Familial dyslipidemia type 1. Treatment to increase high-density lipoprotein levels. Diagnosis of dyslipidemia includes

Dyslipidemia is pathological process occurring in violation of the lipid balance of the blood. This type pathology, is not an illness, 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, increases significantly due to increased education and their development in 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 lipids themselves in the bloodstream - can be detected only during laboratory methods diagnostics. 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. AT 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. Availability similar sign typical for people over 50 years of age. 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).

Primary type - pathological changes 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.
Type secondary - pathological changes of a genetic nature, in which hypercholesterolemia and combined lipidemia are formed.
Type three - characteristic of this type of pathology, is a significant increase in the content of triglycerides and lipoproteins with low density.
The fourth type is lipidemia, which has an endogenous origin. In this type, there is an increase in low density lipoproteins.
Type five - characterized by an increase in chylomicrons in the bloodstream.

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

Primary - 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 of fatty foods of 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:

Violation of genes as a result of mutations;
Endocrine pathologies;
Diseases of an obstructive nature in the hepatobiliary system;
Long course of admission medications;
Reception fatty foods.

The main factors that can cause dyslipidemia are:

Not a mobile way of life;
Not proper 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 clinical manifestations it is not possible to distinguish with 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. With an increased content of 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 ( whole complex violations in the field of fat metabolism, as well as violations of the functions of regulating pressure in the arteries). A similar syndrome manifests itself in the form:

Dyslipidemia;
Obesity by abdominal type;
An increase in blood sugar;
General increase in pressure in the arteries;
Blood supply disorders.

Diagnosis of the disease

Decide accurate diagnosis able only the 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 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 important diagnostic study indicators of the bloodstream, which determine the amount in the bloodstream of specific substances with fat-like features, which are the most important clinical sign 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 medicines;
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 cell structures organism;
for the 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 are medicines that lower the amount of triglycerides in the bloodstream, increase total 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 positive results. They show excellent results complex methods treatment. Positive effect achieved by adjusting the diet, diet regimen and physical activity. base 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 failure from alcoholic beverages that increase in the bloodstream of the patient and become the cause of 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.

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 this condition requires increased 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.

The human body needs fats and fat-like substances to function properly. 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 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. She has a grayish or White color. Lipoid arc is nothing but excess cholesterol.

Reasons and forms

Reasons for violation lipid profile set, 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 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 modern medicine cannot change the defective genetic material. 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 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 provoked internal reasons. 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 violations of the vegetative nervous system that can adversely 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 the child's body. Decline in education bile acids 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, 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. At high cholesterol you will have to refuse 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 allowed vegetable oil and seafood, with the exception of shrimp. Seafood is rich in unsaturated omega fatty acids capable of lowering the level of "bad" cholesterol. The vegetable fats contained in nuts and flax seeds have the same property. 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 excess weight, you need to fight it. In hereditary and secondary dyslipidemia, moderate loads, it is important to exercise regularly, but not to exhaust the body. A destructive genetic program can be launched by non-compliance with the regime of work and rest, increased nervous tension, 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 gives 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. Rich in unsaturated omega acids fish fat. 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 make the right diet, avoid bad habits and stress, do not forget about physical education.

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 severe pathologies 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 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 number 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 belongs to this type hereditary dyslipidemia. 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 exposure factors. environment(nutrition, diseases of internal organs).

Dyslipidemia type 3 is characterized by an increase in LDL and triglycerides in the blood. 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.

The modern medical classification of this disorder 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 because they are common to many diseases. And since hyperlipidemia is only laboratory indicator disorders of fat metabolism, the main diagnostic criterion is lipidogram.

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.

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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 sexual life, as well as problems associated with the development of other conditions that accompany such changes in the body.

Dyslipidemia- this is an imbalance in the ratios of various cholesterol fractions, which does not manifest itself with specific clinical symptoms, but is a provocateur of the development of various pathological conditions in the human body. Thus, as an independent disease, dyslipidemia is not considered by doctors, however, this pathological condition is provocative in relation to the development of such a chronic pathology as atherosclerotic vascular disease. Dyslipidemic disorders inevitably lead to the formation of fatty layers on the inner wall of blood vessels, which makes it difficult for adequate blood flow through them and provokes hemodynamic damage to organs and tissues.

Causes of dyslipidemia

The occurrence of dyslipidemia can be observed under various conditions, for example, when pathological conditions, accompanied by the activation of the process of fat synthesis, as well as their excessive intake with food. In addition, an imbalance in the proportions of fatty particles in the body can be triggered by a violation of their splitting and excretion from the body, which can occur even with their insignificant intake with food.

Depending on the pathogenetic mechanisms the occurrence of dyslipidemic imbalance, there are several etiopathogenetic forms of dyslipidemia. All hereditary forms of dyslipidemia are primary and are divided into monogenic (the occurrence of dyslipidemia develops as a result of the transfer of a defective gene to a child from one or both parents suffering from this pathology) and polygenic (the development of dyslipidemia is due not only to the transmission of a defective gene, but also to the negative influence of the environment) .

The secondary form of dyslipidemia is the most difficult to diagnose, since its occurrence is due to any chronic pathology that the patient has. Background diseases, which can provoke the development of one or another pathogenetic form dyslipidemias are:, and various diffuse diseases of the hepatic parenchyma.

The diagnosis of "alimentary dyslipidemia" is established on the basis of the existing fact of excessive intake of cholesterol into the human body through food. This variant of dyslipidemia can proceed according to a transient type, in which the increase in cholesterol takes place for a short time and is caused by a single intake of a large volume of fatty foods, or in the form of permanent dyslipidemia.

The disease "dyslipidemia", as a rule, is established only when prolonged increase indicators of cholesterol fractions in the blood, despite the fact that this pathology affects a significant part of the population around the world.

Symptoms of dyslipidemia

Due to the fact that dyslipidemia is exclusively a "laboratory diagnosis", that is, its diagnosis is possible only on the basis of laboratory tests, clinical symptoms do not occupy a leading position in terms of diagnostic criteria. However experienced professionals even when visual inspection a patient with a long history of dyslipidemia may be suspected of having this disease. One of these specific clinical markers are , which are small seals on the surface of the skin, the favorite localization of which is the plantar surface of the feet, the skin of the back, the joints of the hands and knees.

Excessive accumulation of cholesterol in the form of various fractions is accompanied by formation, which are neoplasms on the eyelids different size, yellow, dense structure, the internal content of which is cholesterol.

The hereditary form of dyslipidemia is characterized by the formation of a lipoid corneal arch, which is a whitish rim located along the outer contour of the cornea of the eye.

Despite the paucity clinical picture diagnosis of dyslipidemia is not difficult even in outpatient settings and includes a complex of laboratory studies of various directions. top priority laboratory analysis, on the data of which the doctor relies when making a diagnosis of "dyslipidemia" is the so-called "patient's lipid profile". Lipidogramme means the determination of the concentration of various fractions of cholesterol and the determination of the coefficient of atherogenicity, indicating an increased risk of developing atherosclerotic disease in a patient. Due to the fact that the majority clinical forms dyslipidemias are a hereditary pathology, currently genetic testing patients with the definition of defective genes are standard examination.

Types of dyslipidemia

The international classification of dyslipidemias was developed on the basis of data on which of the fat fractions is elevated in the patient's blood. So, all dyslipidemias are divided into isolated ones, in which increased rates lipoproteins, which are cholesterol fractions, and combined, in which there is not only an increase in cholesterol, but also triglycerides.

A more extended version of the division of dyslipidemia is the Fredrickson classification, according to which five types of this pathology are distinguished.

Hereditary primary hyperchylomicronemia, or type 1 dyslipidemia, is accompanied exclusively by an increase in the level of chylomicrons, which are 90% triglycerides and only 10% contain cholesterol. Favorable factor is that this variant of the course of dyslipidemia under no circumstances can become a background for the development of atherosclerotic lesions of blood vessels and the heart.

In type 2a dyslipidemia, there is an increase in the indicators of exclusively low-density lipoproteins, which belong to cholesterol fractions with a high level of atherogenicity. This variant of dyslipidemia is polygenic, that is, for the development of dyslipidemic imbalance, a combination of inheritance of a defective gene and the negative influence of environmental factors is necessary.

The difference between type 2b dyslipidemia is that the patient has not only elevated low-density lipoproteins, but also triglycerides.

Type 3 dyslipidemia is characterized by the appearance in the patient advanced level very low density lipoproteins, which is accompanied by increased risk development of atherosclerotic vascular lesions.

In type 4 dyslipidemia, there is also an increase in very low density lipoproteins, but the development given state due not to a hereditary factor, but to endogenous causes.

Type 5 dyslipidemia is characterized by an increase in the content of chylomicrons in the blood, combined with an increase in very low density lipoproteins.

Due to the variety of laboratory types of dyslipidemic disorders in international classification there are several forms of this pathology, however, dyslipidemia for microbial 10 has a single code E78.

Treatment of dyslipidemia

Therapeutic measures aimed at eliminating the manifestations of dyslipidemia are very diverse and include not only drug correction, but also compliance with the recommendations of a nutritionist, lifestyle modification. Compliance with the recommendations of a non-drug profile should take place both in hereditary forms of dyslipidemia (in order to prevent the progression of the disease), and in the secondary variant. Treatment of secondary dyslipidemia should begin with the elimination of the root cause of its occurrence, that is, the compensation of chronic pathologies.

The main group of drugs, the action of which is aimed at lowering the total cholesterol level and various cholesterol fractions, are statins and bile acid sequestrants. Fibrates and nicotinic acid are the drugs of choice for correcting elevated levels of triglycerides and very low density lipoproteins.

The drugs of the statin group are monocalin antibiotics, the action of which is aimed at the specific suppression of the activity of an enzyme that enhances the production of cholesterol fractions by the liver. Statins like Lovastatin, Atorvastatin, Pravastatin can be developed both microbiologically and synthetically. Therapy of dyslipidemia with the use of statins is accompanied by a stable long-term decrease in the level of not only total cholesterol, but also low-density cholesterol, which has importance for the prevention of atherosclerotic disease. The priority in the use of statins is also due to the fact that this group of drugs has not only a hypolipidemic effect, but also other pleiotropic effects in the form of improved endothelial function, suppression of inflammatory reactions in the vessels.

The hypocholesterolemic effect is observed no later than three days after the start of statin use, however, the maximum therapeutic effect achieved only after 6 weeks of drug use. Perhaps the only negative effect from the use of statins is that after the complete discontinuation of the drug, the patient most often experiences a reverse increase in cholesterol levels, so drugs of this pharmacological group must be taken continuously. Statins are devoid of pronounced adverse reactions, however, some patients with their long-term use note the appearance dyspeptic disorders conditioned by the development drug lesion liver.

Indications for temporary discontinuation of cholesterol-lowering treatment with statins is acute infection organism, surgical interventions, trauma, severe metabolic disorders. An absolute contraindication to the use of drugs of the statin group is diffuse or focal lesions of the hepatic parenchyma and. Primary therapeutic dose statins is 20 mg, which should be taken once in the evening. The maximum dosage of these drugs is not more than 80 mg. Supportive hypocholesterolemic therapy is lifelong, and therefore, it is advisable to monitor transaminase levels in the blood once every 3 months.

In a situation where statin monotherapy does not bring the desired effect, combined treatment is recommended with the use of bile acid sequestrants, representatives of which are Colestipol, Cholesteramine at a dose of 4 g per day orally. This group drugs have an indirect effect on the synthesis of cholesterol, by increasing the excretion of bile acids from the body, provoking the further formation of bile acids from cholesterol fractions. An absolute contraindication to the use of bile acid sequestrants is chronic and significant hypertriglyceridemia.

In isolated hypertriglyceridemia, the drugs of choice are fibrates (Ciprofibrate at a daily dose of 100 mg). Due to the fact that drugs of this pharmacological group can provoke the development cholesterol stones in the gallbladder cavity, all patients taking long-term fibrates should undergo regular ultrasound examination. In addition, with type 5 dyslipidemia, combined with, Nicotinic acid is widely used in daily dosage 2 g. The only limiting factor that prevents the widespread use of nicotinic acid in the treatment of dyslipidemia is its adverse reactions in the form of pronounced redness skin upper body and head.

In addition to the classical drug correction for severe dyslipidemic disorders, hemosorption and cascade plasma filtration are widely used, which belong to the category of extracorporeal methods for the treatment of dyslipidemia. These techniques allow you to change the qualitative composition of the blood and can be used for patients of various age category as well as pregnant women.

Despite the proven theory of the hereditary origin of most forms of dyslipidemia, genetic engineering still does not offer effective methods treatment of primary dyslipidemia, so these methods are only at the development stage.

The prognosis for the recovery of patients suffering from dyslipidemia directly depends on the severity of dyslipidemic disorders, the rate of development of atherosclerotic vascular lesions and the localization of atherosclerotic plaques.

Diet for dyslipidemia

Modification eating behavior patient suffering from dyslipidemia is aimed at eliminating the risk of development and progression of cardiac and vascular pathologies, improving the lipid profile, normalizing blood sugar levels, as well as preventing thrombosis.

The main risk group for the development of dyslipidemia is made up of people with increased nutrition, therefore, the priority medical event should be the normalization of the patient's eating behavior. Dietary guidelines state that the regular diet of a patient suffering from dyslipidemia should severely limit the amount of animal fats. Reception meat products nutrition is allowed no more than once a week, and to enrich the body with protein, it should be enough eat sea fish.

The main menu of patients with dyslipidemic disorders should be saturated with vegetables and fruit dishes containing fiber and important nutrients.

There is a controversial opinion that the use of alcoholic beverages has a beneficial effect on the prevention of atherosclerotic vascular disease. In fact, alcoholic beverages contain a colossal concentration of triglycerides, so their use by patients with dyslipidemia is strictly prohibited.

Prevention for dyslipidemia can be primary, when a person takes preventive measures even before the onset of metabolic disorders, and secondary, the activities of which are aimed at preventing the development of possible complications in the form of.

Dyslipidemia - which doctor will help? If you have or suspect the development of dyslipidemia, you should immediately seek advice from doctors such as a cardiologist and gastroenterologist.

Dyslipidemia is a major and perhaps even a predisposing risk factor for the development of atherosclerotic cardiovascular disease(ASSB) occurring 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 advice for practicing physicians, developed by the American Association of Clinical Endocrinologists (AACE) Board of Directors and the American College of Endocrinology (ACE) Board of Trustees), which are consistent with previously published AACE protocols for standardized provision of clinical practice guidelines.

According to the authors, another reason for the development of this guideline was the controversial 2013 American Heart Association/American College of Cardiology recommendations that eliminated reduction targets. LDL level and instead it is recommended to vary 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 that this information be used in conjunction with best clinical judgment rather than a substitute, and the recommendations presented 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); decline HDL level; diabetes mellitus, arterial hypertension, chronic disease kidneys; 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 level LDL cholesterol and low level HDL cholesterol). 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 humans young age is low, adults over 20 should be assessed for dyslipidemia every 5 years. More frequent assessments are warranted for young adults with a positive family history of premature ASPD (established myocardial infarction or sudden death before age 55 in a father or other first-degree male relative, or before age 65 in a 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-C is within the acceptable risk level (<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. Also, children aged 2–3 years and older who have risk factors for developing ASBP, an average or high risk of other associated diseases, a aggravated family history of premature development of ASBP or dyslipidemia should also be examined.

The AACE also supports the recommendations of other organizations for screening children and adolescents for the following risk factors for ASPD: obesity (or elevated body mass index), insulin resistance, diabetes mellitus, hypertension, tobacco smoking, health conditions with moderate or high risk of complications ( for example, chronic or end-stage kidney disease, kidney transplantation, post-orthotopic heart transplantation, Kawasaki disease with regressed or recurrent aneurysms, chronic inflammatory disease, HIV, or nephrotic syndrome), a positive family history of premature ASPD 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 exercise tests may be less accurate in women due to anatomical and hormonal differences, which should also be considered by practitioners.

The authors have established a list of the main recommended screening methods for identifying risk factors for the development of pathology of the cardiovascular system. These methods include: fasting lipid profile, LDL, HDL, non-HDL cholesterol, apolipoproteins, triglycerides. It is also recommended to rule out secondary causes of dyslipidaemia by examining possible underlying thyroid, liver, and kidney pathologies, as well as to rule out 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 emphasize the importance of treating LDL-C in some people to achieve lower LDL levels than previously stated, as well as measuring coronary artery calcification and inflammatory markers 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