Platelet aggregation, according to the logic of the name, is their association in order to stop bleeding. But this is only one, albeit important, blood clotting factor, which has a numerical value.

The main function is participation in the vascular-platelet (microcirculatory) mechanism of stopping bleeding, that is, in creating a plug (thrombus) that closes the hole in the vascular wall resulting from damage. Thrombus formation occurs as a result of adhesion (sticking to a damaged vascular wall) and platelet aggregation.

As usual, for the ability to aggregate platelets, there are norms in which cell adhesion has a positive role. However, in some cases, the aggregation ability of platelets can play a negative role by disrupting the nutrition of cells of important organs due to the formation of blood clots.

This type of hemostasis is typical for small vessels with small caliber and low blood pressure. For more large vessels the mechanism of coagulation is characteristic, that is, the activation of blood coagulation.

Hemostasis system and blood clotting

Hemostasis is a complex physiological processes in the body, thanks to which the liquid aggregate state of the blood is preserved, and blood loss is minimized in case of violation of the integrity of the vascular bed.

Disturbances in the functioning of this system can manifest as hemorrhagic conditions ( increased bleeding), and thrombotic (a tendency to form small blood clots that prevent normal blood flow due to increased platelet aggregation).

For reference. At normal functioning of the hemostasis system, damage to the vessel activates a sequential chain of events leading to the formation of a stable thrombus and the cessation of bleeding. An important role in this mechanism is played by vascular spasm, which provides a decrease in blood flow at the site of injury, adhesion and aggregation of platelets, as well as activation of the coagulation cascade.

To stop bleeding in small-caliber vessels, a microcirculatory mechanism for stopping bleeding is sufficient. The cessation of bleeding from larger vessels is impossible without the activation of the blood coagulation system. However, it must be understood that the full maintenance of hemostasis is possible only with the normal functioning and interaction of both mechanisms.

In response to damage to the vessel occurs:

• vascular spasm;
• release from damaged cells of the endothelium lining the vessels from the inside, VWF (von Willebrand factor);
• start of the coagulation cascade.

Endothelial cells are endothelial cells that line inner surface vessel, are able to produce anticoagulants (limiting the growth of a thrombus and controlling platelet activity) and procoagulants (activate platelets, contributing to their full adhesion). These include: von Willebrand factor and tissue factor.

That is, after a spasm occurs in response to damage to the vessel and procoagulants are released, active process creating a platelet plug. First of all, platelets begin to stick to the damaged area of ​​the vascular bed (manifestation of adhesive properties). In parallel, they secrete biologically active substances, contributing to increased vascular spasm and a decrease in blood supply to the damaged area, they also release platelet factors that trigger the coagulation mechanism.

Among the substances secreted by platelets, it is necessary to single out ADP and thromboxane A2, which contribute to the active aggregation of platelets, that is, sticking to each other. Due to this, the thrombus begins to rapidly increase in size. The process of platelet aggregation continues until the formed clot reaches a sufficient caliber to close the hole formed in the vessel.

In parallel with the formation of a thrombus, due to the work of the coagulation system, fibrin is released. The strands of this insoluble protein tightly entwine platelets, forming a complete platelet plug (fibrino-platelet structure). Further, platelets secrete thrombosteine, which contributes to the contraction and tight fixation of the cork, and its transformation into a platelet thrombus. This is a temporary structure that firmly closes the damaged area of ​​the vessel and prevents blood loss.

For reference. Platelet activation decreases with distance from the damaged area of ​​the vessel. Platelets that have undergone partial activation, that is, those located at the edge of the clot, are detached from it and returned to the bloodstream.

Further destruction of the formed thrombus, limiting its growth, as well as preventing the formation of small blood clots (increased platelet aggregation) in intact vessels, is carried out by the fibrinolysis system.

Blood test for platelet aggregation

If it is necessary to evaluate the functional activity of platelets, an analysis is performed with their induced aggregation - an aggregogram. In fact, this study allows you to graphically display the ability of platelets to active adhesion and aggregation.

Aggregatogram is performed on a special automatic aggregometer. The analysis is carried out after the addition of aggregation stimulants to the patient's platelet-rich plasma.

Platelet aggregation inducers are divided into:

• weak (adenosine diphosphate (ADP) in small doses, adrenaline);
• strong (ADP in high doses, collagen, thrombin).

As a rule, platelet aggregation is carried out with ADP, collagen, adrenaline and ristomycin (antibiotic ristocetin). The study of platelet activity in the presence of ristocetin is important research in the diagnosis of hereditary hemorrhagic thrombocytopathies (von Willebrand's disease and Bernard-Soulier syndrome).

In these conditions, platelet aggregation is impaired after activation with ristocetin. Under the influence of other inductors (collagen, ADP), activation occurs.

Rules for preparing for taking an analysis

Smoking is prohibited one hour before the test. Within half an hour before taking the material, the patient should be at rest.

Attention. It is important to remember that the results of the platelet activation test change dramatically under the influence of medicines that can affect blood clotting.

The attending physician and laboratory staff must be informed about the medications taken by the patient. High concentrations anticoagulants can reduce platelet aggregation. Antiaggregants dramatically reduce all types of activation of platelet aggregation. The use of antiplatelet agents should be stopped 10 days before the analysis, and non-steroidal anti-inflammatory drugs - at least three days.

Also violate the aggregation ability of platelets:

• high dosages of diuretics (furosemide) and beta-lactams (penicillin, cephalosporins),
• beta-blockers (propranolol),
• vasodilators,
• calcium channel blockers,
• cytostatics,
• antifungal drugs (amphotericin),
• antimalarials.

They can also slightly reduce platelet aggregation:

• Luke,
• garlic,
• ginger,
• turmeric,
• coffee,
• fish oil.

Induced platelet aggregation. Decoding, norm and pathology

Attention. The norms in different laboratories may vary somewhat, therefore, when obtaining the results, it is necessary to focus on the values ​​\u200b\u200bspecified in the form. Also, the result can be presented in the form of a graph (light transmission curve and the presence of disaggregation).

More often, the results of the study are recorded as a percentage. Normal platelet aggregation with:

• ADP 5.0 µmol / ml - from sixty to ninety;
• ADP 0.5 µmol/ml - up to 1.4 to 4.3;
• adrenaline - from forty to seventy;
• collagen - from fifty to eighty;
• ristocetin - from fifty-five to one hundred.

It must be remembered that:

• activation by ristomycin is an indirect reflection of von Willebrand factor activity;
• ADP - platelet aggregation activity;
• collagen induction - the integrity of the vascular endothelium.

The percentage value indicates the degree of light transmission of the plasma after adding the aggregation inductor to it. Platelet-poor plasma is taken as light transmission - 100%. Conversely, platelet-rich plasma is 0%.

Example: an increase in the amplitude of the light transmission curve (an increase in values ​​above the norm) with the addition of an ADP inductor at a high dose (5 μmol / ml) indicates an increased platelet aggregation activity, that is, after the addition of the inductor, the platelets actively stick together and the light transmission of the plasma increases.

Aggregation during pregnancy

Normal platelet aggregation during pregnancy ranges from thirty to sixty percent. V last trimester there may be a slight increase in platelet aggregation.

Decrease in values ​​indicates high risk bleeding during childbirth, and a pronounced increase indicates the risk of thrombosis in postpartum period, as well as possible miscarriage of the fetus (threat of self-abortion).

Indications for analysis

• hemorrhagic disorders (increased bleeding);
• thrombophilia (a bleeding disorder with an increased risk of thrombosis);
• severe atherosclerosis;
• diabetes;
• before carrying out surgical interventions;
• during pregnancy;
• when monitoring the effectiveness of anticoagulant and antiplatelet therapy.

Also, this study is important in the diagnosis of hereditary hemorrhagic thrombocytopathies.

Increased platelet aggregation. Causes

Similar violations in the analyzes are typical for:

• thrombophilia (a clotting disorder characterized by a tendency to form blood clots);
• DM (diabetes mellitus);
• severe atherosclerosis;
• ACS (acute coronary syndrome);
• malignant neoplasms;
• viscous platelet syndrome;
• severe dehydration (dehydration thrombophilia).

Attention! Increased aggregation platelets in the postoperative and postpartum period indicates a high risk of thrombosis. It also increases the risk of heart attack, stroke, and deep vein thrombosis.

Most often, blood clots form in deep veins. lower extremities. The disease is manifested by bursting pains in the legs, aggravated by walking, fatigue, swelling, pallor and cyanosis of the affected limb.

Initial thrombosis predominantly affects veins calf muscle, further with the progression of the disease, blood clots spread higher, affecting the area of ​​the knee, hip and pelvis. The spread of thrombosis and the increase in the size of the thrombus increases the risk of pulmonary thromboembolism.

Reasons for the decrease in aggregation

The decrease in aggregation is typical for:

• aspirin-like syndrome;
• myeloproliferative diseases;
• treatment with drugs that reduce platelet aggregation;
• uremia.

In von Willebrand disease (manifested by nasal, gastrointestinal, uterine bleeding, hemorrhages in the muscles during injuries, light education hematoma) will be:

• sharply impaired activation by ristocetin;
• preserved induction of ADP, collagen and adrenaline;
• von Willebrand factor deficiency.

Bernard-Soulier syndrome (profuse bleeding from mucous membranes) oral cavity, nose, prolonged bleeding from wounds, hemorrhagic rash, extensive hematomas), is also characterized by a sharp decrease in platelet activation by ristomycin, while maintaining normal ADP induction, etc. In this disease, von Willebrand factor activity is normal.

Glantsman's thrombasthenia is manifested by hemorrhages in the joints, prolonged bleeding from wounds, hemorrhagic rash, severe nosebleeds. In the aggregation a sharp decline activation of platelets by ADP, adrenaline and collagen. Induction with ristomycin is not impaired.

In Wiskott-Aldrich syndrome, thrombocytopenia, eczema, and frequent purulent infections are observed. The analyzes are characterized by a decrease in the reaction with collagen, adrenaline and the absence of a second wave with ADP.

Platelets are small blood cells whose main function is to protect the body from internal and external bleeding. The blood stops due to the possibility of gluing blood cells and the appearance. This is called platelet aggregation. Cells stuck together cling to the wall blood vessel. Other elements of blood grow on them, and all this leads to the formation of a large thrombus, which completely closes the flow of blood into the vessel, and the bleeding stops. It is on the speed of this seemingly simple operation that human life depends.

Platelet aggregation in human body occurs only when needed. But there are pathological cases when an unauthorized process of gluing them can harm the body, and even lead to lethal outcome. It's about about the formation of blood clots, which can cause malnutrition of vital internal organs in the development of such serious illnesses and conditions of the body, like, thrombophlebitis,.

First signs pathological process begin to appear in childhood, and have clinical picture long non-healing wounds, large edema at the site of minor bruises. In girls, the presence of thrombocytopathy is expressed in long-lasting and heavy menstruation. The result of pathology is the development of anemia.

The inactivity of blood cells to form blood clots can be caused due to a severe viral or infectious disease, as well as under the influence of regular intake of certain medications.

Secondary thrombocytopathy

The causes of thrombocytopathy are leukemia, anemia of the pernicious form, the development of myeloma. It is also observed when kidney failure disruption of the endocrine system.

Other causes of secondary thrombocytopathy:

• Atherosclerosis.
• Hypertension.
• Heart attack.
• Formation of blood clots in the arteries of the abdominal cavity.
• Stroke.
• Diabetes.

Platelet behavior during pregnancy

During pregnancy, the number of blood cells can differ significantly from the norm. Manifestation - constant small bleeding, bruising. O possible risk discovery of bleeding is necessary in without fail warn medical staff who will take birth.

Increased platelet aggregation during pregnancy is observed mainly in the first trimester and is caused by toxicosis, during which the body loses a large number of liquids.

If the indicator exceeds the norm, there is a risk of unwanted blood clots. The result - complications during pregnancy up to spontaneous miscarriage.

A moderate increase in the level of aggregation in a pregnant woman is the norm, and it is caused by the need to nourish the placenta with blood. Normal indicators it is customary to consider from 30 to 60 percent of any inductors.

The delivery of a blood test to determine the degree of platelet aggregation during pregnancy is required:

• At frequent pregnancies but the inability to bear fruit.
• At therapeutic methods infertility treatment.
• Before you start taking contraceptives, and after completion.
• As one of the measures for diagnosing the state of the body during pregnancy planning.

A timely analysis of platelet aggregation during pregnancy makes it possible to predict the development possible complications and take preventive measures.

Increased aggregation is a marker of hyperaggressive syndrome and thrombophilia. Born's turbidimetric method, based on the registration of changes in the light transmission of platelet-rich plasma, and the method of studying platelet aggregation, based on the analysis of light transmission fluctuations caused by a random change in the number of particles in the optical channel, are most commonly used.

Material for research. Citrated platelet rich plasma

Research method is determined by the order of work on a particular type of aggregometer.

As inductors, solutions of ADP, ristocetin, collagen, adrenaline, and arachidonic acid are most often used. Thrombin, serotonin, etc. solutions can also be used.

Platelet aggregation with ADP

Exposure to small doses of ADP (usually 1*10 -7 mol) leads to the formation of a double wave of aggregation. The first phase (primary wave) depends on the added exogenous ADP, and the second phase (secondary wave of aggregation) occurs due to the release reaction of its own agonists contained in platelet granules. Large doses ADP (usually 1*10 -5 mol) lead to the fusion of the first and second waves of aggregation.

When analyzing aggregation patterns, attention is paid to general character aggregation (one-wave, two-wave; complete, incomplete; reversible, irreversible) and aggregation rate. The appearance of two-wave aggregation upon stimulation of ADP at concentrations that normally cause reversible aggregation (usually 1-5 μmol) indicates an increase in platelet sensitivity, and the development of single-wave incomplete (and often reversible) aggregation upon stimulation of ADP at concentrations of 10 μmol or more indicates violation of the platelet release reaction.

Platelet aggregation with ristocetin

Determination of platelet aggregation with ristocetin in plasma is used to quantify the von Willebrand factor. The method is based on the ability of ristocetin to stimulate in vitro interaction of von Willebrand factor with platelet glycoprotein Ib. In most cases of von Willebrand disease, ristocetin aggregation is impaired with a normal response to ADP, collagen, and adrenaline. Violation of ristocetin aggregation is also detected in Bernard-Soulier disease. For differentiation, a test with the addition of normal plasma is used: in von Willebrand disease, after the addition of normal plasma, ristocetin aggregation is normalized, while this does not occur in Bernard-Soulier syndrome. Ristocetin-induced platelet agglutination is reduced in most cases of von Willebrand's disease except type IIB.

Platelet aggregation with collagen

Aggregation of platelets with collagen is quite pronounced latent phase, during which phospholipase C is activated. Depending on the concentration of the reagent used, the duration of this phase can be 5-7 minutes. After the completion of this period, processes occur in platelets leading to the formation of secondary messengers, as a result of which the secretion of platelet granules and the synthesis of thromboxane A2 develop, which is accompanied by a sharp increase in interplatelet interaction.

In laboratory and clinical practice, collagen is most often used at a final concentration of 50 μg/ml, however, collagens from different companies may have different activities, which must be taken into account when using them.

Platelet aggregation with adrenaline

Adrenaline, upon contact with platelets, interacts with α2-adrenergic receptors, which causes inhibition of adenylate cyclase. It is possible that the mechanism underlying the implementation of the effect of adrenaline and the development of the first wave of aggregation does not depend on the formation of thromboxane A2, the release reaction or synthesis of platelet aggregation factor, but is associated with the ability of adrenaline to directly change the permeability of the cell membrane for calcium ions. The second wave of aggregation occurs as a result of the release reaction and production of thromboxane A2.

Platelet aggregation with arachidonic acid

Arachidonic acid is a natural aggregation agonist, and its action is mediated by the effects of prostaglandins G2 and H2, thromboxane A2, and includes the activation of both phospholipase C with subsequent formation of secondary messengers, mobilization of intracellular calcium and expansion of the cell activation process, and phospholipase A2, which directly leads to release of endogenous arachidonic acid. Aggregation of platelets with arachidonic acid occurs quite quickly, so the curve characterizing this process is more often of a single-wave character.

To induce platelet aggregation, arachidonic acid is used at concentrations of 10 -3 -10 -4 mol. When working with arachidonic acid, it should be borne in mind that this substance oxidizes very quickly in air.

A test for aggregation with arachidonic acid is recommended in cases of using drugs that affect the aggregation reaction (for example, acetylsalicylic acid, penicillin, indomethacin, delagil, diuretics), which must be taken into account when evaluating the results of studies.

Determination of platelet aggregation with various inducers of aggregation plays essential role v differential diagnosis thrombocytopathies.

Platelet aggregation disorders various diseases

(+,-) - has no diagnostic value.

Depending on the functional and morphological characteristics of platelets, the following groups of thrombocytopathies are distinguished.

• Hereditary disaggregation thrombocytopathies without disruption of the release reaction (secondary wave). This group includes:
  • Glyantsmann's thrombasthenia, which is characterized by a violation of ADP-dependent aggregation, with normal ristocetin aggregation;
  • essential athrombia - when exposed to small amounts ADP aggregation is not induced, and when the amount of ADP is doubled, it approaches normal;
  • May-Hegglin anomaly - collagen-dependent aggregation is disturbed, the release reaction during stimulation with ADP and ristocetin is preserved.
• Partial disaggregation thrombocytopathies. This group includes diseases birth defect aggregation with one or another aggregant, or inhibition of the release reaction.
• Violation of the release reaction. This group of diseases is characterized by the absence of a second wave of aggregation upon stimulation with a small amount of ADP and adrenaline. In severe cases, there is no ADP- and adrenaline-dependent aggregation. Collagen-dependent aggregation is not detected.
• Diseases and syndromes with insufficient pool of accumulation and storage of aggregation mediators. This group includes diseases characterized by a violation of the ability of platelets to accumulate and secrete serotonin, adrenaline, ADP and other platelet factors. Laboratory for this group is characterized by a decrease in all types of aggregation and the absence of a second wave of aggregation.

A decrease in platelet aggregation in response to the administration of ADP is observed when pernicious anemia, acute and chronic leukemia, multiple myeloma. In patients with uremia, when stimulated with collagen, adrenaline, ADP, aggregation is reduced. Hypothyroidism is characterized by a decrease in platelet aggregation with ADP stimulation. Acetylsalicylic acid, penicillin, indomethacin, chloroquine, diuretics (in particular, furosemide when used in high doses) help reduce platelet aggregation, which must be taken into account when treating with these drugs.

platelets- the smallest blood cells responsible for clotting biological fluid. They take part:

• in stopping bleeding (hemostasis);
• in the nutrition of the walls of blood vessels.

How does platelet aggregation occur?

As soon as we get the slightest cut, the body signals a problem. Platelets rush to the damaged vessels, which begin to stick together together. This action is called aggregation. It takes place in two stages:

1. First, platelets stick together with each other - this is initial stage thrombosis.
2. Then they are attached to the walls of blood vessels.

After that, other elements, even platelets, stick to the platelet clot, and as a result, the thrombus grows until it covers the ruptured walls of the vessels so that the blood does not leak out. However, there is a danger that threatens with increased blood clots - these are heart attacks, strokes.

For any deviations from the norm, contact a specialist.

Blood clotting test

For the study of platelet aggregation, it is necessary to take a blood test:

1. If bruises form from the slightest blows, wounds heal poorly, often there is blood from the nose - this is a signal that blood clotting is reduced.
2. If edema is observed, on the contrary, clotting is increased.

The analysis is carried out by introducing an aggregation inducer and observing the reaction. Chemical thrombogenic substances similar in composition to natural ones are used as an inductor.

Platelet aggregation is tested using the following inductors:

• adrenalin;
• components vascular wall: adenosine diphosphate (ADP);
• ristocetin (ristomycin);
• collagen;
• serotonin.

Spontaneous platelet aggregation is determined without inducers.

Before taking the test, you need to carefully prepare so that the blood test is accurate. To do this, you must follow these rules:

1. Before passing the analysis, stop taking all aspirin drugs (Dipyridamole, Indomethacin and others) and antidepressants.
2. The analysis is taken on an empty stomach, 12 hours after the last meal, it is especially undesirable to eat fatty foods.
3. Do not overload physically, be calm.
4. Do not drink coffee during the day alcoholic drinks, do not eat garlic and do not smoke.
5. If in body goes inflammatory process analysis should be postponed.
6. It is also important to know that during menstruation, women experience a decrease in blood clotting, and this can affect the result of the analysis.

The rate of platelet aggregation

A normal number of platelets in the blood means that a person has a healthy hematopoiesis, tissues and organs are supplied with oxygen and iron in sufficient quantities.

Increased platelet aggregation

To understand what kind of condition it is when platelet aggregation is increased, you need to pay attention to this: the blood is thick, moves slowly through the vessels, and stagnates. This manifests itself in the form of a feeling of numbness, swelling. Such thrombocytosis occurs when:

• widespread atherosclerosis of vessels;
• hypertension;
• diabetes mellitus;
• leukemia;
• stomach or kidney cancer;
• after removal of the spleen;
• sepsis.

Thick blood threatens with such adverse conditions as:

Decreased platelet aggregation

With a small number of platelets in the blood, the vessels become brittle, bleeding stops with difficulty.

If platelet aggregation is reduced, you need:

1. Avoid injury.
2. Use drugs and alcohol with caution.
3. Eat right, avoid spicy and salty foods.
4. There are foods rich in iron (beets, apples, buckwheat, meat, fish, parsley, peppers, nuts, spinach).