Pyruvic acid in the blood
Clinical diagnostic value research
Normal: 0.05-0.10 mmol/l in the blood serum of adults.
Contents of the PVK increases in hypoxic conditions caused by severe cardiovascular, pulmonary, cardiorespiratory failure, anemia, malignant neoplasms, acute hepatitis and other liver diseases (most pronounced in the terminal stages of liver cirrhosis), toxicosis, insulin-dependent diabetes mellitus, diabetic ketoacidosis, respiratory alkalosis, uremia, hepatocerebral dystrophy, hyperfunction of the pituitary-adrenal and sympathetic-adrenal systems, as well as the administration of camphor, strychnine, adrenaline and during heavy physical exertion, tetany, convulsions (with epilepsy).
Clinical and diagnostic value of determining the content of lactic acid in the blood
Lactic acid(MK) is the end product of glycolysis and glycogenolysis. A significant amount of it is formed in muscles. From muscle tissue MK travels through the bloodstream to the liver, where it is used for glycogen synthesis. In addition, part of the lactic acid from the blood is absorbed by the heart muscle, which utilizes it as an energy material.
SUA level in blood increases in hypoxic conditions, acute purulent inflammatory tissue damage, acute hepatitis, liver cirrhosis, renal failure, malignant neoplasms, diabetes mellitus (approximately 50% of patients), mild degree uremia, infections (especially pyelonephritis), acute septic endocarditis, poliomyelitis, serious illnesses blood vessels, leukemia, intense and prolonged muscle stress, epilepsy, tetany, tetanus, convulsive states, hyperventilation, pregnancy (in the third trimester).
Lipids - varied in chemical structure substances that have a number of common physical, physicochemical and biological properties. They are characterized by the ability to dissolve in ether, chloroform, other fatty solvents and only slightly (and not always) in water, and also form, together with proteins and carbohydrates, the main structural component of living cells. The inherent properties of lipids are determined by characteristic features the structures of their molecules.
The role of lipids in the body is very diverse. Some of them serve as a form of deposition (triacylglycerols, TG) and transport (free fatty acid-FFA) substances, the breakdown of which releases a large amount of energy, others are the most important structural components cell membranes(free cholesterol and phospholipids). Lipids are involved in the processes of thermoregulation, protecting vital organs (for example, kidneys) from mechanical stress (injury), protein loss, creating elasticity of the skin, and protecting them from excessive moisture removal.
Some of the lipids are biologically active substances that have the properties of modulators of hormonal effects (prostaglandins) and vitamins (polyunsaturated fatty acids). Moreover, lipids promote the absorption of fat-soluble vitamins A, D, E, K; act as antioxidants ( vitamins A, E), largely regulating the process of free radical oxidation of physiologically important compounds; determine the permeability of cell membranes to ions and organic compounds.
Lipids serve as precursors for a number of steroids with pronounced biological effects - bile acids, vitamins D, sex hormones, and adrenal hormones.
The concept of “total lipids” in plasma includes neutral fats (triacylglycerols), their phosphorylated derivatives (phospholipids), free and ester-bound cholesterol, glycolipids, and non-esterified (free) fatty acids.
Clinical and diagnostic value of determining the level of total lipids in blood plasma (serum)
The norm is 4.0-8.0 g/l.
Hyperlipidemia (hyperlipemia) – an increase in the concentration of total plasma lipids as a physiological phenomenon can be observed 1.5 hours after a meal. Nutritional hyperlipemia is more pronounced, the lower the level of lipids in the patient’s blood on an empty stomach.
The concentration of lipids in the blood changes under a number of pathological conditions. Thus, in patients with diabetes mellitus, along with hyperglycemia, pronounced hyperlipemia is observed (often up to 10.0-20.0 g/l). With nephrotic syndrome, especially lipoid nephrosis, the content of lipids in the blood can reach even higher numbers - 10.0-50.0 g/l.
Hyperlipemia – constant phenomenon in patients with biliary cirrhosis and in patients with acute hepatitis (especially in the icteric period). Elevated levels of lipids in the blood are usually found in individuals suffering from acute or chronic nephritis, especially if the disease is accompanied by edema (due to the accumulation of LDL and VLDL in the plasma).
The pathophysiological mechanisms that cause changes in the content of all fractions of total lipids, to a greater or lesser extent, determine a pronounced change in the concentration of its constituent subfractions: cholesterol, total phospholipids and triacylglycerols.
Clinical and diagnostic significance of the study of cholesterol (CH) in blood serum (plasma)
A study of cholesterol levels in blood serum (plasma) does not provide accurate diagnostic information about a specific disease, but only reflects the pathology of lipid metabolism in the body.
According to epidemiological studies, the upper level of cholesterol in the blood plasma is almost healthy people at the age of 20-29 years it is 5.17 mmol/l.
In blood plasma, cholesterol is found mainly in LDL and VLDL, with 60-70% of it in the form of esters (bound cholesterol), and 30-40% in the form of free, non-esterified cholesterol. Bound and free cholesterol make up the total cholesterol.
A high risk of developing coronary atherosclerosis in people aged 30-39 and over 40 years old occurs when cholesterol levels exceed 5.20 and 5.70 mmol/l, respectively.
Hypercholesterolemia is the most proven risk factor for coronary atherosclerosis. This has been confirmed by numerous epidemiological and clinical studies who established a connection between hypercholesterolemia and coronary atherosclerosis, the incidence of coronary artery disease and myocardial infarction.
The highest level of cholesterol is observed with genetic disorders in lipid metabolism: familial homo-heterozygous hypercholesterolemia, familial combined hyperlipidemia, polygenic hypercholesterolemia.
In a number of pathological conditions, secondary hypercholesterolemia develops . It is observed in liver diseases, kidney damage, malignant tumors of the pancreas and prostate, gout, ischemic heart disease, acute heart attack myocardium, hypertension, endocrine disorders, chronic alcoholism, glycogenosis type I, obesity (in 50-80% of cases).
A decrease in plasma cholesterol levels is observed in patients with malnutrition, with damage to the central nervous system, mental retardation, chronic failure of cardio-vascular system, cachexia, hyperthyroidism, acute infectious diseases, acute pancreatitis, acute purulent-inflammatory processes in soft tissues, febrile conditions, pulmonary tuberculosis, pneumonia, respiratory sarcoidosis, bronchitis, anemia, hemolytic jaundice, acute hepatitis, malignant liver tumors, rheumatism.
Determination of the fractional composition of cholesterol in blood plasma and its individual lipids (primarily HDL) has acquired great diagnostic significance for judging the functional state of the liver. According to modern concepts, the esterification of free cholesterol into HDL occurs in the blood plasma thanks to the enzyme lecithin-cholesterol acyltransferase, which is formed in the liver (this is an organ-specific liver enzyme). The activator of this enzyme is one of the main components of HDL - apo-Al, which is constantly synthesized in the liver.
A nonspecific activator of the plasma cholesterol esterification system is albumin, also produced by hepatocytes. This process primarily reflects functional state liver. If normally the coefficient of cholesterol esterification (i.e. the ratio of the content of ether-bound cholesterol to total) is 0.6-0.8 (or 60-80%), then with acute hepatitis, exacerbation chronic hepatitis, liver cirrhosis, obstructive jaundice, as well as chronic alcoholism, it decreases. A sharp decrease in the severity of the cholesterol esterification process indicates insufficiency of liver function.
Clinical and diagnostic significance of studying the concentration of total phospholipids in blood serum.
Phospholipids (PL) are a group of lipids containing, in addition to phosphoric acid (as an essential component), alcohol (usually glycerol), fatty acid residues and nitrogenous bases. Depending on the nature of the alcohol, PLs are divided into phosphoglycerides, phosphosphingosines and phosphoinositides.
The level of total PL (lipid phosphorus) in blood serum (plasma) increases in patients with primary and secondary hyperlipoproteinemia types IIa and IIb. This increase is most pronounced in glycogenosis type I, cholestasis, obstructive jaundice, alcoholic and biliary cirrhosis, viral hepatitis(mild), renal coma, posthemorrhagic anemia, chronic pancreatitis, severe diabetes mellitus, nephrotic syndrome.
To diagnose a number of diseases, it is more informative to study the fractional composition of serum phospholipids. To this end, in last years Lipid thin layer chromatography methods are widely used.
Composition and properties of blood plasma lipoproteins
Almost all plasma lipids are bound to proteins, which makes them highly soluble in water. These lipid-protein complexes are commonly referred to as lipoproteins.
According to modern concepts, lipoproteins are high-molecular water-soluble particles, which are complexes of proteins (apoproteins) and lipids formed by weak, non-covalent bonds, in which polar lipids (PL, CXC) and proteins (“apo”) form a surface hydrophilic monomolecular layer surrounding and protecting the internal phase (consisting mainly of ECS, TG) from water.
In other words, lipids are peculiar globules, inside of which there is a fat droplet, a core (formed predominantly by non-polar compounds, mainly triacylglycerols and cholesterol esters), delimited from water by a surface layer of protein, phospholipids and free cholesterol.
The physical characteristics of lipoproteins (their size, molecular weight, density), as well as the manifestations of physicochemical, chemical and biological properties, largely depend, on the one hand, on the ratio between the protein and lipid components of these particles, on the other hand, on the composition of the protein and lipid components, i.e. their nature.
The largest particles, consisting of 98% lipids and a very small (about 2%) proportion of protein, are chylomicrons (CM). They are formed in the cells of the mucous membrane small intestine and are a transport form for neutral dietary fats, i.e. exogenous TG.
Table 7.3 Composition and some properties of serum lipoproteins (Komarov F.I., Korovkin B.F., 2000)
| Criteria for assessing individual classes of lipoproteins | HDL (alpha-LP) | LDL (beta-LP) | VLDL (pre-beta-LP) | HM |
| Density, kg/l | 1,063-1,21 | 1,01-1,063 | 1,01-0,93 | 0,93 |
| Molecular weight of drug, kD | 180-380 | 3000- 128 000 | - | |
| Particle sizes, nm | 7,0-13,0 | 15,0-28,0 | 30,0-70,0 | 500,0 - 800,0 |
| Total proteins, % | 50-57 | 21-22 | 5-12 | |
| Total lipids, % | 43-50 | 78-79 | 88-95 | |
| Free cholesterol, % | 2-3 | 8-10 | 3-5 | |
| Esterified cholesterol, % | 19-20 | 36-37 | 10-13 | 4-5 |
| Phospholipids, % | 22-24 | 20-22 | 13-20 | 4-7 |
| Triacylglycerols,% | ||||
| 4-8 | 11-12 | 50-60 | 84-87 |
If exogenous TGs are transported into the blood by chylomicrons, then the transport form endogenous triglycerides are VLDL. Their formation is a protective reaction of the body aimed at preventing fatty infiltration, and subsequently liver degeneration.
The size of VLDL is on average 10 times smaller than the size of CM (individual VLDL particles are 30-40 times smaller than CM particles). They contain 90% of lipids, of which more than half are TG. 10% of total plasma cholesterol is carried by VLDL. Due to the content of a large amount of TG, VLDL shows insignificant density (less than 1.0). Determined that LDL and VLDL contain 2/3 (60%) of total cholesterol plasma, while 1/3 is HDL.
HDL– the densest lipid-protein complexes, since the protein content in them is about 50% of the mass of the particles. Their lipid component consists half of phospholipids, half of cholesterol, mainly ether-bound. HDL is also constantly formed in the liver and partly in the intestines, as well as in the blood plasma as a result of the “degradation” of VLDL.
If LDL and VLDL deliver Cholesterol from the liver to other tissues(peripheral), including vascular wall, That HDL transports cholesterol from cell membranes (primarily the vascular wall) to the liver. In the liver it goes to the formation of bile acids. In accordance with this participation in cholesterol metabolism, VLDL and themselves LDL are called atherogenic, A HDL– antiatherogenic drugs. Atherogenicity refers to the ability of lipid-protein complexes to introduce (transmit) free cholesterol contained in the drug into tissues.
HDL competes with LDL for cell membrane receptors, thereby counteracting the utilization of atherogenic lipoproteins. Since the surface monolayer of HDL contains a large amount of phospholipids, at the point of contact of the particle with the outer membrane of the endothelial, smooth muscle and any other cell, favorable conditions are created for the transfer of excess free cholesterol to HDL.
However, the latter remains in the surface HDL monolayer only for a very short time, since it undergoes esterification with the participation of the LCAT enzyme. The formed ECS, being a nonpolar substance, moves into the internal lipid phase, releasing vacancies to repeat the act of capturing a new ECS molecule from the cell membrane. From here: the higher the activity of LCAT, the more effective the antiatherogenic effect of HDL, which are considered as LCAT activators.
If the balance is disturbed between the processes of the influx of lipids (cholesterol) into the vascular wall and their outflow from it, conditions can be created for the formation of lipoidosis, the most famous manifestation of which is atherosclerosis.
In accordance with the ABC nomenclature of lipoproteins, primary and secondary lipoproteins are distinguished. Primary LPs are formed by any apoprotein of one chemical nature. These can conditionally include LDL, which contains about 95% apoprotein B. All others are secondary lipoproteins, which are associated complexes of apoproteins.
Normally, approximately 70% of plasma cholesterol is found in “atherogenic” LDL and VLDL, while about 30% circulates in “antiatherogenic” HDL. With this ratio in vascular wall(and other tissues) a balance is maintained between the rates of inflow and outflow of cholesterol. This determines the numerical value cholesterol ratio atherogenicity, component with the indicated lipoprotein distribution of total cholesterol 2,33 (70/30).
According to the results of mass epidemiological observations, at a concentration of total cholesterol in plasma of 5.2 mmol/l, a zero balance of cholesterol in the vascular wall is maintained. An increase in the level of total cholesterol in the blood plasma of more than 5.2 mmol/l leads to its gradual deposition in the vessels, and at a concentration of 4.16-4.68 mmol/l a negative cholesterol balance is observed in the vascular wall. The level of total cholesterol in blood plasma (serum) exceeding 5.2 mmol/l is considered pathological.
Table 7.4 Scale for assessing the likelihood of developing coronary artery disease and other manifestations of atherosclerosis
(Komarov F.I., Korovkin B.F., 2000)
– a group of substances that are heterogeneous in chemical structure and physical and chemical properties. In blood serum they are represented mainly by fatty acids, triglycerides, cholesterol and phospholipids.
Triglycerides are the main form of lipid storage in adipose tissue and lipid transport in the blood. A study of triglyceride levels is necessary to determine the type of hyperlipoproteinemia and assess the risk of developing cardiovascular diseases.
Cholesterol performs the most important functions: it is part of cell membranes, is a precursor of bile acids, steroid hormones and vitamin D, and acts as an antioxidant. About 10% of the Russian population have high blood cholesterol levels. This condition is asymptomatic and can lead to serious diseases (atherosclerotic vascular disease, coronary heart disease).
Lipids are insoluble in water, so they are transported by blood serum in combination with proteins. Lipid+protein complexes are called lipoproteins. And proteins that are involved in lipid transport are called apoproteins.
Several classes are present in blood serum lipoproteins: chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL).
Each lipoprotein fraction has its own function. synthesized in the liver and transport mainly triglycerides. playing important role in atherogenesis. Low-density lipoproteins (LDL) rich in cholesterol, deliver cholesterol to peripheral tissues. Levels of VLDL and LDL promote the deposition of cholesterol in the vascular wall and are considered atherogenic factors. High density lipoproteins (HDL) participate in the reverse transport of cholesterol from tissues, taking it away from overloaded tissue cells and transferring it to the liver, which “utilizes” it and removes it from the body. High HDL level is considered as an antiatherogenic factor (protects the body from atherosclerosis).
The role of cholesterol and the risk of developing atherosclerosis depends on which lipoprotein fractions it is included in. To assess the ratio of atherogenic and antiatherogenic lipoproteins, it is used atherogenic index.
Apolipoproteins- These are proteins that are located on the surface of lipoproteins.
Apolipoprotein A (ApoA protein) is the main protein component of lipoproteins (HDL), which transports cholesterol from peripheral tissue cells to the liver.
Apolipoprotein B (ApoB protein) is part of lipoproteins that transport lipids to peripheral tissues.
Measuring the concentration of apolipoprotein A and apolipoprotein B in blood serum provides the most accurate and unambiguous determination of the ratio of atherogenic and antiatherogenic properties of lipoproteins, which is assessed as the risk of developing atherosclerotic vascular lesions and coronary heart disease over the next five years.
To the study lipid profile includes the following indicators: cholesterol, triglycerides, VLDL, LDL, HDL, atherogenicity coefficient, cholesterol/triglycerides ratio, glucose. This profile provides complete information about lipid metabolism, allows you to determine the risks of developing atherosclerotic vascular lesions, coronary heart disease, identify the presence of dyslipoproteinemia and type it, and, if necessary, choose the right lipid-lowering therapy.
Indications
Increased concentrationcholesterol has diagnostic value for primary familial hyperlipidemia (hereditary forms of the disease); pregnancy, hypothyroidism, nephrotic syndrome, obstructive liver diseases, pancreatic diseases ( chronic pancreatitis, malignant neoplasms), diabetes mellitus.
Decreased concentrationcholesterol has diagnostic value for liver diseases (cirrhosis, hepatitis), starvation, sepsis, hyperthyroidism, megaloblastic anemia.
Increased concentrationtriglycerides has diagnostic value for primary hyperlipidemia (hereditary forms of the disease); obesity, excessive consumption carbohydrates, alcoholism, diabetes mellitus, hypothyroidism, nephrotic syndrome, chronic renal failure, gout, acute and chronic pancreatitis.
Decreased concentrationtriglycerides has diagnostic value for hypolipoproteinemia, hyperthyroidism, malabsorption syndrome.
Very low density lipoproteins (VLDL) used to diagnose dyslipidemia (types IIb, III, IV and V). High concentrations of VLDL in the blood serum indirectly reflect the atherogenic properties of the serum.
Increased concentrationlow density lipoprotein (LDL) has diagnostic value for primary hypercholesterolemia, dislipoproteinemia (types IIa and IIb); for obesity, obstructive jaundice, nephrotic syndrome, diabetes mellitus, hypothyroidism. Determination of LDL level is necessary for prescribing long-term treatment, the purpose of which is to reduce lipid concentrations.
Increased concentration has diagnostic value for liver cirrhosis and alcoholism.
Decreased concentrationhigh density lipoprotein (HDL) has diagnostic value for hypertriglyceridemia, atherosclerosis, nephrotic syndrome, diabetes mellitus, acute infections, obesity, smoking.
Level determination apolipoprotein A indicated for early assessment of the risk of coronary heart disease; identifying patients with a hereditary predisposition to atherosclerosis at a relatively young age; monitoring treatment with lipid-lowering drugs.
Increased concentrationapolipoprotein A has diagnostic value for liver diseases and pregnancy.
Decreased concentrationapolipoprotein A has diagnostic value for nephrotic syndrome, chronic renal failure, triglyceridemia, cholestasis, sepsis.
Diagnostic valueapolipoprotein B- the most accurate indicator of the risk of developing cardiovascular diseases, is also the most adequate indicator of the effectiveness of statin therapy.
Increased concentrationapolipoprotein B has diagnostic value for dyslipoproteinemia (IIa, IIb, IV and V types), coronary heart disease, diabetes mellitus, hypothyroidism, nephrotic syndrome, liver diseases, Itsenko-Cushing syndrome, porphyria.
Decreased concentrationapolipoprotein B has diagnostic value for hyperthyroidism, malabsorption syndrome, chronic anemia, inflammatory joint diseases, myeloma.
Methodology
The determination is carried out on the “Architect 8000” biochemical analyzer.
Preparation
to study the lipid profile (cholesterol, triglycerides, HDL-C, LDL-C, Apo-proteins of lipoproteins (Apo A1 and Apo-B)
It is necessary to refrain from physical activity, drinking alcohol, smoking and medicines, dietary changes for at least two weeks before blood collection.
Blood is taken only on an empty stomach, 12-14 hours after the last meal.
Preferably morning reception drugs after taking blood (if possible).
The following procedures should not be performed before donating blood: injections, punctures, general body massage, endoscopy, biopsy, ECG, X-ray examination, especially with the introduction of a contrast agent, dialysis.
If there was still minor physical activity, you need to rest for at least 15 minutes before donating blood.
Lipid testing is not performed when infectious diseases, since there is a decrease in the level of total cholesterol and HDL-C, regardless of the type of infectious agent or the clinical condition of the patient. The lipid profile should only be checked after full recovery patient.
It is very important that these recommendations are strictly followed, since only in this case will reliable blood test results be obtained.
Determination of blood lipid profile indicators is necessary for the diagnosis, treatment and prevention of cardiovascular diseases. The most important mechanism for the development of such a pathology is considered to be the formation on the inner wall of blood vessels. atherosclerotic plaques. Plaques are accumulations of fat-containing compounds (cholesterol and triglycerides) and fibrin. The higher the concentration of lipids in the blood, the more likely the occurrence of atherosclerosis. Therefore, it is necessary to systematically take a blood test for lipids (lipidogram), this will help to promptly identify deviations in fat metabolism from the norm.
Lipidogram - a study that determines the level of lipids of various fractions
Atherosclerosis is dangerous due to the high probability of developing complications - stroke, myocardial infarction, gangrene of the lower extremities. These diseases often result in disability of the patient, and in some cases, death.
The role of lipids
Functions of lipids:
- Structural. Glycolipids, phospholipids, cholesterol are the most important components of cell membranes.
- Thermal insulation and protective. Excess fat is deposited in subcutaneous fat, reducing heat loss and protecting internal organs. If necessary, the lipid supply is used by the body to obtain energy and simple compounds.
- Regulatory. Cholesterol is necessary for the synthesis of adrenal steroid hormones, sex hormones, vitamin D, bile acids, is part of the myelin sheaths of the brain, and is needed for the normal functioning of serotonin receptors.
Lipidogram
A lipidogram can be prescribed by a doctor both if an existing pathology is suspected, and for preventive purposes, for example, during a medical examination. It includes several indicators that allow you to fully assess the state of fat metabolism in the body.
Lipid profile indicators:
- Total cholesterol (TC). This the most important indicator lipid spectrum blood, includes free cholesterol, as well as cholesterol contained in lipoproteins and associated with fatty acids. A significant portion of cholesterol is synthesized by the liver, intestines, and gonads; only 1/5 of the TC comes from food. With normally functioning mechanisms of lipid metabolism, a slight deficiency or excess of cholesterol supplied from food is compensated by an increase or decrease in its synthesis in the body. Therefore, hypercholesterolemia is most often caused not by excess cholesterol intake from foods, but by a failure of the fat metabolism process.
- High density lipoproteins (HDL). This indicator has an inverse relationship with the likelihood of developing atherosclerosis - an increased level of HDL is considered an anti-atherogenic factor. HDL transports cholesterol to the liver, where it is utilized. Women have higher HDL levels than men.
- Low density lipoproteins (LDL). LDL carries cholesterol from the liver to tissues, otherwise known as “bad” cholesterol. This is due to the fact that LDL is capable of forming atherosclerotic plaques, narrowing the lumen of blood vessels.
This is what an LDL particle looks like
- Very low density lipoproteins (VLDL). The main function of this group of particles, heterogeneous in size and composition, is the transport of triglycerides from the liver to tissues. A high concentration of VLDL in the blood leads to clouding of the serum (chylosis), and the possibility of the appearance of atherosclerotic plaques also increases, especially in patients with diabetes mellitus and kidney pathologies.
- Triglycerides (TG). Like cholesterol, triglycerides are transported through the bloodstream as part of lipoproteins. Therefore, an increase in the concentration of TG in the blood is always accompanied by an increase in cholesterol levels. Triglycerides are considered the main source of energy for cells.
- Atherogenic coefficient. It allows you to assess the risk of developing vascular pathology and is a kind of summary of the lipid profile. To determine the indicator, you need to know the value of TC and HDL.
Atherogenic coefficient = (TC - HDL)/HDL
Optimal blood lipid profile values
| Floor | Indicator, mmol/l | |||||
| OH | HDL | LDL | VLDL | TG | CA | |
| Male | 3,21 — 6,32 | 0,78 — 1,63 | 1,71 — 4,27 | 0,26 — 1,4 | 0,5 — 2,81 | 2,2 — 3,5 |
| Female | 3,16 — 5,75 | 0,85 — 2,15 | 1,48 — 4,25 | 0,41 — 1,63 | ||
It should be taken into account that the value of the measured indicators may vary depending on the units of measurement and the analysis methodology. Normal values also vary depending on the age of the patient; the above figures are averaged for persons 20 - 30 years old. The level of cholesterol and LDL in men after 30 years tends to increase. In women, indicators increase sharply with the onset of menopause, this is due to the cessation of the antiatherogenic activity of the ovaries. The interpretation of the lipid profile must be carried out by a specialist, taking into account the individual characteristics of the person.
A study of blood lipid levels may be prescribed by a doctor to diagnose dyslipidemia, assess the likelihood of developing atherosclerosis, and in some cases chronic diseases(diabetes mellitus, kidney and liver diseases, thyroid gland), and also as a screening test for early detection persons with lipid profile deviations from the norm.
The doctor gives the patient a referral for a lipid profile
Preparing for the study
Lipid profile values can fluctuate not only depending on the gender and age of the subject, but also on the impact on the body of various external and internal factors. To minimize the likelihood unreliable result, you must adhere to several rules:
- You should donate blood strictly in the morning on an empty stomach; in the evening of the previous day, a light dietary dinner is recommended.
- Do not smoke or drink alcohol the night before the test.
- Avoid 2-3 days before donating blood stressful situations and intense physical activity.
- Stop using all medications and dietary supplements except those that are vital.
Methodology
There are several methods for laboratory assessment of lipid profiles. In medical laboratories, analysis can be carried out manually or using automatic analyzers. The advantage of an automated measurement system is the minimal risk of erroneous results, speed of analysis, and high accuracy of the study.
The analysis requires the patient's venous blood serum. Blood is drawn into vacuum tube using a syringe or vacutainer. To avoid clot formation, the blood tube should be inverted several times and then centrifuged to obtain serum. The sample can be stored in the refrigerator for 5 days.
Taking blood for lipid profile
Nowadays, blood lipids can be measured without leaving home. To do this, you need to purchase a portable biochemical analyzer that allows you to assess the level of total cholesterol in the blood or several indicators at once in a matter of minutes. For the test, a drop of capillary blood is needed; it is applied to the test strip. The test strip is impregnated with a special composition, for each indicator it is different. The results are read automatically after inserting the strip into the device. Thanks to the small size of the analyzer and the ability to operate on batteries, it is convenient to use at home and take with you on a trip. Therefore, persons with a predisposition to cardiovascular diseases It is recommended to have it at home.
Interpretation of results
The most ideal result of the analysis for the patient will be a laboratory conclusion that there are no deviations from the norm. In this case, a person need not fear for the condition of his circulatory system- the risk of atherosclerosis is practically absent.
Unfortunately, this is not always the case. Sometimes the doctor, after reviewing the laboratory data, makes a conclusion about the presence of hypercholesterolemia. What it is? Hypercholesterolemia - an increase in the concentration of total cholesterol in the blood above normal values, with high risk development of atherosclerosis and related diseases. This condition may be due to a number of reasons:
- Heredity. Science knows cases of familial hypercholesterolemia (FH), in such a situation the defective gene responsible for lipid metabolism is inherited. Patients experience constantly elevated levels of TC and LDL; the disease is especially severe in the homozygous form of FH. Such patients have an early onset of coronary artery disease (at the age of 5-10 years); in the absence of proper treatment, the prognosis is unfavorable and in most cases ends in death before reaching 30 years of age.
- Chronic diseases. Elevated cholesterol levels are observed in diabetes mellitus, hypothyroidism, kidney and liver pathologies, and are caused by lipid metabolism disorders due to these diseases.
For patients suffering from diabetes, it is important to constantly monitor cholesterol levels
- Poor nutrition. Long-term abuse of fast food, fatty, salty foods leads to obesity, and, as a rule, there is a deviation in lipid levels from the norm.
- Bad habits. Alcoholism and smoking lead to disruptions in the mechanism of fat metabolism, as a result of which lipid profile indicators increase.
With hypercholesterolemia, it is necessary to adhere to a diet with limited fat and salt, but in no case should you completely abandon all foods rich in cholesterol. Only mayonnaise, fast food and all products containing trans fats should be excluded from the diet. But eggs, cheese, meat, sour cream must be present on the table, you just need to choose products with a lower percentage of fat content. Also important in the diet is the presence of greens, vegetables, cereals, nuts, and seafood. The vitamins and minerals they contain perfectly help stabilize lipid metabolism.
An important condition for normalizing cholesterol is also avoiding bad habits. Constant physical activity is also beneficial for the body.
In case if healthy image life in combination with diet did not lead to a decrease in cholesterol, it is necessary to prescribe appropriate drug treatment.
Drug treatment of hypercholesterolemia includes the prescription of statins
Sometimes specialists are faced with a decrease in cholesterol levels - hypocholesterolemia. Most often, this condition is caused by insufficient intake of cholesterol from food. Fat deficiency is especially dangerous for children; in such a situation, there will be a lag in physical and mental development, cholesterol is vital for a growing body. In adults, hypocholesteremia leads to disorders emotional state due to malfunctions of the nervous system, problems with reproductive function, decreased immunity, etc.
Changes in the blood lipid profile inevitably affect the functioning of the entire body as a whole, so it is important to systematically monitor fat metabolism indicators for timely treatment and prevention.
Lipids are called fats that enter the body with food and are formed in the liver. Blood (plasma or serum) contains 3 main classes of lipids: triglycerides (TG), cholesterol (CS) and its esters, phospholipids (PL).
Lipids are able to attract water, but most of them do not dissolve in the blood. They are transported in a protein-bound state (in the form of lipoproteins or, in other words, lipoproteins). Lipoproteins differ not only in composition, but also in size and density, but their structure is almost the same. central part(core) is represented by cholesterol and its esters, fatty acids, triglycerides. The shell of the molecule consists of proteins (apoproteins) and water-soluble lipids (phospholipids and non-esterified cholesterol). The outer part of apoproteins is capable of forming hydrogen bonds with water molecules. Thus, lipoproteins can be partially dissolved in fats and partially in water.
Chylomicrons, after entering the blood, break down into glycerol and fatty acids, resulting in the formation of lipoproteins. Cholesterol-containing chylomicron residues are processed in the liver.
Cholesterol and triglycerides are formed in the liver into very low-density lipoproteins (VLDL), which release some of the triglycerides to peripheral tissues, while the remainder goes back to the liver and is converted into low-density lipoproteins (LDL).
L PN II are transporters of cholesterol for peripheral tissues, which is used to build cell membranes and metabolic reactions. In this case, non-esterified cholesterol enters the blood plasma and binds to high-density lipoproteins (HDL). Esterified cholesterol (bound to esters) is converted into VLDL. Then the cycle repeats.
The blood also contains intermediate density lipoproteins (IDL), which are remnants of chylomicrons and VLDL and contain large amounts of cholesterol. DILI in liver cells with the participation of lipase are converted into LDL.
Blood plasma contains 3.5-8 g/l of lipids. An increase in blood lipid levels is called hyperlipidemia, and a decrease is called hypolipidemia. The indicator of total blood lipids does not provide a detailed picture of the state of fat metabolism in the body.
Quantitative determination of specific lipids is of diagnostic importance. The lipid composition of blood plasma is presented in the table.
Lipid composition of blood plasma
| Lipid fraction | Normal indicator | |
| General lipids | 4.6-10.4 mmol/l | |
| Phospholipids | 1.95-4.9 mmol/l | |
| Lipid phosphorus | 1.97-4.68 mmol/l | |
| Neutral fats | 0-200 mg% | |
| Triglycerides | 0.565-1.695 mmol/l (serum) | |
| Non-esterified fatty acids | 400-800 mmol/l | |
| Free fatty acids | 0.3-0.8 µmol/l | |
| Total cholesterol (there are age-specific norms) | 3.9-6.5 mmol/l (unified method) | |
| Free cholesterol | 1.04-2.33 mmol/l | |
| Cholesterol esters | 2.33-3.49 mmol/l | |
| HDL | M | 1.25-4.25 g/l |
| AND | 2.5-6.5 g/l | |
| LDL | 3-4.5 g/l | |
Dyslipidemias are divided into primary, associated with inborn errors of metabolism, and secondary. The causes of secondary dyslipidemia are physical inactivity and excess nutrition, alcoholism, diabetes mellitus, hyperthyroidism, liver cirrhosis, chronic renal failure. In addition, they can develop during treatment with glucocorticosteroids, B-blockers, progestins and estrogens. The classification of dyslipidemias is presented in the table.
Classification of dyslipidemias
| Type | Increased blood levels | |
| Lipoproteins | Lipids | |
| I | Chylomicrons | Cholesterol, triglycerides |
| On | LDL | Cholesterol (not always) |
| Type | Increased blood levels | |
| Lipoproteins | Lipids | |
| Nb | LDL, VLDL | Cholesterol, triglycerides |
| III | VLDL, LPPP | Cholesterol, triglycerides |
| IV | VLDL | Cholesterol (not always), triglycerides |
| V | Chylomicrons, VLDL | Cholesterol, triglycerides |
They have different densities and are indicators of lipid metabolism. There are various methods quantification total lipids: colorimetric, nephelometric.
Principle of the method. The hydrolysis products of unsaturated lipids form a red compound with the phosphovanillin reagent, the color intensity of which is directly proportional to the content of total lipids.
Most lipids are not found in the blood free state, and as part of protein-lipid complexes: chylomicrons, α-lipoproteins, β-lipoproteins. Lipoproteins can be separated various methods: centrifugation in saline solutions various densities, electrophoresis, thin layer chromatography. During ultracentrifugation, chylomicrons and lipoproteins of different densities are isolated: high (HDL - α-lipoproteins), low (LDL - β-lipoproteins), very low (VLDL - pre-β-lipoproteins), etc.
Lipoprotein fractions differ in the amount of protein, the relative molecular weight of the lipoproteins, and the percentage of individual lipid components. Thus, α-lipoproteins, containing a large amount of protein (50-60%), have a higher relative density (1.063-1.21), while β-lipoproteins and pre-β-lipoproteins contain less protein and a significant amount of lipids - up to 95% of the total relative molecular weight and low relative density (1.01-1.063).
Principle of the method. When serum LDL interacts with the heparin reagent, turbidity appears, the intensity of which is determined photometrically. Heparin reagent is a mixture of heparin and calcium chloride.
Material under study: blood serum.
Reagents: 0.27% CaCl 2 solution, 1% heparin solution.
Equipment: micropipette, FEC, cuvette with an optical path length of 5 mm, test tubes.
PROGRESS. Add 2 ml of a 0.27% CaCl 2 solution and 0.2 ml of blood serum into a test tube and mix. Determine the optical density of the solution (E 1) against a 0.27% CaCl 2 solution in cuvettes using a red filter (630 nm). The solution from the cuvette is poured into a test tube, 0.04 ml of a 1% heparin solution is added with a micropipette, mixed, and exactly 4 minutes later, the optical density of the solution (E 2) is determined again under the same conditions.
The difference in optical density is calculated and multiplied by 1000 - an empirical coefficient proposed by Ledvina, since constructing a calibration curve is associated with a number of difficulties. The answer is expressed in g/l.
x(g/l) = (E 2 - E 1) 1000.
. The content of LDL (b-lipoproteins) in the blood varies depending on age, gender and is normally 3.0-4.5 g/l. An increase in LDL concentration is observed in atherosclerosis, obstructive jaundice, acute hepatitis, chronic liver diseases, diabetes, glycogenosis, xanthomatosis and obesity, a decrease is observed in b-plasmocytoma. The average LDL cholesterol content is about 47%.
Determination of total cholesterol in blood serum based on the Liebermann-Burkhard reaction (Ilk method)
Exogenous cholesterol in the amount of 0.3-0.5 g comes from food products, and endogenous is synthesized in the body in an amount of 0.8-2 g per day. Especially a lot of cholesterol is synthesized in the liver, kidneys, adrenal glands, and arterial wall. Cholesterol is synthesized from 18 molecules of acetyl-CoA, 14 molecules of NADPH, 18 molecules of ATP.
When acetic anhydride and concentrated sulfuric acid are added to blood serum, the liquid turns successively red, blue and finally green color. The reaction is caused by the formation of green sulfonic acid cholesterylene.
Reagents: Liebermann-Burkhard reagent (a mixture of glacial acetic acid, acetic anhydride and concentrated sulfuric acid in a ratio of 1:5:1), standard (1.8 g/l) cholesterol solution.
Equipment: dry test tubes, dry pipettes, FEC, cuvettes with an optical path length of 5 mm, thermostat.
PROGRESS. All test tubes, pipettes, cuvettes must be dry. You need to be very careful when working with the Liebermann-Burkhard reagent. 2.1 ml of Liebermann-Burkhard reagent is placed in a dry test tube, 0.1 ml of non-hemolyzed blood serum is added very slowly along the wall of the test tube, the test tube is shaken vigorously, and then thermostated for 20 minutes at 37ºC. An emerald green color develops, which is colorimeterized on FEC with a red filter (630-690 nm) against the Liebermann-Burkhard reagent. The optical density obtained on the FEC is used to determine the cholesterol concentration according to the calibration graph. The found cholesterol concentration is multiplied by 1000, since 0.1 ml of serum is taken into the experiment. The conversion factor to SI units (mmol/l) is 0.0258. Normal content total cholesterol (free and esterified) in blood serum 2.97-8.79 mmol/l (115-340 mg%).
Building a calibration graph. From a standard cholesterol solution, where 1 ml contains 1.8 mg of cholesterol, take 0.05; 0.1; 0.15; 0.2; 0.25 ml and adjusted to a volume of 2.2 ml with the Liebermann-Burkhard reagent (2.15; 2.1; 2.05; 2.0; 1.95 ml, respectively). The amount of cholesterol in the sample is 0.09; 0.18; 0.27; 0.36; 0.45 mg. The resulting standard cholesterol solutions, as well as the test tubes, are shaken vigorously and placed in a thermostat for 20 minutes, after which they are photometered. The calibration graph is constructed based on the extinction values obtained as a result of photometry of standard solutions.
Clinical and diagnostic value. If lipid metabolism is disrupted, cholesterol can accumulate in the blood. An increase in cholesterol in the blood (hypercholesterolemia) is observed in atherosclerosis, diabetes mellitus, obstructive jaundice, nephritis, nephrosis (especially lipoid nephrosis), hypothyroidism. A decrease in cholesterol in the blood (hypocholesterolemia) is observed with anemia, fasting, tuberculosis, hyperthyroidism, cancer cachexia, parenchymal jaundice, damage to the central nervous system, febrile states, when administered
