Causes of dyslipidemia, diagnosis and treatment

The pathological condition, which is provoked by changes in the concentration of triglycerides and lipoproteins in the blood, is called dyslipidemia or hyperlipidemia, hyperlipoproteinemia. You will learn about the clinic of the pathology, its affiliation with leptin, diagnosis and treatment from the article.


  1. General Information.
  2. Causes of dyslipidemia.
  3. Risk factors.
  4. Pathogenesis.
  5. Classification and symptoms.
  6. Complications.
  7. Diagnostics.
  8. Dislipidemia treatment.
  9. Prognosis and prevention.

General Information

Dyslipidemia translates as abnormal blood fat content and is found, according to statistics, in more than half of the adult population. In elderly people this figure reaches 80%. The disease has a gender tint: up to 50 years old men more often suffer from the pathology, after 50 (with the onset of menopause) the equilibrium is restored – 1:1. There is no seasonality, endemicity, racial preferences in lipid metabolism disorder.

Causes of dyslipidemia

Hyperlipidemia has many triggers; it is a polyethylological disease with several mechanisms of development. No single, main cause has been identified. Scientists believe that a combination of several exogenous and endogenous factors is necessary for the development of dyslipidemia.

The main ones include:

  1. Gene mutations with abnormal lipoprotein production: minimum of useful high-density lipids and maximum of harmful low-density lipids.
  2. A diet in which leptin, a hormone in adipose tissue that controls eating behavior, plays a key role. Increased lipid levels provoke excessive consumption of saturated fats. Especially dangerous are trans-isomers of fatty acids, with which ready-made foods are overloaded.
  3. Concomitant somatic and endocrine diseases: diabetes mellitus, CVD, biliary cirrhosis, hypothyroidism in women.
  4. Taking medications: diuretics, hypotensive drugs, hormones increase blood fat levels. Increase in cholesterol concentration occurs against the background of taking immunosuppressants, antiretroviral therapy.

Risk factors

Uncontrollable and controllable risk factors can accelerate the pathological process or provoke it:

  • age over 45;
  • male gender;
  • addiction to alcohol and cigarettes;
  • hypodynamia;
  • excess weight.


The main mechanism of dyslipidemia is genetically caused by an insufficient amount of low-density lipoproteins or an abnormal structure of their receptors. As a result, atherogenic lipids circulate in the bloodstream in large quantities. Another variant of dyslipidemia development is a disorder of liver enzyme systems, which influence the process of fat transformation. In case of diabetes it is non-enzymatic glycation of apolipoproteins, which prolongs the time of low and very low density lipoproteins in blood.

Classification and symptoms

Depending on the cause of the pathology, a distinction is made between primary or familial, genetically mediated dyslipidemia, and secondary, developed as a result of eating disorders, where leptin disorders become the key, as well as – caused by comorbidities. WHO proposes a division of hyperlipidemia according to phenotypes, taking into account laboratory data.

According to this gradation, a distinction is made between:

  1. I phenotype, which is accompanied by an increase in total cholesterol, triglycerides, excessive accumulation of transport fat molecules in the serum. Such dyslipidemia is often associated with alimentary factors, has low atherogenic potential and is affiliated with blindin resistance.
  2. Phenotype II has two subtypes, “a” and “b.” The first is typified by an isolated increase in low-density lipoproteins while triglycerides are normal. In the second, cholesterol and triglyceride levels increase, which puts the risk of coronary atherosclerosis formation.
  3. III phenotype is a rare variant of the pathology, in which the level of intermediate lipoproteins and triglycerides increases. Genetic abnormalities in hepatocyte receptors often accompany the process.
  4. IV phenotype is the most common (up to 40%). It increases the level of very low density lipoproteins, triglycerides against the background of normal total cholesterol. Atherogenicity is maximal.
  5. V phenotype is the rarest type, combining features of types I and IV. The pathology is not associated with the formation of atherosclerosis, but it is dangerous with the development of acute pancreatitis.

Dyslipidemia without cardiovascular pathology is asymptomatic.

High levels of lipoproteins guarantee their cumulation in tissues:

  1. On the eyelids – xanthelasma, dense yellowish, painless plaques that do not inflame, but gradually grow.
  2. On the skin of the hands, in the area of large joints, Achilles – tuberous xanthomas, hard nodules without pain, yellow in color, not changing shape when pressed.
  3. At dyslipidemia type III – yellowish palms.
  4. Eruptive xanthomas, fatty plaques with local inflammation and hyperemia are typical for combined forms of pathology.


Among the consequences of dyslipidemia, the most common is atherosclerosis. The highest risk occurs with an increase in low-density lipoproteins: a 1% increase increases the risk of CHD by 2-3%. In dyslipidemia, blood vessels are blocked by lipid plaques, and the rate of blood flow is inhibited. Another serious complication is myocardial infarction, stroke. In addition, visceral obesity, leptin and insulin resistance with the development of metabolic syndrome occur.


Since there are no symptoms of dyslipidemia as such, it is impossible to make a diagnosis without laboratory data. Screening of lipid levels is necessary for all patients at risk and at the first visit to the outpatient clinic of each new patient.

Diagnosis involves:

  1. Lipid profile is the basis of the diagnostic method, which clearly gives an idea of the amount of all lipid fractions. Dyslipidemia is diagnosed if the level of total cholesterol exceeds 6, 2 mmol/l, low-density lipids exceed 4.1 mmol/l, triglycerides exceed 2.3 mmol/l.
  2. Additional testing is performed to confirm the diabetic nature of dyslipidemia, determining the concentration of glucose and glycosylated hemoglobin. To exclude hyperlipidemia of other genesis liver tests, thyrotropic hormone level measurement, BMV are prescribed.
  3. Instrumental diagnostics: ECG, ECHO CG, coronarography.

Treatment of dyslipidemia

The approach to the correction of dyslipidemia is differentiated, taking into account the degree of impairment of lipid metabolism, organic changes in the blood vessels and heart. People without clinical symptoms are recommended to start therapy with a diet, most often a leptin diet. This involves minimizing fat to one-third of daily calories, a balance of saturated and unsaturated fats. Nonmedicamental measures make cholesterol decrease by 5-10%.

Medication correction with hypolipidemic agents is indicated in patients with cardiovascular pathology or with a high probability of their development according to the SCORE scale. Long-term, sometimes up to the end of the day, administration of drugs balancing blood lipids is recommended.

These are used for this purpose:

  1. Statins, which directly affect fat metabolism and have anti-inflammatory and vasodilatory effects. Taking these drugs prevents the development of CHF and reduces mortality from cardiac causes by one-third.
  2. Fibrates, which minimize triglyceride concentration, cause growth of atherogenic fractions of high-density lipoproteins, inhibit the progression of atherosclerosis of coronary vessels, reduce the risk of cardiovascular complications by more than 20%.
  3. Bile acid sequestrants, which are used to minimize the level of total cholesterol in the blood. Especially effective in combination with diet and other fat-lowering agents.
  4. Other drugs: nicotinic acid, polyunsaturated fatty acids, cholesterol absorption inhibitors are selected individually according to the severity of the pathology and the general condition of the patient.

Prognosis and prevention

Reasonable and adequate correction of dyslipidemia significantly reduces the risk of cardiovascular pathology and improves patients’ quality of life. The prognosis is always favorable if there is no dangerous concomitant pathology. Primary prevention is aimed at eliminating the underlying causes, the balance of leptin and ghrelin, the hormones that control satiety and hunger. Secondary – includes dispensary monitoring of the patient and prevention of complications.

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