• Primary - an independent disease, subdivided into:
• Monogenic - a hereditary type of pathology that occurs against the background of gene mutations;
• Homozygous - in this case, a small child receives the affected genes from each parent one at a time;
• Heterozygous - the inheritance of the affected gene directly from only one of the parents of the child.
• Secondary - occurs as a complication, against the background of other ailments.
• Alimentary - develops with increased consumption fatty foods animal origin.

Causes of dyslipidemia

The underlying reasons why the disease arose is not possible. Depending on the stages of development, the causes of lipid metabolism disorders can be:

1. Violation of genes as a result of mutations;
2. Endocrine pathologies;
3. Diseases of an obstructive nature in the hepatobiliary system;
4. Long-term course of taking medications;
5. Fatty food intake.

The main factors that can cause dyslipidemia are:

• Not a mobile way of life;
• Improper nutrition;
• Bad habits - smoking and alcohol abuse;
• High blood pressure;
• Obesity of the abdominal type;
• Men over the age of 43.

Clinical manifestations

one big picture it is not possible to distinguish clinical manifestations in this type of pathology. In most cases, the disease is accompanied by the development of symptoms resembling atherosclerosis, ischemia of the heart muscle and other types of diseases associated with the heart and blood vessels. At elevated content lipid complexes, inflammation of the pancreas may occur in an acute course.

The manifestations of the clinical map of the disease are characterized by such a concept as a metabolic syndrome (a whole complex of disorders in the field of the entire fat metabolism, as well as violations of the functions of regulating pressure in the arteries). A similar syndrome manifests itself in the form:

1. Dyslipidemia;
2. Obesity by abdominal type;
3. An increase in blood sugar;
4. General increase in pressure in the arteries;
5. Blood supply disorders.

Diagnosis of the disease

An accurate diagnosis can only be made by a doctor who performed additional methods diagnostics. An important point in making a correct diagnosis is the collection of the patient's history. During this period, the doctor can learn about the first manifestations of the disease, find out the factor of genetic heredity and possible diseases of the vascular system and myocardium in relatives.

• A full diagnostic examination of the patient - mucous membranes, skin, measurement of pressure in the arteries;
• Analysis of urine of a general nature;
• Biochemistry of blood;
• Lipidogram is an important diagnostic study of blood flow indicators, which determines the amount of specific substances with fat-like features in the bloodstream, which are the most important clinical sign of dyslipidemia;
• Atherogenic index - good method diagnosis, which allows you to find out the general indicator of atherogenicity. If the indicator exceeds the norm, this primarily means that the process of significant progression of atherosclerosis is taking place in the human body.

Treatment of dyslipidemia

Therapy of the disease is based on the severity of dyslipidemia and its specific features. Treatment should be selected individually, based on the characteristics of each individual patient. Several types of therapy are used:

• With the use of medicinal substances;
• Without drugs;
• Special diet food;
• Therapy is extracorporeal.

Treatment with medication

For therapy, several types of drugs are used, the main of which are:

• Statites - substances that act on the formation of cholesterol by liver cells and its composition inside the cellular structures of the body;
• for absorption of cholesterol medications that prevent the absorption of cholesterol in the intestinal tract;
• Exchange-ionic resins - drugs that have the ability to bind specific acids in the secretion of bile, with the cholesterol they contain, removing them from the lumen of the intestinal tract;
• Clofibrates - drugs that reduce the content of triglycerides in the bloodstream, increasing the total amount of protective substances;
• Omega-3 - substances formed from the muscle fibers of fish that help strengthen the heart muscle and protect the myocardium from possible development arrhythmias.

Treatment without medication

It is important to remember that treating dyslipidemia without medication will not give positive results. They show excellent results complex methods treatment. A positive effect is achieved by adjusting the diet, diet and physical activity. The basic points without drug therapy are:

• Reducing the amount of animal fats in the diet. In some cases, it is necessary to exclude them completely;
• Decrease in body weight;
• Increased physical activity;
• The transition to proper nutrition, with fractional portions and saturated with vitamin complexes;
• Restriction or complete rejection of alcoholic beverages, which increase the blood flow of the patient and cause the thickness of the walls of the vascular endothelium, accelerating the onset of atherosclerosis.

Dietary nutrition for dyslipidemia is not a temporary measure, but a way of eating for life. It is advisable to consume more fermented milk products, as well as enrich your diet with various vegetables and fresh seasonal fruits. From meat, it is desirable to eat chicken and turkey fillet.

Dyslipidemia is a disorder in the ratios of different cholesterol fractions, which is not expressed by specific clinical symptoms. However, it is a provoking factor in the development of various pathological conditions in the human body.

From this it follows that dyslipidemia as an independent disease is not considered by experts, but it is a "provoker" in relation to the occurrence of a chronic pathology called "atherosclerotic vascular disease".

Violations of a dyslipidemic nature inevitably lead to the deposition of fatty layers on the inner walls of the vessels. As a result, the free flow of blood along the channel becomes difficult and hemodynamic damage to tissues and organs develops.

Reasons for the development of the disease

Dyslipidemia can occur under a variety of conditions, such as disorders accompanied by increased fat synthesis and excessive dietary intake of fat.

In addition, an imbalance in the ratio of body fat particles can be caused by the pathology of their splitting and output. This is possible even with a small intake of fats in the body with food.

In accordance with the pathogenetic mechanism of the development of dyslipidemic imbalance, there are several forms of etiopathogenetic dyslipidemia. Absolutely all hereditary types of dyslipidemia are primary forms and are divided into monogenic and polygenic.

1. Monogenic forms are characterized by the development of dyslipidemia as a result of the child receiving a defective gene from one of the parents suffering from this pathology, or from both at once.
2. The polygenic development of dyslipidemia is determined not only by the inheritance of the defective gene, but also negative impact environment.

Important! The most difficult to diagnose is the secondary form of dyslipidemia, since the occurrence of this pathology is due to any chronic disease that the patient has.

The main diseases that can provoke one form or another of pathogenetic dyslipidemia are:

• hypothyroidism;
• various diffuse liver diseases.

Diagnosis of "alimentary dyslipidemia" occurs on the basis of the proven fact of excessive intake of cholesterol along with food. A similar variant of dyslipidemia can take place according to a transient type, in which cholesterol rises only for a short time, and this happens due to a single consumption of a large amount of fatty foods.

In most cases, dyslipidemia is diagnosed only with a prolonged increase in cholesterol fractions in the bloodstream. And this is despite the fact that a significant part of people all over the world have pathology.

Symptoms

Dyslipidemia is diagnosed exclusively in the laboratory. For this reason, it is possible to identify the disease only based on the indications of laboratory tests. Because of this leading position clinical symptoms does not take.

Experienced professionals, however, even with visual inspection a patient who has been suffering from dyslipidemia for a long time may be suspected of the disease. Such specific clinical markers include xanthomas - small seals on the skin. Favorite localization sites for xanthoma are;

1. plantar part of feet;
2. knee and hand joints;
3. back skin.

Excessive accumulation of cholesterol, which is expressed in the form of various fractions, is accompanied by the appearance of xanthelasmas. These are yellow neoplasms different size located on the eyelids. Xanthelasma have a dense structure, and their internal content is cholesterol.

With the hereditary nature of dyslipidemia, a lipoid arch of the cornea occurs. This is a whitish rim located along the outer edge of the cornea of ​​\u200b\u200bthe eye.

Despite the poverty of clinical manifestations, it is possible to diagnose dyslipidemia even on an outpatient basis. This complex includes research in various areas.

The most popular laboratory analysis today, the data of which a specialist counts on when making a diagnosis of dyslipidemia, is the patient's lipid profile. This term means:

• determination of the concentration of different cholesterol fractions;
• determination of the value of atherogenicity.

Both of these indicators indicate a high risk of a patient developing atherosclerotic disease. Due to the fact that the main number of clinical forms of dyslipidemia is a hereditary pathology, today genetic testing patients with the definition of a set of defective genes is a standard examination. In addition, you can use and take measurements at home.

Disease types

The international classification of the forms of the disease was developed on the basis of information about which fraction of fats is increased in the patient's bloodstream. All dyslipidemias are divided into isolated and combined.

1. Isolated - these are those in which the indicators of lipoproteins, which are cholesterol fractions, are increased.
2. Combined - with these dyslipidemias, in addition to cholesterol, there is an increase in triglycerides.

A broader version of the distinction between dyslipidemia is the Fredrickson classification, according to which this pathology divided into five types:

• Hereditary primary hyperchylomicronemia, otherwise type 1 dyslipidemia. The disease is accompanied only by an increase in the index of chylomicrons, consisting of 90% of triglycerides and 10% of cholesterol. It is encouraging that this variant of dyslipidemia can never become the main one for the development of atherosclerotic lesions of the heart and blood vessels.
• The second type of dyslipidemia is characterized only by an increase in low-density lipoproteins, which are cholesterol fractions with a high level of atherogenicity. This type of disease is polygenic, since a combination of an inherited defective gene and adverse environmental factors is required for the occurrence of a dyslipidemic imbalance. A distinctive characteristic of type 2 dyslipidemia is the fact that the patient has an increase not only in the level of low-density lipoproteins, but also in the level of triglycerides.
• The third type of dyslipidemia is characterized by the appearance of a high rate of very low density lipoproteins in a patient, this is accompanied by high probability occurrence of atherosclerotic vascular disease.
• In the fourth type, there is also an increase in the level of very low density lipoproteins. But in this case, the condition develops not because of hereditary factors, but for endogenous reasons.
• The fifth type of dyslipidemia is an increase in the number of chylomicrons in the blood, which is combined with an increase in the number of very low density lipoproteins.

Due to the variety of laboratory types of dyslipidemic disorders in international classification There are several types of this pathology. However, according to microbial 10, dyslipidemia has a single code E78.

Treatment

Therapeutic and preventive measures aimed at the destruction of the symptoms of the disease are very diverse. They consist not only in the correction with drugs, but also in compliance with the prescriptions of a nutritionist, in a change in lifestyle.

Note! Non-drug recommendations should be followed both in hereditary types of the disease (in order to prevent progress) and in secondary forms. For the treatment of secondary dyslipidemia, it is required to eliminate the original cause of its occurrence, that is, chronic pathology.

The main list of medicines aimed at lowering the level of cholesterol and its various fractions are bile acid sequestrants and statins,. Fibrates and nicotinic acid are used to correct high levels of very low density lipoproteins and triglycerides.

The drugs included in the group of statins are monocaline antibiotics, the effect of which extends to the specific inhibition of the activity of an enzyme that increases the production of cholesterol fractions by the liver.

The drugs Atorvastatin, Lovastatin, Pravastatin, which are part of the statin group, are being developed today both by microbiological methods and synthetic ones. Treatment of dyslipidemia with statins is accompanied by a long-term stable decrease in the level of not only total cholesterol, but also low-density cholesterol. It plays an important role in the prevention of atherosclerosis of the vessels.

The advantage in the use of statins is also due to the fact that such treatment has not only a hypolipidemic effect, but also pleiotropic effects, in the form of an improvement in the function of suppressing inflammatory processes in the vessels.

If monotherapy with statins does not bring a positive result, complex therapy is prescribed using bile acid sequestrants, for example, Colestipol or Cholestyramine at a dosage of 4 g. per day orally.

This group of drugs has a direct effect on cholesterol synthesis. This happens by increasing the excretion of bile acids from the body and their further formation from cholesterol fractions.

Significant hypertriglyceridemia and chronic colitis are complete contraindications to the use of bile acid sequestrants. For isolated hypertriglyceridemia, fibrates are used, for example, Ciprofibrate - 100 mg / day.

Due to the fact that this group of drugs can cause cholesterol stones in the gallbladder cavity, all patients who have taken fibrates for a long period should undergo regular ultrasound scans.

In addition, if type 5 dyslipidemia is accompanied by pancreatitis, it is advisable to use nicotinic acid - 2g / day.

But this substance has side effect, which does not allow the widespread use of nicotinic acid in the fight against dyslipidemia. The reaction is expressed as redness of the skin in the upper body and head.

Making adjustments to the diet of a patient suffering from any form of dyslipidemia is aimed at:

• destruction of the risk of occurrence and progression of vascular and cardiac pathologies;
• normalization of blood glucose levels;
• improvement of lipid parameters;
• prevention of thrombophlebitis.

The main risk group for developing dyslipidemia includes people with enhanced nutrition, therefore medical event of primary importance is the normalization eating behavior sick. The dietary guidelines state that daily diet A patient with dyslipidemia should drastically limit the intake of animal fats.