The causes of dyslipidemia in children are all about cholesterol. Treatment of dyslipidemia in various clinical situations

In Rome (Italy) at the annual congress of the European Society of Cardiology (ESC), new recommendations for the treatment of dyslipidemia, which were created jointly by experts (ESC) and the European Society for the Study of Atherosclerosis (EAS), are presented. The new paper was published simultaneously in the European Heart Journal and on the ESC website.

Cardiovascular disease (CVD) kills more than four million people in Europe every year, and at least 80% of all CVD cases are potentially preventable by avoiding medically risky behavior patterns. As Professor Ian Graham from Ireland (ESC Rep.) commented in a press release, lipids are perhaps the most fundamental risk factor for CVD. He noted that the relationship between lipids, especially low-density lipoprotein (LDL) cholesterol, is strong and dose-dependent, and the causal relationship between them has been proven quite unequivocally. Heart attacks rarely develop in populations with extremely low lipid levels, even if these people smoke.

The new guidelines highlight the need to lower lipid levels both at the population level and in high-risk groups. As Professor Graham explained, people at high risk should be the first priority for doctors who treat individual patients, but most deaths still occur in people with only slightly elevated cholesterol - simply because there are so many such people. This means that population-based approaches to lipid reduction are also needed, in particular lifestyle changes.

With regard to specific recommendations for patients, the new guidance suggests selecting individual LDL-cholesterol targets based on the level of risk (which is determined by comorbidities and estimated 10-year risk of death from CVD). For example, for patients at high risk, the target LDL cholesterol level would be less than 2.6 mmol/L (100 mg/dL). At the same time, in all patients, regardless of their risk, at least a 50% reduction in LDL cholesterol should be achieved. As explained by the co-chair of the working group, Professor Alberico Catapano from Italy (representative of the EAS), in order to guarantee at least 50% reduction in LDL cholesterol in all patients, the experts made a kind of mixture of target levels of LDL cholesterol and a target level of cholesterol reduction.

This individualized approach differs from US guidelines, which prescribe statins to all high-risk patients, even if they have low cholesterol levels. According to Professor Graham, the implementation in Europe of the same approach as in America would mean that significantly more people would receive statins. However, the task force decided to abandon this one-size-fits-all approach due to concerns that many high-risk, obese, and inactive patients will lower their cholesterol levels with medication but then ignore other risk factors.

Fasting is no longer required prior to lipid screening as new studies have shown that non-fasting blood samples give the same cholesterol results as after the previously recommended fasting period.

The lifestyle and nutrition recommendations from the previous version of the ESC/EAS guidelines have been improved, and target levels for body mass index and other weight parameters have been added. Recommendations are specified on preferred foods, foods for moderate consumption and those foods that should be chosen only occasionally and in limited quantities. Professor Graham explained that the experts focused more on the need for foods such as cereals, vegetables, fruits and fish than on limiting fat. This decision was made after receiving the results of two studies, which found a surprisingly large effect on mortality in the Mediterranean diet. In a press release, Professor Graham said, "We're not saying you shouldn't be careful with saturated fats, we're saying that if you choose the right foods, especially if you find foods that you enjoy, it will be easier to deal with it.”

The document also provides recommendations for combination therapy in patients with refractory high cholesterol levels. Statins are the first line of treatment. The combination of a statin with ezetimibe may provide an additional 15–20% reduction in LDL cholesterol levels. Inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9) may be considered in those patients who have a persistent increase in LDL cholesterol during the combination of a statin and ezetimibe. As Professor Catapano explained, PCSK9 inhibitors are significantly more effective than the maximum therapy described above and are a real breakthrough, for example, for patients with severe familial hypercholesterolemia. However, due to their extremely high cost, their use in some countries should be limited. He concluded by stating, “We hope practitioners will make every effort to lower LDL cholesterol as much as possible in their patients. To help achieve this, we have determined the sequence of drugs. The basis should be statins, then combination treatment with ezetimibe, and as a third line, new PCSK9 inhibitors.”

Dyslipidemia- this is a violation of the ratio of different types of lipids (fat-like substances) in human blood.

Dyslipidemia- the main cause of atherosclerosis, a chronic disease characterized by thickening of the walls of arteries (vessels that bring blood to organs) and narrowing of their lumen, followed by impaired blood supply to organs).

Cholesterol - a fat-like substance, it mainly consists of atherosclerotic plaque and is the main culprit in the development of atherosclerosis - a disease of the human arteries.

*So, cholesterol(fat-like substance) in the blood is present in the composition of various complexes, the violation of the ratio of which is dyslipidemia. Cholesterol is necessary for the body: it is used to build some hormones (substances that regulate body functions), restore cell membranes (especially the brain), etc.

Forms

According to the mechanism of occurrence, dyslipidemia is divided into several forms:

1. Primary(that is, it is not a consequence of any disease).

1.1. Primary monogenic dyslipidemia is a hereditary dyslipidemia (passed from parents to children) associated with disorders in genes (carriers of hereditary information).

• Homozygous hereditary dyslipidemia (the patient received defective genes from both parents) is rare: 1 case per 1 million population.
• Heterozygous hereditary dyslipidemia (the patient received a defective gene from one of the parents) is much more common: 1 case per 500 people of the population.

1.2 Primary polygenic dyslipidemia is a dyslipidemia due to both hereditary factors and the influence of the environment - the most common form of dyslipidemia.

2. Secondary dyslipidemia(develops due to certain diseases).

3. Alimentary dyslipidemia(develops with excessive consumption of animal fats).

The reasons

There are three groups of causes of dyslipidemia:

1. Cause of primary dyslipidemias- inheritance from one or both parents of an abnormal gene (a disturbed carrier of hereditary information) responsible for the synthesis of cholesterol.

2. Cause of secondary dyslipidemias- the following diseases and conditions:

• hypothyroidism (decrease in thyroid function due to inflammation, surgical removal, etc.);
• diabetes mellitus (a disease in which the flow of glucose - a simple carbohydrate - into cells is disrupted);
• obstructive liver diseases (diseases in which the outflow of bile from the liver, a fluid secreted by the liver and accumulated in the gallbladder), is disturbed, for example, cholelithiasis (the formation of stones in the gallbladder);
• taking medications (some of the diuretics, beta-blockers, immunosuppressants, etc.);

3. Cause of alimentary(related to nutritional habits) dyslipidemia- high content of animal fats in food.

• Transient (that is, transient) hypercholesterolemia is noted the next day after taking a large amount of fatty foods.
• Permanent alimentary hypercholesterolemia is observed with regular consumption of food with a large amount of animal fats.

Factors

In the development and progression of dyslipidemia, the same factors play a role as for atherosclerosis:

Modifiable (that is, those that can be eliminated or corrected).

1. Lifestyle (diet, exercise, smoking, overweight directly or indirectly (through the mechanisms of insulin resistance) affect lipid metabolism):

• physical inactivity (a sedentary lifestyle);
• abuse of fatty, cholesterol-rich foods;
• features of personality and behavior - a stressful type of character (the presence of a violent emotional reaction to various stimuli). Psycho-emotional stress contributes to lipid metabolism disorders through neuroendocrine stimulation, in particular due to an increase in the activity of the autonomic nervous system .;
• alcohol abuse;
• smoking.

2. Arterial hypertension(persistent increase in blood pressure).

3. Diabetes (a disease in which the entry of glucose into cells, a simple carbohydrate, is impaired) with a fasting blood glucose level of more than 6 mmol / l (the norm is 3.3-5.5 mmol / l).

4. Abdominal obesity (about waist circumference in men more than 102 cm, waist circumference in women more than 88 cm). Obesity, especially abdominal (intra-abdominal), is associated with an increase in triglycerides, a low concentration of high-density cholesterol and an increase in the concentration of low-density cholesterol, which is a major factor contributing to the formation of vascular atherosclerosis.

It should be noted that dyslipidemia is the earliest manifestation of the so-called metabolic syndrome.

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Non-modifiable factors (those that cannot be changed) include several factors.

1. Age: men over 45 years old (women over 55 years old or with early menopause (complete cessation of menstruation due to stoppage of ovarian function - female gonads).

2. Presence in a family history (among close relatives: under the age of 55 years for men and up to 65 years for women) of cases of early atherosclerosis:

• familial dyslipidemia (hereditary predisposition to increased formation of lipids in the liver);
• myocardial infarction (death of a section of the heart muscle due to the cessation of blood flow to it);
• ischemic stroke (death of a part of the brain due to the cessation of blood flow to it);
• sudden death (non-violent death within 1 hour of onset of acute symptoms).

Treatment of dyslipidemia

In the treatment of secondary dyslipidemias (developing as a result of any disease, alcohol or certain drugs), the identification and treatment of the underlying disease and the abolition of alcohol and drugs that cause dyslipidemia are of primary importance.

1. Non-drug treatment of dyslipidemia.

• Normalization of body weight.

• Dosed physical activity under sufficient oxygen supply. The load regimen is selected individually, taking into account the localization and severity of atherosclerosis, as well as concomitant diseases.

• Animal fat restricted diet, enriched with vitamins and dietary fiber, the calorie content of which corresponds to the patient's loads. Refraining from fatty and fried foods is recommended. It is advisable to replace meat in the diet with fish (preferably sea) 2-3 times a week. Vegetables and fruits, rich in fiber and vitamins, should make up the bulk of the diet.

• Restriction of alcohol consumption. Alcohol increases the level of triglycerides (chemical compounds - esters of triglycerol with fatty acids that contribute to the development of atherosclerosis - a chronic disease characterized by thickening of the walls of arteries (vessels that bring blood to organs) and narrowing of their lumen, followed by impaired blood supply to organs), contributes to an increase in body weight, aggravation of the course of gout (impaired uric acid metabolism), provokes muscle damage in patients taking statins (a group of drugs that affect the synthesis of lipids by the liver).

• To give up smoking. Smoking significantly increases the risk of developing cardiovascular diseases, especially myocardial infarction and damage to the arteries of the lower extremities. Quitting smoking, on the contrary, is accompanied by an increase in blood levels of anti-atherogenic substances (substances that prevent atherosclerotic vascular damage).

• ​statins- reduce the synthesis of cholesterol by the liver and intracellular cholesterol, increase the destruction of lipids (fat-like substances), have an anti-inflammatory effect, prevent damage to new sections of blood vessels, increase the life of patients, reduce the incidence of complications of atherosclerosis. The decision to prescribe statins for prevention or treatment is made only by a doctor. By itself, taking statins does not replace the correction of lifestyle and nutrition, as they affect various mechanisms of the development and progression of the disease and complement each other. Statins can cause damage to the liver and muscles, therefore, when taking them, it is necessary to regularly monitor blood tests for the presence of liver damage products (alanine aminotransferase - ALT) and muscles (creatine phosphokinase - CPK) in them. Statins should not be used in active liver disease (if ALT levels are more than 3 times normal). Statins are prohibited for use in children, pregnant and lactating women;

• intestinal cholesterol absorption inhibitors (a group of drugs that prevent the absorption of cholesterol in the intestines). The effect of this group of drugs is limited, since dietary cholesterol is approximately 1/5 of the total cholesterol in the body, and 4/5 of cholesterol is formed in the liver. Forbidden to children;

• bile acid sequestrants (ion-exchange resins) - a group of drugs that bind bile acids containing cholesterol in the intestinal lumen and remove them from the body. May cause constipation, bloating, taste disturbances. Approved for use by children, pregnant and lactating women;

• fibrates- a group of drugs that reduce the level of triglycerides (small molecules of fat-like substances) and increase the level of high-density lipoproteins (protective substances that prevent atherosclerosis). Can be used in conjunction with statins. It is not recommended to use fibrates for children, pregnant and lactating women;

• omega-3 polyunsaturated fatty acids - a group of drugs derived from the muscles of fish. Reduce the level of triglycerides, reduce the risk of heart rhythm disturbances, prolong the life of patients after myocardial infarction (death of a section of the heart muscle due to the complete cessation of blood flow to it).

3. Extracorporeal treatments(immunosorption of lipoproteins, cascade plasma filtration, plasma sorption, hemosorption, etc.) is a change in the composition and properties of the patient's blood outside the body using special devices. Used to treat severe forms of dyslipidemia. Allowed for children (weighing at least 20 kg) and pregnant women.

4. Genetic engineering methods(changing the hereditary material of cells to obtain the desired qualities) in the future can be used in patients with hereditary dyslipidemia.

Complications and consequences

The main natural consequence and complication of dyslipidemia is atherosclerosis(a chronic disease characterized by thickening of the walls of the arteries (vessels that bring blood to the organs) and narrowing of their lumen, followed by a violation of the blood supply to the organs).

Depending on the location of the vessels containing atherosclerotic plaques (dense thickening of the inner lining of the vessel containing cholesterol), there are:

1. aortic atherosclerosis(the largest vessel in the human body), which leads to arterial hypertension (persistent increase in blood pressure) and can contribute to the formation

2. atherosclerotic heart disease: stenosis (narrowing) and insufficiency (inability to prevent backflow of blood) of the aortic valve;
atherosclerosis of the heart vessels is called coronary heart disease and can lead to the development of:

• myocardial infarction (death of a section of the heart muscle due to the cessation of blood flow to it);
• heart rhythm disturbances;
• heart defects (structural disorders of the heart);
• heart failure (a disease associated with insufficient blood supply to organs at rest and during exercise, often accompanied by blood stasis);

3. atherosclerosis of cerebral vessels leads to various disorders of mental activity, and with complete closure of the vessel - to ischemic stroke (death of a part of the brain due to the cessation of blood flow to it);

4. atherosclerosis of the renal arteries usually manifested by arterial hypertension;

5. atherosclerosis of the arteries of the intestine can lead to a heart attack of the intestine (death of a section of the intestine due to the complete cessation of blood flow to it);

6. atherosclerosis of the vessels of the lower extremities leads to the development of intermittent claudication (sudden onset of pain in the legs when walking, passing after stopping), the development of ulcers (deep defects of the skin and underlying tissues), etc.

For atherosclerosis, regardless of its localization, two groups of complications are distinguished: chronic and acute:

chronic complications. Atherosclerotic plaque leads to stenosis (narrowing) of the lumen of the vessel (stenosing atherosclerosis). Since the formation of a plaque invessels - the process is slow, chronic ischemia occurs (insufficient supply of nutrients and oxygen due to reduced blood flow) in the blood supply zone of this vessel.

Acute complications. They are caused by the occurrence of thrombi (blood clots), emboli (blood clots that have broken away from the place of formation, carried by the blood flow and closed the lumen of the vessel), spasm (compression) of the vessels. There is an acute closure of the lumen of the vessels, accompanied by acute vascular insufficiency (acute ischemia), which leads to the development of heart attacks (death of an organ site due to a cessation of blood flow to it) of various organs (for example, myocardial infarction, kidney, intestines, ischemic stroke, etc.). Sometimes there may be a rupture of the vessel.

Forecastdyslipidemia depends on:

• the level of pro-atherogenic (causing atherosclerosis) and anti-atherogenic (preventing the development of atherosclerosis) blood lipids (fat-like substances);
• the rate of development of atherosclerotic changes;
• localization of atherosclerosis. The most favorable course is atherosclerosis of the aorta, the least favorable is atherosclerosis of the own arteries of the heart.

Elimination of modifiable (that is, those that can be influenced) risk factors and timely full-fledged treatment can significantly extend the life of patients and improve its quality.

Prevention

Primary prevention of dyslipidemia

(i.e. before it came out)

1. Non-drug effects on modifiable (which can be changed) risk factors:

• normalization of body weight;
• following a diet low in fat and salt (up to 5 g per day), enriched with vitamins and fiber;
• refusal to take alcohol and smoking;
• individually selected level of physical activity;
• limitation of emotional overload;
• normal blood glucose (simple carbohydrate) levels;
• blood pressure below 140/90 mm Hg.

2. Timely full treatment of diseases that can lead to dyslipidemia, for example, diseases of the thyroid gland and liver.

Secondary prevention

(that is, in people with existing dyslipidemia)

It is aimed at preventing the appearance and progression of atherosclerotic vascular changes and the development of complications.

• Non-drug effects on modifiable (which can be changed) risk factors.

Cm.

Dyslipidemia is a condition in which fat metabolism is disturbed, which leads to the appearance of atherosclerosis.

With this disease, the vascular walls thicken, the gap between them narrows, which causes a violation of the movement of blood in all organs of the body. This is fraught with the development of ischemic disease of the heart muscle or brain, stroke, heart attack, hypertension.

General information about the disease

If the level of lipids is excessively elevated, then the pathology is called hyperlipidemia. The development of the disease is influenced by lifestyle, diet, taking certain drugs, lack of activity and bad habits.

Dyslipidemia indicates a violation of the balance of fatty elements. These low molecular weight compounds are synthesized in the liver with subsequent transportation to all cellular and tissue structures by lipoproteins - complex complexes of lipid protein composition. Three types can be classified, in which low, high or very low density.

LDL and VLDL are large structures that have a pronounced ability to be deposited in a cholesterol precipitate. It is they who cause diseases of the vascular bed and heart, and this cholesterol is “bad”. LDL provoke the formation of plaques on the endothelium, which reduces the lumen of the vessels.

HDL refers to molecules that dissolve in water and promote the excretion of cholesterol, preventing its deposition in the vessels. In the liver, they can be converted into bile acids that leave the body through the intestines.

The atherogenic value (coefficient) is the ratio of the sum of LDL and VLDL to high-density components. is called the excess of the number of such elements in human blood.

Against the background of these problems, as well as dyslipidemia, atherosclerosis may appear, which causes tissue hypoxia. To identify such a condition, it is enough to analyze blood samples and evaluate lipid metabolism.

We talk about imbalance when:

• The level of cholesterol (total) exceeds 6.3 mmol / l.
• KA is greater than 3.
• TG more than 2.5 mmol / l.
• LDL exceeds 3 mmol / l.
• HDL less than 1 mmol/l for men and below 1.2 mmol/l for women.

Factors of the occurrence of pathology

The causes of the formation of the disease can be divided into several groups:

• hereditary predisposition. Primary dyslipidemias are mainly transmitted from parents who have an abnormal element in their DNA that is responsible for cholesterol synthesis.
• Factors that cause secondary dyslipidemia are found:
  1. With hypothyroidism, when the functionality of the thyroid gland is reduced.
  2. In patients with diabetes mellitus, when glucose processing is impaired.
  3. If there is liver disease in a state of obstruction, when the outflow of bile is disturbed.
  4. When using certain medications.

• Nutritional errors. There are two forms: transient and permanent. The first is characterized by the appearance of hypercholesterolemia immediately or a day after a significant intake of fatty foods. Permanent alimentary pathology is observed in individuals who regularly consume foods with a large amount of animal fats.

Risk group

It should be borne in mind that factors that provoke the progression of atherosclerosis are involved in the formation of dyslipidemia. They can be divided into modifiable and non-modifiable. There is a risk group of people who are most susceptible to developing the disease.

Modified factors:

• Improper diet, in which fatty cholesterol foods predominate.
• Passive lifestyle.
• The presence of stress.
• Bad habits: alcohol, smoking.
• Obesity.
• High blood pressure.
• Decompensation of diabetes mellitus.

These factors are subject to correction at the request of the patient.

An unmodified reason cannot be changed. They are typical for men who are over 45 years old. Persons with a family history who have had cases of early onset of atherosclerosis, dyslipidemia, heart attack, stroke, and sudden death are also susceptible to disease.

Signs of illness

External symptoms can manifest as:

• xanthomas. These are nodules, dense to the touch, which contain particles of cholesterol. They are located above the tendon layers. Most often they can be found on the hands, less often they appear on the palms and soles, back or other areas of the skin.
• Xanthelasma. Manifested in the accumulation of cholesterol under the folds of the eyelids. In appearance, they resemble nodules of a yellowish tint or normal skin color.
• Lipoid corneal arch. In appearance, this is a rim that is deposited along the edge of the cornea of ​​\u200b\u200bthe eye. It comes in white or grey. If problems occur in patients who are not yet 50 years old, then this suggests that the cause of the disease is hereditary dyslipidemia.

The disease has the peculiarity of not manifesting itself for a long time, when significant harm has already been done to the body. At an early stage of the pathology, the problem can be identified by passing the analysis on the lipidogram.

The violations are based on the metabolic syndrome, in general, this is a complex of failures between the metabolism of fats and the normalization of blood pressure. Characteristic manifestations may be a change in the amount of lipids in the blood test, hypertension, hyperglycemia, hemostasis errors.

Disease classification

Based on the amount of lipids, the following types of pathology are distinguished:

• Isolated hypercholesterolemia, when cholesterol, which is part of lipoproteins, is elevated.
• Mixed hyperlipidemia, when the analysis reveals an increase in cholesterol and triglycerides.

Dyslipidemia according to the mechanism of occurrence can be primary (this includes hereditary pathologies) or secondary, which appeared under the influence of adverse factors.

In addition, there is a classification according to Fredrickson, in which the types of the disease depend on the type of lipid that is elevated. In most cases, the disease can lead to atherosclerosis. The following forms are distinguished:

• Hereditary hyperchylomicronemia. It differs in that only chylomicrons are elevated in the blood test. This is the only subspecies in which the risk of developing atherosclerosis is minimal.
• Type 2a is hereditary hypercholesterolemia or arising under the influence of unfavorable external factors. At the same time, LDL levels were increased.
• Type 2b, this includes combined hyperlipidemia, when lipoproteins of very low and low density, as well as triglycerides, increase.
• The third type is hereditary dys-beta-lipoproteinemia, when LDL is elevated.
• Type 4 is called endogenous hyperlipidemia, with elevated levels of very low density lipoproteins.
• The last 5 types include hereditary hypertriglyceridemia, in which chylomicrons and very low density lipoproteins are increased.

Diagnostics

In most cases, dyslipidemia can be detected by conducting a series of special examinations. The final diagnosis is made after:

• An initial examination is carried out with the collection of complaints and anamnesis. The doctor tries to identify the characteristic signs of the disease in the patient, and also studies information about hereditary and past pathologies.
• The presence of xanthelasma, xanthoma, lipoid corneal arch is detected.
• They donate blood and urine for analysis.
• . It helps to determine the coefficient of atherogenicity.
• Class M and G immunoglobulins are determined in the blood.

Treatment of the disease

To normalize fat metabolism, doctors can prescribe special drugs, dietary nutrition, an active lifestyle, and traditional medicine methods.

The medical way of treatment consists in taking:

• Statins are drugs that help reduce the biosynthesis of cholesterol in liver cells. These drugs have an anti-inflammatory effect. The most common are Atorvastatin, Lovastatin, Fluvastatin.
• Fibrates prescribed for. Treatment promotes an increase in HDL, which prevents the appearance of atherosclerosis. The combination of statins and fibrates is most effective, however, severe adverse effects such as myopathy may occur. From this group, Clofibrate, Fenofibrate are used.
• Nicotinic acid in the composition of Niacin, Enduracin. These drugs have hypolipidemic properties.
• Polyunsaturated fatty acids, omega-3. They can be found in fish oils. This treatment helps to reduce cholesterol, lipids, LDL and VLDL levels in the blood. Such drugs are anti-atherogenic, can improve the rheological functions of the blood and inhibit the formation of blood clots.
• Cholesterol absorption inhibitors that help stop absorption in the small intestine. The most famous drug is Ezetimibe.
• Resins for the connection of bile acids: Colestipol, Cholestyramine. These funds are needed as monotherapy for hyperlipidemia or as part of complex treatment with other hypocholesterolemic drugs.

home methods

Folk remedies help lower cholesterol levels and improve the condition of blood vessels. They can be used as additional help.

The most common methods are:

• Taking potato juice. It must be drunk daily on an empty stomach. To do this, raw potatoes are peeled, washed and rubbed, the contents are squeezed out. The resulting drink is drunk fresh.
• A mixture of lemon, honey, vegetable oil. It is necessary to drink such a medicine for a long time, at least 2-3 months.
• Melissa tea. It soothes and tones well, improves the vessels of the brain and heart.
• Nettle baths. To do this, a freshly cut plant is placed in a hot bath. After insisting for half an hour, bring to the required temperature, and the feet are immersed in this water. It helps to stop atherosclerosis in the lower extremities.

Principles of nutrition in case of illness

A diet with this pathology is necessary to lower cholesterol levels. A balanced diet helps to reduce excess weight and normalize blood glucose levels.

When dyslipidemic syndrome is observed, the patient should refrain from large amounts of animal fats consumed.

Fat, sour cream, egg yolks, butter, fatty meats, sausages, sausages, offal, shrimp, squid, caviar, cheese over 40% fat should be excluded from the diet.

To keep the nutrition complete, you can replace animal fats with vegetable ones. It will be useful for patients to take corn, sunflower, cottonseed, linseed, soybean oils.

In addition, it is necessary to introduce other foods of plant origin, namely:

• Fruits, berries, vegetables, legumes. All these substances contain dietary fiber, which requires at least 30 g per day.
• Rapeseed and soybean oil, which contain stanols. Their daily amount should be 3 g.
• Fresh plums, apricots, peaches, black currants, beets, carrots. These foods are rich in pectins. During the day, you need to eat about 15 g of such food.

• Regular intake of fruits, vegetables, berries.
• The use of polyunsaturated fats, mono- and saturated fats should occur in a ratio of 1:1:1.
• Restriction of high-fat dairy products.
• Reducing the consumption of eggs to 3 pieces in 7 days.

Alcohol abuse is contraindicated, however, dry red wine, taken in small amounts before meals, is useful for patients.

Complications of pathology

All the negative consequences of the disease can be divided into acute and chronic. The first includes stroke, myocardial infarction. Pathology is rapidly developing and very often ends in death.

Chronic complications include thrombi, arrhythmia, hypertension, aortic valve stenosis, renal failure, angina pectoris, trophic ulcers, and intermittent claudication syndrome.

Considering where vascular damage is observed due to the accumulation of atherosclerotic plaques, atherosclerosis is distinguished:

• Aorta. It causes arterial hypertension, in some cases it can provoke heart defects, aortic valve insufficiency, stenosis.
• Vessels of the heart. Can lead to myocardial infarction, heart rhythm failure, heart disease or failure.
• Cerebral vessels. At the same time, the activity of the organ worsens. Vascular occlusion can occur, causing ischemia and stroke.
• renal arteries. It manifests itself in hypertension.
• intestinal arteries. Often leads to intestinal infarction.
• Vessels of the lower extremities. May cause intermittent claudication or ulceration.

How to prevent illness

Prevention of dyslipidemia is:

• Weight normalization.
• Leading an active lifestyle.
• Exclusion of stressful situations.
• Passing preventive examinations.
• Proper nutrition.
• Achieving compensation for chronic pathologies such as diabetes. They need to be treated in a timely manner, avoiding complications.

Lipid metabolism disorders can occur at any age if you do not monitor your body. In order not to know what it is - dyslipidemia, it is very important to eat right and give up bad habits.

The most dangerous complication that a patient may face is the development of atherosclerosis, heart attack, stroke, heart failure.

Treatment mainly consists in correcting fat metabolism, prescribing statins, fibrates, nicotinic acid, cholesterol absorption inhibitors, bile acid binding resins, polyunsaturated fatty acids.

Dyslipidemia (ICD code E78) is a congenital or acquired pathology of fat metabolism, which is accompanied by a violation of the synthesis, transport and excretion of fats from the blood. It is for this reason that their increased content in the circulating blood is observed.

There are several classifications of this disease:

• according to Fredrickson;
• depending on the mechanism of development;
• depending on the type of lipids.

According to Fredrickson, the classification of dyslipidemia has not gained wide popularity among doctors, but still it is sometimes remembered, because it is adopted by WHO. The main factor taken into account in this classification is the type of lipid that is elevated. There are 6 types of dyslipidemia, among which only 5 have an atherogenic ability, that is, they lead to the rapid development of atherosclerosis.

• The first type is a hereditary pathology in which an increased content of chylomicrons is observed in the patient's blood (ICD E78.3). It is also the only type that does not cause the development of atherosclerosis.
• The second type (a and b) is a hereditary pathology, which is characterized by hypercholesterolemia (a) or combined hyperlipidemia (b).
• The third type is dysbetalipoproteinemia, which is characterized by an increase in the level of triglycerides and low-density lipoproteins.
• The fourth type is hyperlipidemia of endogenous origin, in which the level of very low density lipoproteins is elevated.
• The fifth type is hereditary hypertriglyceridemia, which is characterized by an increased content of chylomicrons in the blood.

According to the mechanism of occurrence, the classification of dyslipidemia has several forms:

1. Primary - is an independent disease and happens:
   • monogenic - hereditary pathology associated with gene mutations;
   • homozygous - a very rare form when a child receives defective genes one by one from both parents;
   • heterozygous - receiving a defective gene from one of the parents.
2. Secondary - develops as a complication of other diseases.
3. Alimentary - the development of this type of disease is directly related to the excessive consumption of animal fats.

Depending on what fats are contained in the blood in an increased amount, they secrete:

• isolated (pure) (according to the ICD code e78.0) - the content of cholesterol in the blood in combination with protein and lipids, lipoproteins.
• combined (mixed) hyperlipidemia (ICD e78.2) - an increased amount of cholesterol and triglycerides in the blood (chemical compounds of fatty acids and triglycerol).

The reasons

It is impossible to name one reason that causes this disease. Depending on the mechanism of development, the following factors can be the causes of dyslipidemia:

1. Primary dyslipidemia occurs as a result of the pathology of the genes of one or two parents and is inherited.
2. The causes of secondary dyslipidemia can be diseases of such organs and systems:
3. Nutritional dyslipidemia can be caused by a balanced diet, that is, excessive consumption of animal fats. Moreover, this type of disease can be of several forms:
   • endocrine diseases (hypothyroidism, diabetes mellitus);
   • obstructive diseases of the hepatobiliary system (for example, cholelithiasis);
   • long-term use of medications (diuretics, immunosuppressants, beta-blockers);
   • transient - occurs after abundant and fatty food on the next day after its use;
   • constant - observed in people who constantly consume fatty foods.

Factors contributing to the onset and progression of the disease can be:

• sedentary lifestyle;
• gross violations of diet and nutrition;
• smoking, alcohol abuse;
• arterial hypertension;
• abdominal type of obesity;
• male gender;
• age over 45;
• burdened family history (stroke, atherosclerosis, ischemic heart disease).

Clinic

It is impossible to single out one clinical syndrome in dyslipidemia. Very often, such a disease is accompanied by the development of symptoms resembling atherosclerosis, coronary artery disease and other diseases of the cardiovascular system. The syndrome of acute pancreatitis may also appear, which is more typical with a high content of triglycerides. With a high content of high-density lipoprotein (HDL), patients note the appearance of:

The syndrome of damage to internal organs manifests itself with the development of atherosclerosis of the vessels.

Speaking about the clinical manifestation of dyslipidemia, one should not forget about such a concept as. Metabolic syndrome is a complex of disorders of lipid and fat metabolism, as well as dysfunction of the mechanisms of regulation of blood pressure. In practice, the metabolic syndrome is represented by:

• dyslipidemia;
• abdominal obesity;
• hyperglycemia;
• arterial hypertension;
• violation of hemostasis.

Diagnostics

The diagnosis of dyslipidemia can only be made by a highly qualified doctor, after additional diagnostics:

Treatment

Treatment of dyslipidemia depends on the type, severity and type of dyslipidemia and is selected strictly individually for each patient. There are several types of treatment for dyslipidemia:

• drug treatment;
• non-drug treatment;
• diet therapy;
• extracorporeal therapy;
• genetic engineering methods.

All methods of treatment are aimed at normalizing lipid metabolism, lowering cholesterol and lipoprotein levels.

Medical treatment:

• - drugs, the action of which is aimed at reducing the synthesis of cholesterol by hepatocytes and its intracellular content;
• Cholesterol adsorption inhibitors are a group of drugs that prevent intestinal absorption of cholesterol;
• Ion-exchange resins (bile acid sequestrants) are a group of pharmaceuticals that have the ability to bind bile acids and the cholesterol they contain and remove them from the intestinal lumen;
• - drugs that reduce the level of triglycerides in the blood and increase the amount of protective HDL substances;
• Omega-3 polyunsaturated fatty acids are drugs synthesized from the muscles of fish that protect the heart from a heart attack, reduce the risk of developing arrhythmias.

Non-drug treatment

It is not advisable to treat dyslipidemia with medications, without the use of non-pharmacological methods. After all, by adjusting the diet, the regime of work and rest, as well as physical activity, you can achieve a very good therapeutic effect. For this you need:

• reduce the amount of animal fats in the daily diet, and sometimes completely abandon them;
• normalize body weight;
• increase physical activity, corresponding to the strengths and capabilities of the patient;
• switch to a balanced, fortified and fractional diet;
• sharply limit or completely abandon the use of alcohol, which increases the amount of triglycerides in the patient's blood, contributes to the thickening of the walls of blood vessels and accelerates the development of atherosclerosis.
• Smoking also plays an important role in the development of this disease.

diet therapy

As mentioned above, diet for dyslipidemia is one of the main factors in effective treatment. Diet is not a temporary phenomenon, but a way of life and nutrition, on which the prevention of atherosclerosis is based. The diet for this disease is aimed at the patient and has several principles:

• limit the use of fatty meats, fish, lard, shrimp, butter, fatty varieties of fermented milk products, industrial cheeses, sausages and sausages;
• enrich your diet with fats, vegetable origin, vegetables, fruits, low-fat varieties of poultry and fish;
• low-fat dairy products are also indicated for this type of disease;
• , in small portions at regular intervals.

Extracorporeal treatment

Such treatment is used to change the properties and composition of the blood, outside the human body. Severe atherogenic dyslipidemia is an indication for the use of this method. Indeed, atherogenic dyslipidemia is a factor contributing to the development of complications in the form of cardiovascular diseases.

Genetic engineering methods

This type of treatment in the future may become one of the main ones in the treatment of hereditary dyslipidemia. Developments in genetic engineering are used to change the genetic material and give it the desired qualities. This type of treatment is being developed for the future.

Possible complications and consequences

The disease is treatable, but this process is quite lengthy and requires discipline and willpower from the patient. But these efforts are worth it to prevent complex and dangerous complications in the form of:

• atherosclerosis;
• ischemic heart disease;
• heart attack;
• stroke
• heart rhythm disturbances;
• arterial hypertension and;
• intestinal atherosclerosis;
• atherosclerosis of the lower extremities.

According to the mechanism of development, all complications can be divided into two groups:

• sharp;
• chronic.

Complications can be different, from atherosclerosis to stroke

Acute complications are the occurrence of stenosis (compression) of the vessel and the separation of the thrombus from the place of its attachment. Simply put, a thrombus closes completely or partially the lumen of the vessel and an embolism occurs. This pathology is often fatal. Chronic complications are the gradual narrowing of the lumen of the vessel and the formation of a thrombus in it, which leads to chronic ischemia of the area that is supplied with blood by this vessel. The prognosis for dyslipidemia depends on:

• severity and type of disease;
• localization of the focus of atherosclerosis;
• the rate of development of the pathological process;
• timeliness of diagnosis and treatment.

Prevention

This disease, like all others, is easier to prevent than to treat for a long and difficult time. Therefore, dyslipidemia can be of several types:

1. Primary prevention is a set of measures aimed at preventing the onset and development of a disease. To this end, it is recommended:
2. Secondary prevention - measures aimed at preventing the development of complications and the progression of the disease. This type of prophylaxis will be used for already diagnosed dyslipidemia. For this purpose, you can apply:
   • normalization of body weight;
   • active way of life;
   • avoidance of stress;
   • rational distribution of time for work and rest;
   • regular medical examination with mandatory blood and urine tests, as well as blood pressure measurement;
   • diet therapy;
   • drug prophylaxis;
   • non-drug effect on the cause of the disease.

When the first alarming symptoms appear, you should seek qualified medical help.

Prevention, diagnosis and treatment, carried out in a timely manner, can prolong and preserve the patient's life and its quality. Only the main condition for such a forecast is discipline and respect for one's health.

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

ICD-10 code

E78 Disorders of lipoprotein metabolism and other lipidemias

Causes of dyslipidemia

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

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

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

Pathogenesis

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

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

Symptoms of dyslipidemia

By itself, dyslipidemia does not have its own symptoms, but it can lead to clinical symptoms of cardiovascular disease, including coronary artery disease and obliterating atherosclerosis of the vessels of the lower extremities. High triglyceride levels [> 1000 mg/dL (> 11.3 mmol/L)] may be a cause of acute pancreatitis.

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

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

Forms

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

Diagnosis of dyslipidemia

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

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

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

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

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

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

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

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

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

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

Treatment of dyslipidemia

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

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

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

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

Elevated LDL levels

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

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

The therapeutic approach includes lifestyle changes (including dietary and exercise needs), medications, nutritional supplements, physiotherapy and other treatments, and experimental therapies. Much of the above is also effective for the treatment of other lipid disorders. Sufficient physical activity has a direct direct effect on lowering LDL levels in some patients, which is also beneficial for ideal weight control.

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

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

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

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

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

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

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

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

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

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

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

Elevated triglyceride levels

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

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

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

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

Statins may be used in patients with triglyceride levels

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

Low HDL

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

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

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

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

Elevated lipoprotein levels (a)

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

How is secondary dyslipidemia treated?

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

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

Dyslipidemia Monitoring

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

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

Forecast

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