Dyslipidemia, treatment of dyslipidemia in Moscow

Lipid metabolism disorders (dyslipidemia) affect the processes of absorption, transformation and metabolism of fats in the body. In addition to their energy function, fats are an important component of cell membranes, participate in the synthesis of hormones, transmit nerve impulses, and perform a host of other vital tasks. Therefore, a violation of lipid metabolism significantly affects the condition of the entire organism as a whole and can lead to the development of severe consequences.

Causes of dyslipidemia

Nutritional – eating large amounts of animal and vegetable fats. The norm is set individually for each person, the average is from 0.8 to 1 g. fat per kilogram of body weight per day.
Congenital disorders of lipid metabolism. They arise as a result of mutations in genes that are responsible for the processes of synthesis, breakdown, and transportation of fats. These mutations are passed on from generation to generation, so the disease can occur in young children for no apparent reason. Examples of genetic disorders of lipid metabolism are Gaucher disease, Tay-Sachs disease, and Niemann-Pick disease.
Secondary disorders of lipid metabolism. Caused by other diseases that can affect the gastrointestinal tract, endocrine and enzyme systems, various internal organs (liver, kidneys).

Among the provoking factors that increase the risk of developing lipid metabolism disorders are bad habits (smoking, alcohol abuse), a sedentary lifestyle, excess weight, chronic stress, and taking hormonal medications.

Symptoms, causes, diagnosis and treatment of lipid metabolism disorders

The increase in the content of fat-like substances - lipids - in the blood is influenced by three main factors: excess intake of fat into the body from food, impaired excretion and increased synthesis in the body.
Depending on the mechanism of development of the disease, the causes of dyslipidemia are different.

Pathology can be:

primary (due to hereditary factors);
secondary (as a result of complications of any diseases);
nutritional (if the human diet is oversaturated with animal fats).

An anomaly is often recognized after the fact, when problems with the cardiovascular system arise, since lipid metabolism disorders are most often asymptomatic. But in some patients, due to high levels of LDL, clouding of the cornea occurs, and xanthomas appear on the elbows and knees, and on the soles. With very high triglyceride levels (exceeding 11.3 mmol/l), pancreatitis develops and xanthomatous rashes are observed on the body.

Diet

Diet for vascular atherosclerosis

Efficacy: therapeutic effect after 2 months
Dates: no data
Cost of products: 1700-1800 rubles. in Week

DASH Diet

Efficacy: therapeutic effect after 21 days
Timing: constantly
Cost of products: 1700-1800 rubles. in Week

Patients are prescribed a diet low in fat, simple carbohydrates and an increased intake of dietary fiber up to 40 g. In the diet of patients, the amount of unsweetened fruits and vegetables with a low starch content, vegetable oils, beans, nuts, chickpeas, soybeans, fish, whole grain products, low-fat yoghurts At the same time, red meat, processed meats and salt are reduced. The traditional diet for hypercholesterolemia is the DASH and Mediterranean . These diets are effective in reducing cardiovascular disease factors. The Mediterranean diet includes olive oil or nuts.

When following this diet, there is a 30% decrease in cardiovascular diseases. Canola, flax, corn, olive and soybean oils reduce LDL cholesterol levels.

The main points of nutrition for patients are:

Avoiding consumption of trans fats.
Limiting saturated fats (only 7% of them are allowed in the diet).
Limiting the intake of cholesterol from food (less than 300 mg/day - one chicken egg covers the need for cholesterol).
Reducing the amount of carbohydrates, it is advisable to completely eliminate simple carbohydrates from the diet. Carbohydrates have a neutral effect on low-density lipoproteins, but excessive consumption of highly refined carbohydrates indirectly (via insulin) adversely affects triglycerides and low-density lipoproteins.
Reduce consumption of foods with cholesterol.
Increase in dietary fiber, which has a hypolipidemic effect. Soluble dietary fiber, which is found in fruits, vegetables, legumes, and whole grain cereals, is effective in this regard. Coarse plant fiber (cabbage, lettuce, carrots, grapefruits, apples, pears) partially adsorbs cholesterol and also prevents the absorption of fats.
Eating foods rich in phytosterols . Regular consumption of such foods reduces cholesterol levels by 10%. Phytosterols are found in corn, soybeans, lentils, peas, vegetable oils, beans, whole grains, pumpkin seeds, sesame seeds, pistachios, and walnuts.
Consuming omega-3 PUFAs.

Classification of lipid metabolism disorders

Today, the Fredrickson classification of dyslipidemias is considered the main one:

The cause of type 1 dyslipidemia is enzyme deficiency. Violations of this type are quite rare.
Dyslipidemia 2a occurs due to mutations in genes and is one of the most common types of lipid metabolism disorders.
Dyslipidemia 2b also occurs quite often and can be either hereditary or combined (the cause may be previous diseases and a diet oversaturated with animal fats).
Type 3 lipid metabolism disorders are characterized by an increase in triglycerides and LDL in the blood.
Type 4 hyperlipidemia, characterized by an increase in VLDL, is of endogenous origin.
Dyslipidemia type 5 occurs when the level of cholinomicrons in the blood increases and also refers to hereditary disorders.

Pathogenesis

Lipoproteins whose diameter is less than 70 nm pass through the vascular endothelium. ApoB-containing lipoproteins in the arterial wall become trapped and trigger a process whereby lipids are deposited in the wall. Low-density lipoproteins are oxidized and, together with monocytes, form the core of an atherosclerotic plaque. The active substances released during this process are involved in the proliferation of smooth muscle cells in blood vessels and the breakdown of collagen. In patients with high levels of apoB-containing lipoproteins, more particles are deposited, and the atherosclerotic plaque progresses faster. Over time, other particles are deposited in the vessel wall, and the atherosclerotic plaque, reaching a critical point, ruptures with the formation of a blood clot on the surface. It becomes the cause of blockage of the vessel with the development of angina or myocardial infarction .

Dyslipidemia develops with
insulin resistance .
Under conditions of increased insulin secretion with decreased tissue sensitivity to insulin, increased breakdown of fats into fatty acids occurs. The latter are delivered to the liver, where they produce low-density lipoprotein cholesterol. Dyslipidemia causes increased blood pressure. The role of very low-density and low-density lipoproteins in the development of vascular endothelial dysfunction has been proven, which causes disruption of the synthesis of nitric oxide and an increase in the production of the vasoconstrictor peptide endothelin-1. As a result, vasoconstriction occurs and systemic blood pressure increases. Primary hyperlipidemia type 1 is associated with a mutation in the lipoprotein lipase gene. A defect in this enzyme blocks the metabolism of chylomicrons and they accumulate in large quantities in the plasma. With reduced lipoprotein lipase activity, triglycerides are not broken down and severe triglyceridemia .

Diagnostic measures

Diagnostic procedures include a consultation with a physician, physical examination, medical history, and blood chemistry tests.

During a physical examination, the doctor notes the possible presence of xanthelasma, xanthomas, and lipoid arch of the cornea. Patients often experience high blood pressure. Auscultation (listening) and percussion (tapping) are not informative, since they are not accompanied by changes in dyslipidemia.

To identify inflammation and concomitant diseases, a laboratory test of blood and urine is prescribed. Genetic analysis identifies genes that carry hereditary information and are responsible for the development of type 2 dyslipidemia.

A biochemical blood test allows you to determine the level of total blood protein and sugar, uric acid and creatinine to detect concomitant organ damage. Immunological analysis determines the content of antibodies to cytomegalovirus and chlamydia, as well as the level of C-reactive protein.

But the main method for diagnosing dyslipidemia is a lipidogram - a blood test for fat-like substances, lipids. When measuring the lipid spectrum

The levels of triglycerides, total cholesterol, LDL and HDL are determined.

The studies are carried out on an empty stomach, in NEARMEDIC's own laboratory.

Treatment of dyslipidemia is prescribed after a complete diagnosis, accurate diagnosis and determination of the cause of the pathology.

Procedures and operations

Patients in whom drug treatment is ineffective undergo extracorporeal removal of low-density lipids. Most often, this method is used for familial hypercholesterolemia (homozygous and heterozygous). These are hardware methods based on plasma filtration and plasma sorption. Other types of techniques are also used: immunosorption, heparin precipitation, plasmapheresis. During the procedure, lipoproteins are precipitated and removed by membrane filtration, and the plasma is returned to the patient. There are diseases for which plasmapheresis is used as the first line of treatment, while for others it is used as the second line or in combination with other treatments.

Treatment of dyslipidemia

Treatment of dyslipidemia is complex and includes:

Drug therapy - fibrates, vitamins, statins and other drugs that correct lipid metabolism disorders;
Non-drug treatment - weight normalization through fractional meals, dosed physical activity, limiting alcohol and smoking, and stressful situations.
Diet therapy - foods rich in dietary fiber and vitamins are recommended (vegetables, cereals, fruits, beans, low-fat lactic acid products); fatty and fried meats are not allowed.

If lipid imbalance is a secondary pathology resulting from exposure to negative factors or any disease, NEARMEDIC cardiologists prescribe therapy aimed at timely detection and treatment of the underlying disease.

Dyslipidemia develops over years and requires equally long-term treatment. You can prevent further disturbances in lipid metabolism by strictly following the recommendations of doctors: move more, watch your weight, quit bad habits.

Contact your doctors on time!

In the early stages, stopping the pathological process is much easier. Timely therapy, elimination of risk factors and disciplined implementation of doctors’ recommendations significantly prolong and improve the lives of patients

Contact our clinics, do not delay your visit to the doctor. You will be consulted by experienced doctors, and you will undergo an expert examination using high-tech diagnostic equipment. Based on the results obtained, the cardiologist will prescribe competent treatment for dyslipidemia and recommend preventive measures.

To make an appointment with a cardiologist, call or fill out a request on the website.

List of sources

ESC/EAS 2021 recommendations for the treatment of dyslipidemia: modification of lipids to reduce cardiovascular risk/Russian Journal of Cardiology 2020; 25 (5), pp. 121-193.
Ershova A.I., Al Rashi D.O., Ivanova A.A., Aksenova Yu.O., Meshkov A.N. Secondary hyperlipidemia: etiology and pathogenesis. Russian Journal of Cardiology. 2019; (5): 74-81.
Diagnosis and correction of lipid metabolism disorders for the prevention and treatment of atherosclerosis. Russian recommendations VI revision. Atherosclerosis and dyslipidemia. 2017; 3 (28): 5-22.
Cronenberg G. M. et al. Obesity and lipid metabolism disorders / Trans. from English edited by I. I. Dedova, G. F. Melnichenko. M.: Read Elsiver LLC, 2010. 264 p.
Vizir V.A., Berezin A.E. Modern approaches to the treatment of hyperlipidemia/Zaporozhye Medical Journal. - 2011. - volume 13, no. 1, pp. 108-117.

Fatty degeneration

Diabetes

3735 10 September

IMPORTANT!

The information in this section cannot be used for self-diagnosis and self-treatment.
In case of pain or other exacerbation of the disease, diagnostic tests should be prescribed only by the attending physician. To make a diagnosis and properly prescribe treatment, you should contact your doctor. Fatty degeneration: causes, symptoms, diagnosis and treatment methods.

Definition

Fatty degeneration, or lipodystrophy, is a group of rare disorders that are characterized by complete or partial loss of subcutaneous fat, as well as its abnormal distribution, in the absence of a previous fasting or catabolic state. These diseases are accompanied by various metabolic disorders: insulin resistance, specific diabetes mellitus (lipoatrophic diabetes), fatty hepatosis, steatohepatitis, lipid metabolism disorders, arterial hypertension.

Fatty degenerations are quite rare conditions; according to various sources, their incidence ranges from 1 to 60 cases per 1 million population.
Causes of fatty degeneration
Fatty degenerations are divided into congenital and acquired. Congenital lipodystrophies are always hereditary and associated with genetic mutations that lead to metabolic disorders in adipose tissue, resulting in its atrophy.

The mechanism of development of acquired generalized lipodystrophy is unknown; the disease is assumed to be related to genetic mutations and autoimmune processes.

Genetic mutations are also suspected in the occurrence of acquired partial lipodystrophies. Today, the most common type of lipodystrophy is a special variant of acquired partial dystrophy - lipodystrophy, which develops as a result of highly active antiretroviral therapy in HIV-infected patients. In addition, there are local lipodystrophies, which are usually associated with injections of drugs, for example, insulin.

Classification of the disease

Fatty degenerations are divided according to the degree of fat loss into generalized, when subcutaneous fatty tissue is absent over most of the body, and partial, or segmental, when adipose tissue atrophies in certain areas of the body.

Hereditary and acquired lipodystrophies are divided into 4 types:

congenital generalized lipodystrophy (CHL, Berardinelli-Seyp syndrome) with 4 types depending on the gene in which the mutation occurred;
acquired generalized lipodystrophies (PGL, Lawrence syndrome);
familial partial lipodystrophy (FPL, Dunnigan-Cobberling syndrome) with 3 types;
acquired partial lipodystrophy (PPL, Barraquer-Simons syndrome).

Separately, there are fatty degenerations that develop as a result of other genetic syndromes and those associated with drug injections.
Symptoms of fatty degeneration
With congenital generalized lipodystrophy, immediately after birth or in the first year of life, the child develops a complete absence of subcutaneous fat. Lipoatrophy can occur on the trunk, limbs, and face. In severe cases of the disease, there is a significant risk of intrauterine growth retardation. Due to the lack of fatty tissue, the patient experiences pseudohypertrophy of skeletal muscles, as a result of which the patient has an “athletic” appearance (usually observed in children over 10 years of age). Patients with generalized lipodystrophy are tall (ahead of bone age), they may have an enlarged lower jaw, hands and feet, there is an enlargement of the clitoris in women and external genitalia in men, children have a very high appetite - they are “insatiable.” Due to the difficulty in digesting fats, the level of lipids (triglycerides, cholesterol) in the blood increases and the load on the organs involved in their metabolism increases. There is an abnormal accumulation of fat in the liver, kidneys, myocardium, and skeletal muscles, which disrupts their functions.

This type of lipodystrophy is characterized by severe fatty hepatosis, leading to liver enlargement, steatohepatitis, liver cirrhosis and liver failure.

Since metabolism is a balanced system, when lipid metabolism is disturbed, both protein and carbohydrate metabolism suffer. Disorders of carbohydrate metabolism lead to insulin resistance from the first years of life and to the development of type 2 diabetes mellitus by the age of 15-20 years. Such patients experience hyperpigmentation of the groin area, neck, armpits, weight loss, increased thirst, and excessive urination. Some forms of congenital generalized lipodystrophy are accompanied by damage not only to adipocytes (adipose tissue cells), but also to skeletal muscle cells and myocardium (heart muscle), which can lead to hypertrophic cardiomyopathy, heart failure and subsequently to an unfavorable outcome.

In addition, with this type of lipodystrophy, psychomotor retardation, intellectual impairment, hirsutism (excessive hair growth in women according to the male pattern - in the armpits, on the pubis, above the upper lip) or hypertrichosis (excessive hair growth in all areas of the body and head, not associated with the secretion of sex hormones). Due to the lack of subcutaneous fat, the veins of the upper and lower extremities bulge - this is called phlebomegaly. The characteristic appearance of the patient is a thin face against the backdrop of a developed figure, noticeable saphenous veins, increased size of the feet and hands, areas of hyperpigmentation (acanthosis nigricans) in the area of skin folds.

With acquired generalized lipodystrophy, a child is born with a normal amount of subcutaneous fatty tissue, and its degradation begins in childhood or adolescence and occurs gradually. Large areas of the body are affected, especially the face and extremities, including the palms and soles. In approximately a quarter of cases, patients with PGL are first diagnosed with panniculitis (inflammation of subcutaneous fat tissue), which manifests itself as local lipodystrophies. There are also PGL associated with autoimmune diseases (~25%) and idiopathic (~50%).

Familial partial lipodystrophies appear in childhood or adolescence. A progressive loss of adipose tissue begins in the chest, anterior abdominal wall and limbs with its redistribution to other areas - the face, neck and inside the abdominal cavity. This redistribution of subcutaneous fat may resemble Cushing's syndrome or create a false impression of an “athletic” physique in women. In men, the redistribution of adipose tissue and the expression of skeletal muscles are often perceived as a normal physique. Metabolic disorders develop after puberty and are more severe in women.

SPF is characterized by insulin resistance, a significant increase in the concentration of free fatty acids and triglycerides in the blood, accumulation of fat in skeletal muscle cells and hepatocytes, and impaired leptin secretion.

Patients have a high risk of developing diabetes mellitus and insulin resistance, dyslipidemia, mainly due to increased triglyceride levels, pancreatitis, liver steatosis, hyperpigmentation in skin folds (this symptom is less pronounced than with VHL), arterial hypertension. In rare cases, myopathies and cardiomyopathies may develop, as well as hirsutism, menstrual irregularities and polycystic ovary syndrome, however, in most patients, reproductive function remains intact.

Acquired partial lipodystrophy is characterized by a progressive loss of subcutaneous fat in the upper body - in the face, neck, chest, upper extremities, and epigastric region.

This process can begin at any age, lasts from several months to several years and moves from top to bottom from the head to the feet, but, as a rule, does not affect the lower limbs. On the contrary, some patients may develop excess accumulation of fatty tissue in the lower abdomen, buttocks and thighs. Metabolic disorders are less common than in other types of fatty degeneration, but PPL is associated with the development of chronic kidney disease.

Diagnosis of fatty degeneration

When collecting complaints and anamnesis, the doctor pays attention to the patient’s appearance, and also studies the family history of the disease to identify the nature of its inheritance.

From laboratory examinations the patient is given:

general blood analysis;