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Types of aggregation

In medicine it is customary to distinguish the following types of aggregation platelets:

1. Spontaneous, which is determined without an inductor. To do this, venous blood is poured into a test tube and heated to a temperature of 37 o C.
2. Induced, during the study of which inducers are added to the plasma, which are collagen, ADP, ristomycin or adrenaline. The method is used in the diagnosis of certain blood diseases.
3. Moderate. Caused by blood circulation in the placenta during pregnancy.
4. Low. It is observed in the presence of diseases of the circulatory system, and can cause bleeding.
5. Increased, which leads to an increased risk of blood clots.

Increased blood aggregation ability leads to an increase in its viscosity, and a characteristic slow movement of blood with an increased ability to clot (at normal levels up to 2 minutes). Pathology manifests itself when:

1. Increased blood pressure.
2. Diabetes mellitus.
3. Oncology of blood, kidneys and stomach.
4. Thrombocytopathies.
5. Atherosclerotic changes in blood vessels.

Hyperaggregation leads to the following pathologies:

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Anna Poniaeva. She graduated from the Nizhny Novgorod Medical Academy (2007-2014) and Residency in Clinical Laboratory Diagnostics (2014-2016).

1. Myocardial infarction due to insufficient blood supply.
2. Stroke due to cerebrovascular accident.
3. Vein thrombosis in the legs.

Normal values

The aggregation rate in a healthy person is in the range of 25-75%, which indicates normal hematopoiesis and the absence of a lack of oxygen in tissues and organs. The normal indicator for various inductors is as follows.

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Thrombocytopenia

What is Thrombocytopenia -

Thrombocytopenia is understood as a group of diseases characterized by a decrease in platelet count below normal levels (150 H 109/L).

A decrease in platelet count is associated with both increased platelet destruction and decreased production.

Thrombocytopenia is divided into hereditary and acquired forms.

Acquired forms of thrombocytopenia are differentiated according to the mechanism of damage to the megakaryocyte-platelet apparatus. Among such mechanisms, immune mechanisms occupy a special place. Their development can be characterized by a number of factors, the main of which are: mechanical damage to platelets, replacement of bone marrow with tumor tissue, inhibition of bone marrow cell division, increased platelet consumption, mutations, deficiency of vitamin B12 or folic acid.

There are 4 groups of immune thrombocytopenia:

1) isoimmune (alloimmune), in which the destruction of platelets is associated with incompatibility in one of the blood group systems or is caused by the transfusion of foreign platelets to the recipient in the presence of antibodies to them or the penetration of antibodies to the child from a mother previously immunized with an antigen that she does not have, but has child;

2) transimmune, in which autoantibodies of a mother suffering from autoimmune thrombocytopenia penetrate the placenta and cause thrombocytopenia in the child;

3) heteroimmune, associated with a violation of the antigenic structure of the platelet under the influence of a virus or with the appearance of a new antigen;

4) autoimmune, in which antibodies are produced against one’s own unchanged antigen.

It should be noted that most patients with both hereditary and acquired thrombocytopenic purpura have a similar bone marrow reaction without spleen enlargement.

Thrombocytopenia caused by immune changes constitutes the majority of all thrombocytopenia. In childhood, as a rule, a heteroimmune form of the disease develops, and at an older age, autoimmune variants predominate. Antibodies directly involved in development can be directed against various cells of the blood and hematopoietic system. These cells are platelets, megakaryocytes or the common precursor of platelets, leukocytes and erythrocytes. Thrombocytopenias are classified similarly.

An autoimmune process is called idiopathic if the cause of autoaggression cannot be identified, and symptomatic if it is a consequence of another, underlying disease.

Idiopathic autoimmune thrombocytopenia The ratio of men and women suffering from this pathology is approximately 1: 1.5 per 100,000 population. In most cases, idiopathic thrombocytopenia is autoimmune.

Pathogenesis (what happens?) during Thrombocytopenia:

In 1915, I.M. Frank suggested that the basis of the disease was a violation of the maturation of megakaryocytes under the influence of some factor, presumably located in the spleen. In 1946, Dameshek and Miller showed that the number of megakaryocytes in thrombocytopenic purpura is not reduced, but even increased. They suggested that the detachment of platelets from megakaryocytes is disrupted. In 1916, Kaznelson suggested that in thrombocytopenic purpura the intensity of platelet destruction in the spleen increases. For many years, Frank's hypothesis was more popular.

However, studies have found that the lifespan of platelets in any type of thrombocytopenic purpura is acutely reduced. Normally, the duration of existence of these blood cells is 7-10 days, and with the development of pathology - only a few hours.

Further studies revealed that in a larger percentage of cases of thrombocytopenia, the content of blood platelets formed per unit time does not decrease, as previously assumed, but increases significantly compared to their normal number - 26 times. The increase in the number of megakaryocytes and platelets is associated with an increase in the number of thrombocytopoietins (factors that promote the formation and growth of the above blood cells) in response to a decrease in the number of platelets.

The number of functionally complete megakaryocytes is not reduced, but increased. A large number of young megakaryocytes, rapid detachment of platelets from megakaryocytes and their rapid release into the bloodstream create the erroneous impression that the function of megakaryocytes in idiopathic thrombocytopenic purpura is impaired.

In hereditary forms of thrombocytopenic purpura, the lifespan of platelets is shortened as a result of a defect in the structure of their membrane or as a result of a defect in the energy metabolism in them. In immune thrombocytopenia, platelet destruction occurs due to the effect of antibodies on them.

The process of megakaryocyte formation is disrupted, as a rule, if the amount of antibodies against platelets is excessively large or if the resulting antibodies direct their action against the megakaryocyte antigen, which is absent on the platelet membrane.

The determination of antiplatelet antibodies (antiplatelet antibodies) is associated with great methodological difficulties, which has caused most of the discrepancies in the classifications of thrombocytopenia. Thus, in many works, Werlhof's disease is divided into two forms: immune and non-immune. To prove the immune form of Werlhof's disease, serum thromboagtlutinins (substances that promote the “gluing” of platelets) are determined. However, in immune thrombocytopenia, antibodies in most cases attach to the surface of platelets, thereby disrupting their function and leading to their death. However, antibodies do not cause platelet agglutination. The thromboagglutination method allows you to determine only antibodies that cause agglutination (“gluing”) of platelets when mixing the patient’s serum with the donor’s blood. Often, “sticking” occurs when exposed to not only the test serum, but also the control serum. This is due to the ability of platelets to aggregate (form aggregates of various sizes), and their aggregation is practically indistinguishable from agglutination. In this regard, it turned out to be impossible to use not only thromboagglutination, but also direct and indirect Coombs tests to determine antiplatelet antibodies.

The Steffen test has been widely used to detect antiplatelet antibodies, but its sensitivity has been found to be poor. The results often turned out to be false positive when using donor serum and serum from patients with other diseases.

In recent years, new, more sensitive and more reliable, tests have been proposed for the determination of antibodies against platelets (antiplatelet antibodies). Some methods are based on determining the ability of antibodies in the patient’s serum to damage platelets of healthy people, as well as on determining platelet breakdown products. In 65% of patients with thrombocytopenic purpura, antibodies belonging to the IgG class are detected in the serum. It has also been established that these antibodies can be isolated from extracts of the spleen removed from a patient with thrombocytopenic purpura. All these methods determine only the antibodies present in the blood serum, which, firstly, reduces sensitivity, since not all patients have antibodies in the serum, and secondly, does not allow the differentiation of allo- and autoantibodies.

The Dixon method is of greatest interest. This method is based on the quantitative determination of antibodies located on the platelet membrane. Normally, the platelet membrane contains a certain amount of class G immunoglobulin. With immune thrombocytopenia, its amount increases several tens of times.

Dixon's method is of great informative value, but it is more labor-intensive and cannot be used in widespread practice. In addition, there is a certain lower limit on the number of platelets at which antibodies on their surface can be examined. For very low numbers, Dixon's method is not suitable.

To study antiplatelet antibodies, it is recommended to use the immunofluorescent method. This technique uses paraformaldehyde, which extinguishes the nonspecific glow formed during the formation of antigen + antibody complexes, leaving only those associated with antiplatelet antibodies.

Using all of these methods, antiplatelet antibodies are detected on the surface of platelets in most patients with thrombocytopenic purpura.

An organ such as the spleen produces the bulk of all platelets in the human body.

Symptoms of Thrombocytopenia:

The disease sometimes begins suddenly, progresses either with exacerbations, or is prone to a protracted course.

Some classifications use traditional terminology to define different forms of thrombocytopenic purpura: it is divided into acute and chronic. By chronic form of idiopathic thrombocytopenia is meant essentially autoimmune thrombocytopenia, and by acute form is meant heteroimmune thrombocytopenia. This terminology cannot be considered successful, since the first clinical manifestations of the disease do not allow us to classify a specific case of idiopathic thrombopenic purpura as a specific form.

The idiopathic form of the disease develops without a clear connection with any previous disease, and symptomatic forms are observed in chronic lymphocytic leukemia, multiple myeloma, chronic active hepatitis, systemic lupus erythematosus, and rheumatoid arthritis. Idiopathic and symptomatic thrombocytopenia often occur in the same way, but their forms still have a certain impact on the clinical picture.

Thrombocytopenic hemorrhagic syndrome is characterized by skin hemorrhages and bleeding from the mucous membranes. Skin hemorrhages are more often observed on the limbs and torso, mainly along the anterior surface. There are often hemorrhages at the injection sites. Minor hemorrhages most often occur on the legs. Hemorrhages sometimes occur on the face, in the conjunctiva, and on the lips. The appearance of such hemorrhages is considered a serious symptom, indicating the possibility of hemorrhages in the brain.

Bleeding in case of tooth extraction does not always occur; it begins immediately after the intervention and continues for several hours or days. However, after stopping, they, as a rule, do not resume, which is why they differ from worsening bleeding in hemophilia.

Capillary fragility tests are often positive.

An enlarged spleen is not typical for idiopathic thrombocytopenic purpura and occurs in some symptomatic forms of autoimmune thrombocytopenia associated with hematological malignancies, lymphocytic leukemia, chronic hepatitis and other diseases. The spleen is often enlarged in patients in whom thrombocytopenia is combined with autoimmune hemolytic anemia. Liver enlargement is not characteristic of thrombocytopenia. In some patients, during an exacerbation of the disease, the lymph nodes become slightly enlarged, especially in the neck, and the temperature becomes low-grade (up to 38°C). Lymphadenopathy (damage to the lymph nodes), arthralgic syndrome (joint pain) and accelerated ESR require the exclusion of systemic lupus erythematosus, which can begin with autoimmune thrombocytopenia.

In a general analysis of peripheral blood, a decrease in the number of platelets (in some cases until their complete disappearance) is noted with normal or increased levels of plasma coagulation factors. It is hardly possible to talk about a critical number of platelets at which signs of hemorrhagic diathesis appear. This figure depends on the functional state of platelets. If the platelet count exceeds 50 × 109/l, then hemorrhagic diathesis is rarely observed.

Morphological changes in platelets are often detected, such as an increase in their size and the appearance of blue cells. Sometimes there are small forms of plates, their poikilocytosis is noted. The number of process platelets, which can be visualized by phase contrast microscopy, decreases.

The content of red blood cells and hemoglobin in some cases does not differ from that in the absence of pathology. Posthemorrhagic anemia is sometimes observed. In a number of patients, thrombocytopenia of autoimmune origin occurs in combination with autoimmune hemolytic anemia. The morphology of red blood cells depends on whether the patient has anemia and what its origin is. The increase in the number of reticulocytes in the blood depends on the intensity of blood loss or hemolysis (destruction of red blood cells). The leukocyte count in most patients is normal or slightly increased.

Leukopenia (decrease in the number of leukocytes) is observed with combined damage to 2 or 3 hematopoietic lineages. In some cases, eosinophilia (increased number of eosinophils) is possible.

The majority of patients with this pathology have an increased number of megakaryocytes in the bone marrow. Sometimes it remains within normal limits. Only with exacerbation of the disease does the number of megakaryocytes temporarily decrease until they disappear completely. Enlarged megakaryocytes are often found. Sometimes red germ irritation is found in the bone marrow, associated with bleeding or increased destruction of red blood cells.

Histological examination of the bone marrow in most cases reveals a normal ratio between fat and hematopoietic tissue. The number of megakaryocytes usually increases.

Bleeding time is often prolonged. Blood clot retraction is reduced. Blood clotting is normal in most patients. Often with autoimmune thrombocytopenia, functional platelet disorders are observed.

Diagnosis of Thrombocytopenia:

Diagnosis of the disease is based on the clinical picture and laboratory tests. First of all, aplasia of hematopoiesis, hemoblastosis, Marchiafava-Micheli disease, vitamin B12-deficiency anemia, cancer metastases are excluded, for which a sternal puncture (sternum puncture), trepanobiopsy of the bone marrow is performed, and hemosiderin in the urine is examined.

In Marchiafava-Miceli disease, platelets, erythrocytes and leukocytes with a defective membrane are formed in the bone marrow as a result of mutation, which are easily destroyed in the peripheral blood under the influence of certain substances. Despite thrombocytopenia, which is sometimes pronounced in this disease, bleeding is rare and there is a tendency to thrombosis.

Thrombocytopenia in combination with anemia is observed with a deficiency of vitamin B12 or folic acid. In this case, thrombocytopenia is often mildly expressed, and with extremely rare exceptions, patients do not experience bleeding.

A special group consists of consumption thrombocytopenia, which is a fairly common accompaniment of thrombosis and disseminated intravascular coagulation syndrome. These processes cause an intense loss of platelets and fibrinogen from the circulation. In most cases, the history and examination data allow us to determine symptomatic thrombocytopenia, but great diagnostic difficulties are possible. Thrombocytopenic syndrome at a certain stage may be the only manifestation of latent thrombosis or DIC syndrome. The origin of the deficiency of blood platelets is clarified during dynamic monitoring of patients and treatment.

In differentiating forms in the group of hereditary and immune thrombocytopenias, family history in some cases can be of irreplaceable help, but sometimes, especially with recessively inherited forms, the examined patient remains the only person suffering from this disease in the family.

Important assistance for the correct diagnosis of hereditary thrombocytopenic purpura is provided by a morphological study of platelets, determination of their size, structure, functional properties, as well as other laboratory and clinical manifestations of hereditary pathology inherent in some forms of thrombocytopathy with thrombocytopenic syndrome.

The functional state of platelets is disrupted in both hereditary and immune forms of thrombocytopenic purpura, since antibodies not only shorten the lifespan of platelets, but also disrupt their functional activity.

The number of megakaryocytes in bone marrow examination in most cases remains within the physiological norm or is increased, only occasionally during periods of exacerbation of the disease or in its especially severe forms it is reduced.

Thus, the diagnosis of autoimmune thrombocytopenia is based on the following signs:

1) absence of symptoms of the disease in early childhood;

2) absence of morphological and laboratory signs of hereditary forms of thrombocytopenia;

3) absence of clinical or laboratory signs of the disease in blood relatives;

4) the effectiveness of glucocorticosteroid therapy in sufficient doses;

5) detection, if possible, of antiplatelet antibodies.

Autoimmune thrombocytopenic purpura is indirectly indicated by the combination of thrombocytopenia with autoimmune hemolytic anemia and the detection of anti-erythrocyte antibodies (anti-erythrocyte antibodies). However, the absence of signs of hemolytic anemia does not exclude the autoimmune origin of thrombocytopenia.

In all cases of autoimmune thrombocytopenic purpura, symptomatic forms associated with systemic lupus erythematosus, chronic lymphocytic leukemia, chronic hepatitis in the acute phase, or a number of other diseases should be excluded.

Treatment of Thrombocytopenia:

Treatment autoimmune thrombocytopenia of any origin consists of the use of glucocorticosteroid hormones, removal of the spleen and treatment with immunosuppressants.

Treatment always begins with prednisolone at an average dose of 1 mg/kg per day. In severe cases, this dose may be insufficient, then after 5-7 days it is increased by 1.5-2 times. The effect of therapy usually appears in the first days of treatment. First, the hemorrhagic syndrome disappears, then the platelet count begins to increase. Treatment continues until the full effect is achieved. Then they begin to reduce the dose and gradually, slowly discontinue glucocorticosteroids.

In some cases, just one such course of hormonal therapy can lead to a final cure. However, more often, after discontinuation of hormones or even when trying to reduce the dose, a relapse occurs (exacerbation of the disease), requiring a return to the original high doses of the drug. In approximately 10% of patients, the effect of glucocorticosteroid therapy is completely absent or incomplete: bleeding stops, but thrombocytopenia remains.

If the effect of treatment with glucocorticosteroid hormones is incomplete and unstable (usually 3-4 months from the start of therapy), indications arise for removal of the spleen or the prescription of immunosuppressants. In more than 75% of patients with autoimmune thrombocytopenia, removal of the spleen leads to practical recovery, especially if glucocorticosteroid hormones provide a good but unstable effect. The results of spleen removal are better when platelet normalization occurs with a small dose of prednisolone. Improvement after removal of the spleen is almost always permanent if in the first days after surgery the platelet count rises to 1000 H 109/l or more.

Removal of the spleen is usually performed against the background of glucocorticosteroid therapy, and the dose of prednisolone is increased 4-5 days before surgery so that the platelet level becomes as normal or subnormal as possible. 1-2 days before surgery, regardless of whether it was possible or not to normalize platelet levels, the dose of prednisolone is doubled. Due to the faster elimination (removal) from the body of prednisolone administered intramuscularly, a dose of prednisolone should be prescribed 2 times higher than when administered orally; when administered intravenously, the dose of the drug should be 3 times higher. Thus, on the day of surgery, prednisolone should be administered intramuscularly at a dose 4 times higher than the original dose. This ensures improved hemostasis during and after the intervention. From the 3rd day after removal of the spleen, the dose of prednisolone is quickly reduced and by the 5-6th day of the postoperative period it is brought to the original dose, and then, depending on the effect of the operation, a slow dose reduction and gradual withdrawal of glucocorticosteroid hormones begin. With a decrease in the number of platelets along with a decrease in prednisolone, its intensity is slowed down.

Even with ineffective removal of the spleen, in more than half of patients, bleeding disappears, although the platelet level remains low. Some of them have a delayed effect of the operation - a slow increase in platelet levels over the next 56 months or more. Often, after removal of the spleen, the therapeutic effect of previously ineffective glucocorticosteroids appears, and it is possible to use intermittent courses of relatively small doses of hormones for a long time.

The greatest difficulties in therapeutic terms are patients with autoimmune thrombocytopenia after ineffective removal of the spleen, in whom a return to hormonal therapy is ineffective or gives a temporary and unstable effect even when using high doses of hormones. These patients are indicated for therapy with cytostatic immunosuppressants in combination with glucocorticosteroid hormones. The effect of immunosuppressive chemotherapy appears after 1.5-2 months, after which glucocorticosteroid hormones are gradually withdrawn.

Imuran (azathioprine) is used as an immunosuppressant at a dose of 2-3 mg/kg per day, course duration is up to 3-5 months; cyclophosphamide (cyclophosphamide) 200 mg/day (usually 400 mg/day), about 6-8 g per course; vincristine - 1-2 mg/m2 of body surface once a week, course duration - 1.5-2 months. Vincristine has some advantage over other immunosuppressive drugs, but it sometimes causes polyneuritis.

For symptomatic autoimmune thrombocytopenia, complicating systemic lupus erythematosus and other diffuse connective tissue diseases, hemoblastosis, treatment with immunosuppressants begins early, splenectomy is usually performed only if cytostatic drugs are ineffective and severe hemorrhagic syndrome, sometimes for health reasons. This tactic applies only to severe forms of connective tissue diseases. In erased forms of the disease, especially in young people, it is more rational to remove the spleen followed by treatment with cytostatic agents in the absence of effect from surgery and the use of glucocorticosteroid hormones.

The use of immunosuppressants before removal of the spleen in the case of autoimmune thrombocytopenia is irrational. Cytostatic treatment requires individual selection of an effective drug, since there are no criteria to predict the effectiveness of a particular drug. At the same time, doctors prescribe fairly large doses of cytostatics and hormonal drugs to patients for a long period of time. This treatment sharply worsens the conditions for subsequent removal of the spleen, which cannot be avoided in more than half of the patients. The effectiveness of treatment using immunosuppressants is significantly lower than removal of the spleen. Finally, in children and young people, cytostatic treatment is fraught with a mutagenic effect (the occurrence of mutations of various types), infertility or pathology in the offspring. Based on these considerations, removal of the spleen should be considered the treatment of choice in the treatment of idiopathic thrombocytopenia, and cytostatic treatment should be considered a “method of despair” in case of ineffective splenectomy.

Treatment of acquired thrombocytopenia of a non-immune nature consists of treating the underlying disease.

Symptomatic treatment of hemorrhagic syndrome with thrombocytopenia includes local and general hemostatic agents. The use of aminocaproic acid, estrogens, progestins, adroxon and other agents is rational.

Locally, especially for nosebleeds, a hemostatic sponge, oxidized cellulose, adroxon, local cryotherapy, and aminocaproic acid are widely used.

Hemotransfusions (blood transfusions), especially massive ones, sharply reduce the aggregation properties of platelets, which often leads to worsening thrombocytopenic purpura due to the consumption of young cells in microthrombi. Indications for blood transfusions are strictly limited, and only washed red blood cells, selected individually, are transfused. For all types of autoimmune thrombocytopenia, platelet infusion is not indicated, as it threatens to worsen thrombocytolysis (“melting” of platelets).

Patients should carefully avoid all substances and medications that interfere with platelet aggregation properties.

Patients with thrombocytopathies are subject to clinical observation by hematologists. In the process of such observation and a complete clinical and laboratory examination, the form of thrombocytopathies and its connection with certain diseases or exposures are determined. Family history is carefully studied, the function and morphology of blood platelets in the patient’s relatives is examined. It is advisable to examine those relatives who do not have bleeding, since thrombocytopathies can be asymptomatic or with minimal hemorrhagic phenomena.

Particular attention should be paid to eliminating exposures that may cause or increase bleeding. Drinking alcohol is prohibited; It is necessary to exclude from the diet all dishes that contain vinegar and home-canned products prepared with salicylates. Food should be rich in vitamins C, P and A, the latter is especially indicated for frequent nosebleeds. These vitamins are also prescribed in the form of medications, especially in winter and spring. It is useful to include peanuts in your diet.

It is necessary to exclude in the treatment of drugs concomitant with the disease that affect blood clotting, as well as platelet function. Particularly dangerous are salicylates, brufen, butazolidines, indomethacin, carbenicillin, chlorpromazine, indirect anticoagulants, and fibrinolytics. Heparin can only be prescribed for disseminated intravascular coagulation syndrome.

Relatively small doses of aminocaproic acid (0.2 g/kg or 6-12 g/day for an adult patient) significantly reduce bleeding in many disaggregation thrombocytopathies and at the same time increase the rates of collagen, ADP and thrombin aggregation, and reduce the time of capillary bleeding. The drug is most effective for essential athrombia, partial disaggregation thrombocytopathies with both normal and impaired “release reaction”, and mild to moderate von Willebrand disease. Of the symptomatic thrombocytopathies, aminocaproic acid is most effective in post-transfusion forms, hypoestrogenic uterine bleeding, dysfunction of blood platelets of drug origin, and leukemia.

The stopping effect of aminocaproic acid on uterine bleeding (except for the most severe forms of Glanzmann thrombasthenia and von Willebrand disease) and nosebleeds is especially noticeable. Patients with uterine bleeding are prescribed regular use of the drug from the 1st to the 6th day of each menstrual cycle. Select the minimum dose and the shortest course of taking the drug, which will stop heavy and prolonged menstrual bleeding.

In some patients, after a course of treatment with aminocaproic acid, a temporary absence of menstrual bleeding occurs, which does not require special treatment, but in such cases pregnancy should be excluded.

Aminocaproic acid is prescribed orally, and the daily dose is divided into 6-8 doses (the first dose can be a shock dose, double).

With intravenous administration, it is difficult to achieve continuous action of the drug, vein thrombosis occurs, and when large doses are administered, disseminated intravascular coagulation syndrome occurs, and therefore intravenous administration is permissible only in the presence of emergency indications.

The hemostatic effect of aminocaproic acid is explained by its complex effect on different parts of the hemostasis system - platelet function, fibrinolysis, and blood coagulation system. This apparently explains the decrease in bleeding not only with qualitative platelet defects, but also with their severe deficiency.

In the treatment of thrombocytopathies, it is possible to use cyclic amino acids related to aminocaproic acid with antifibrinolytic action - paraaminomethylbenzoic acid, tranexamic acid. They significantly reduce microcirculatory bleeding and especially menstrual bleeding.

Synthetic hormonal contraceptive drugs significantly increase the adhesive function of platelets. They significantly reduce bleeding in a number of primary and symptomatic thrombocytopathies. However, even when there is deep thrombocytopenia or platelet function does not improve, synthetic contraceptives stop and prevent uterine bleeding, which is valuable in the treatment of uterine bleeding in hematological patients.

They cause the same structural changes in the endometrium as pregnancy, and menstruation either stops altogether or becomes scanty and short-lived.

All these features also conceal the negative aspects of the action of synthetic contraceptives - their ability to increase the likelihood of thrombosis and provoke disseminated intravascular coagulation. In case of thrombocytopathy and thrombocytopenia caused by intravascular coagulation, or with a high probability of its development, these drugs should not be prescribed, as they can increase bleeding, including uterine bleeding.

The above forms include promyelocytic leukemia, thrombocytopathies in myeloproliferative diseases, collagenosis, massive transfusions, and liver diseases.

The combined use of contraceptives and aminocaproic acid is dangerous. Prevention of disseminated intravascular coagulation is necessary.

In the treatment of thrombocytopathy, ATP is traditionally used (2 ml of a 1% solution daily intramuscularly for 3-4 weeks) with the simultaneous administration of magnesium sulfate (intramuscularly 5-10 ml of a 25% solution for 5-10 days) with the appointment subsequently magnesium thiosulfate orally (0.5 g 3 times a day before meals).

This treatment provides some benefit for partial disaggregation thrombocytopathies with impaired “release reaction”, but is almost ineffective for advanced forms (Glanzmann thrombasthenia, essential athrombia) and forms of insufficient accumulation of dense granule components.

Adroxon (chromadren, adrenoxyl) gives a good hemostatic effect both when applied topically and when administered subcutaneously or intramuscularly. The drug stimulates the hemostatic function of platelets and improves microcirculatory hemostasis (helps stop parenchymal bleeding, bleeding from mucous membranes) and at the same time does not activate blood coagulation or inhibit fibrinolysis. This makes it possible to widely use adroxon for any thrombocytopathy and thrombocytopenia, including forms associated with disseminated intravascular coagulation syndrome.

Adroxon is used in the form of subcutaneous or intramuscular injections of 1-2 ml of a 0.025% solution 2-4 times a day: the course of treatment can last 1-2 weeks. The drug is irrigated on the bleeding surface or napkins soaked in adroxon solution are applied to it.

For thrombocytopathic bleeding, dicinone is also widely used, either subcutaneously and intramuscularly, or in tablets orally.

Undoubtedly, bradykinin antagonists - pyridinol carbamate (anginin, prodectin, parmidin) have a positive effect in a number of thrombocytopathy. When taken orally in a course of 1-3 g/day, bleeding decreases both in many thrombocytopathies and in thrombocytopenias (idiopathic, hypoplastic, leukemic). For menstrual bleeding, this drug can be combined with synthetic progestins, and for immune thrombocytopenia - with glucocorticosteroids.

In von Willebrand disease, a synthetic derivative of vasopressin is highly effective; when administered intravenously, it causes an increase in the activity of von Willebrand factor and the coagulation activity of factor VIII in plasma, stopping bleeding. The drug is used in the form of intravenous injections at a dosage of 0.2-0.4 mg/kg 2 times a day during periods of bleeding or before and after surgical interventions. It can be combined with cryoprecipitate and aminocaproic acid (or tramexanoic acid).

Blood transfusions in most thrombocytopathy do not stop bleeding, and excessively massive ones aggravate platelet dysfunction and contribute to the development of disseminated intravascular coagulation with consumption thrombocytopenia.

Transfusions of native, antihemophilic plasma and administration of cryoprecipitate remain the main methods of replacement therapy for von Willebrand disease. They stop bleeding and prevent hemorrhagic complications during operations. Less clear, but in many cases the effect of antihemophilic plasma and cryoprecipitate is undoubtedly pronounced in Glanzmann thrombasthenia, essential athrombia and some secondary platelet dysfunctions.

Local stopping of bleeding is ensured by irrigating the bleeding surface with a 5% solution of aminocaproic acid cooled to 6-8°C, followed by application of a fibrin film with thrombin, application of adroxon to the bleeding surface, application of collagen or connective tissue extract with thrombin.

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Other diseases from the group Diseases of the blood, hematopoietic organs and certain disorders involving the immune mechanism:

Platelets are responsible for several processes in our body, but their main task is to organize stable blood clotting. In case of damage to blood vessels, platelets stick together, forming a clot, and replace the damaged area, restoring tissue.

One of the problems that can arise with them is low platelets.

If the level of blood cell coagulation falls, the number of platelets in the blood decreases, thereby increasing the possibility of bleeding and slow wound healing.

What processes do platelets perform in the body?

Originating primarily in the bone marrow, these blood platelets have a circular or oval shape, and never contain a nucleus. The diameter of platelets reaches from 2 to 4 microns.

Glycoprotein complexes are located directly on the membrane, as receptors, and assist platelets in activation, in establishing a spherical shape and forming pseudopodia (outgrowths of single-celled organisms used by cells for movement).

The gluing of platelets and their attachment to damaged areas of blood vessels are all the tasks of such complexes. They are attached to fibrin, after which they release thrombostenin (an enzyme), resulting in tissue compaction.

The main function of platelets is blood clotting.

Stimulating these blood cells directly also produces benefits. Components involved in blood clotting, while at the same time other useful and active substances are released.

Platelets are distributed throughout all vessels and participate in the following actions:

• Formation of blood clots, the initial thrombus that will stop bleeding by closing the damaged area;
• Nourishes blood vessels and also narrows them if necessary;
• Processes related to the immune system;
• They also take part in the dissolution of a blood clot, this process is called fibrinolysis;

The lifespan of platelets is from 8 to 10 days; towards the end of their existence, they decrease in size and lose their shape slightly.

Note! More than 75% of bloody discharge from the nose, prolonged menstruation, subcutaneous hemorrhages and gum blood flow are attributed to pathologies of the platelet formation system.

Normal in blood

Indicators of the normal level for the human body are 180-400*/l.

Low platelets are diagnosed if the level is below 140*/l.

Thrombocytopenia can be a symptom of another serious disease or an independent pathology.

Symptoms of Low Platelets

A situation in which the saturation of platelets in the blood is low is called thrombocytopenia.

If platelets are low, the following symptoms may occur:

• Bleeding from the nasal cavity;
• Prolonged menstruation, and in greater quantities;
• Bleeding gums;
• Formation of red dots on the skin;
• Accelerated formation of bruises and hematomas, even with slight pressure on the tissue.
• Profuse and slowly stopping bleeding when soft tissue is damaged;
• Less common is an enlarged spleen.

Slow stops of external hemorrhage, with this pathology, occur because the concentration of platelets in the blood is low, and the process of gluing and replacing the damaged area takes much longer.

Prolonged thrombocytopenia contributes to severe pathologies, which, if not given attention, can result in death.

They are:

• Large tissue damage with severe hemorrhages. With low blood clotting, severe bleeding caused by large-scale injuries is almost impossible to stop, which can lead to large blood loss;
• Hemorrhages can also occur in soft tissues, contributing to a stroke, which can cause significant complications or end in failure.

Existing types of thrombocytopenia

This pathology can be either congenital or develop over time. The majority of cases are acquired over time. And directly in a larger number of acquired ones, the factor of low platelets is reactions of an immune nature.

They are divided according to mechanisms into 4 groups:

• Autoimmune. Noticing platelet protein in the blood, the body secretes antibodies against it, considering it harmful; this disease is called autoimmune thrombocytopenia. Cancer, rubella, HIV, as well as autoimmune diseases and the use of certain drugs contribute to their development;
• Alloimmune. Appear as a result of platelet collapse, in the case of incompatible blood group, or during the production of antibodies;
• Transimmune. Antibodies in this scenario penetrate directly from the mother infected with autoimmune platelet disease to the child, transmitted through the placenta;
• Heteroimmune. The body produces antibodies due to the formation of a new antigen in the body, or infection of the red plate protein with viral diseases.

What is spontaneous thrombocytopenia?

During pregnancy, the drop in blood clotting is insignificant and within normal limits. But if you notice symptoms of a more severe fall, you should immediately consult a doctor. Also, a strong fall is fraught with large loss of blood during childbirth, which can be fatal for the mother.

What foods to exclude to increase clotting?

Certain foods can affect blood thinning or thickening. If coagulation rates are low, it is necessary to remove or reduce the consumption of foods that are not allowed for thrombocytopenia.

They are as follows:

• Green tea;
• Blueberry;
• Fresh tomatoes;
• Pepper;
• Garlic;
• Ginger;
• Celery juice, raspberry juice;
• Sea fish;
• Yogurts and kefir;
• Low-fat meat (turkey and chicken);
• Nuts;
• Sunflower seeds
• Olive oil;
• and others.

The following herbs also lead to low platelets:

• Fresh nettle;
• Yarrow;
• Burdock;
• Needles;
• Burnet;
• and others.

A certain list of medications also affects greater blood thinning, so you should stop using the following medications:

• Aspirin;
• Phenilin;
• Chime;
• ThromboAss;
• Cardiomagnyl;
• Ginko Biloba;
• Aspecard.

How to diagnose low platelets?

It is necessary to consult a doctor, he will be able to conduct an examination, prescribe tests, and the correct therapy, identify a possible more serious disease that provoked thrombocytopenia, and help you choose the right diet to normalize the thickening.

How to treat slow clotting?

There are no specific medications aimed at quantitatively increasing platelets. Treatment in this case depends more on the pathology that caused this state of platelets in the blood. For minor deviations from the norm, no specialized treatment is required; you just need to bring your diet back to normal.

To bring clotting rates back to normal, you should not only eliminate thinning foods, but also add foods that help thicken the blood to your diet.

Products

The following list of products will help in increasing clotting processes:

• Cheese and cottage cheese, which contain large amounts of calcium;
• Legumes (almonds, peanuts, hazelnuts) containing fatty acids;
• Products rich in iron, such as meat, apples, buckwheat, etc.;
• Rose hip;
• Carrot;
• Fish oil (omega-3);
• Spinach, parsley;
• Potato;
• Peas;
• Corn;
• Beef liver;
• and others.

Drugs

Immune system stimulation agents are also prescribed:

• Immunal;
• Echinacea tincture.

Folk remedies

There are also methods to reduce the increase in blood density with folk remedies, these include:

• Currant leaves;
• Dog-rose fruit;
• Thyme leaves;
• Coltsfoot;

All herbs are brewed as tea and taken orally. Doctors also recommend including sesame oil (10 g per day) in your diet; along with these remedies, you need to consume more onions and garlic.

Note! You can thicken the blood with a decoction of dried nettle leaves. It is very important that the leaves are dry, as fresh leaves help thin the blood.

If the patient’s condition is very serious, then in a clinical setting a transfusion of platelets and plasma is performed.

Important! If antibodies to platelets are detected, platelet transfusions should be abandoned, as there is a risk of increased bleeding.

If low platelets are caused by a disease, then a narrow spectrum of the disease is determined and the disease itself is referred for additional research (oncology, hepatitis, etc.). And after this, the drugs are coordinated with a qualified doctor in this field.

Video. Thrombocytopenic purpura

Conclusion

Any deviation of platelets from the specified norm is fraught with serious consequences. Low platelets provoke bleeding and cerebral hemorrhages, which is very dangerous for health.

If factors of thrombocytopenia are detected, you should immediately urgently go to a qualified doctor, take a test to study blood density, and introduce foods that affect blood thickening into your diet.

Clotting during pregnancy requires special attention, as it can be dangerous for both the expectant mother and the unborn child.

In order not to experience serious illnesses and consequences, it is better not to self-medicate!

Platelets, colorless blood cells, play a vital role in protecting the body from blood loss. They can be called ambulances, since they instantly rush to the site of damage and block it. This process is called aggregation.

Platelet aggregation - what is it?

Platelet aggregation is a process in which cells stick together. This forms a plug that closes the wound. At the initial stage, blood cells stick together and later adhere to the walls of the vessel. The result is a blood clot called a thrombus.

In a healthy body, aggregation is protective: platelets clog the wound and bleeding stops. In some cases, the formation of blood clots is undesirable because they block blood vessels in vital organs and tissues.

1. Increased activity of colorless blood cells can lead to stroke and heart attack.
2. Decreased platelet production often leads to large blood loss. Frequent bleeding that does not stop for a long time leads to exhaustion and anemia (anemia).

According to statistics, one in 250 people die from thrombosis every year.

In order to prevent the disease, it is necessary to control the level of platelets and their ability to aggregate.

• frequent bleeding - uterine, from the nose;
• the appearance of bruises from the slightest injury;
• poorly healing wounds;
• swelling.

Normal indicators

Normally, aggregation is 25–75%. Such indicators indicate good hematopoiesis and sufficient oxygen supply to tissues and organs.

Platelet norm - table

Platelet Aggregation Test

A blood test allows you to identify deviations from the norm and diagnose pathologies of the hematopoietic and cardiovascular systems. In addition, the procedure is prescribed to monitor the dynamics of a number of diseases and prescribe appropriate treatment.

The analysis is carried out in laboratory conditions. To do this, blood is taken from a vein. Before the study, the patient is recommended:

• follow a diet prepared by a specialist for 1–3 days;
• 8 hours before the procedure, avoid foods high in fat, as well as take medications, including Voltaren gel (if possible);
• 24 hours in advance, avoid the use of immunostimulants, including coffee, alcohol, garlic, and stop smoking.

The study is carried out in the morning on an empty stomach. Before the procedure, you are allowed to drink only clean, still water.

After collecting venous blood, special substances are added to it - inducers, which in their composition are similar to the cells of the human body, promoting thrombus formation. For this purpose use:

• ADP - adenosine diphosphate;
• ristomycin;
• adrenalin;
• arachidonic acid;
• collagen;
• serotonin.

The method for determining aggregation is based on transmitting light waves through blood plasma before and after clotting. The nature, shape and speed of the light wave are also taken into account.

It should be noted that the study is not carried out if there is an inflammatory process in the body.

The indicator depends on the substance that was added to the blood and its concentration.

Aggregation rate depending on the inductor - table

Types of aggregation

Doctors distinguish several types of aggregation:

• spontaneous - determined without an inductor substance. To determine the aggregation activity of platelets, blood taken from a vein is placed in a test tube, which is placed in a special device, where it is heated to a temperature of 37°C;
• induced - the study is carried out with the addition of inducers to the plasma. Typically, four substances are used: ADP, collagen, epinephrine and ristomycin. The method is used to determine a number of blood diseases;
• moderate - observed during pregnancy. Caused by placental circulation;
• low - occurs in pathologies of the circulatory system. A decrease in platelet levels can lead to various types of bleeding. Observed in women during menstruation;
• increased - leads to increased thrombus formation. This manifests itself in the form of swelling and a feeling of numbness.

Platelet hyperaggregation

If the level of aggregation (hyperaggregation) increases, increased thrombus formation occurs. In this condition, the blood moves slowly through the vessels and clots quickly (the norm is up to two minutes).

Herbs for thinning thick blood and strengthening the walls of blood vessels:

Hyperaggregation occurs when:

• diabetes mellitus;
• hypertension - high blood pressure;
• cancer of the kidneys, stomach, blood;
• vascular atherosclerosis;
• thrombocytopathy.

Increased levels of aggregation can lead to the following conditions:

• myocardial infarction - an acute disease of the heart muscle that develops due to insufficient blood supply;
• stroke - cerebrovascular accident;
• thrombosis of the veins of the lower extremities.

Ignoring the problem can be fatal.

Treatment methods depend on the complexity of the disease.

Drug therapy

At the initial stage, it is recommended to take medications whose action is aimed at thinning the blood. Regular aspirin is suitable for this purpose. To prevent bleeding, the drug in a protective shell is taken after meals.

The use of special medications will help prevent the formation of new blood clots. All medications are taken only after consultation with the attending physician.

After additional studies, the patient is prescribed:

• anticoagulants - medications that prevent rapid blood clotting;
• novocaine blockade, painkillers;
• drugs that promote vasodilation.

Diet

• seafood;
• greenery;
• citrus;
• garlic;
• green and red vegetables;
• ginger.

It is very important to maintain a drinking regime, since an insufficient amount of fluid causes vasoconstriction, as a result of which the blood thickens even more. You should consume at least 2–2.5 liters of water per day.

Avoid foods that promote hematopoiesis:

• buckwheat;
• pomegranate;
• chokeberry.

Prohibited products - gallery

1. Sweet clover. Pour 1 tbsp boiling water over a glass. l. ground herbs, leave for 30 minutes. Divide the liquid into 3-4 equal parts and drink throughout the day. The course of therapy is a month. If necessary, repeat treatment.
2. Peony. Grind the root and pour 70% alcohol in a proportion of 1 tbsp. l. for 250 ml. Leave in a dark place for 21 days. Take 30 drops before meals 3 times a day for two weeks. Then you need to take a break for a week and repeat the course.
3. Green tea. Mix 1 tsp. ginger root and green tea, pour 500 ml of boiling water, add cinnamon on the tip of a knife. Infuse tea for about 15 minutes. You can add lemon for taste. Drink during the day.
4. Oranges. It is recommended to drink 100 ml of freshly squeezed orange juice daily. Can be mixed with pumpkin juice in a 1:1 ratio.

Platelet hypoaggregation

A reduced level of aggregation is no less dangerous for the health and life of the patient. Insufficient platelet aggregation (hypoaggregation) causes poor blood clotting (thrombocytopenia). As a result, the formation of clots (thrombi) does not occur, which leads to severe bleeding.

Doctors distinguish between hereditary and acquired platelet hypoaggregation.

According to WHO, the disease affects about 10% of the world's population.

Low aggregation ability is activated by a viral or bacterial infection, physiotherapy, or taking medications.

Hypoaggregation occurs when:

• renal failure;
• chronic leukemia - a malignant disease of the circulatory system;
• decreased thyroid function;
• anemia (anemia).

Diet

Nutrition is an important factor in normalizing platelet levels. The diet should contain foods that promote hematopoiesis:

• buckwheat;
• fish;
• red meat - prepared in any way;
• beef liver;
• eggs;
• greenery;
• salads with carrots, nettles, bell peppers, beets;
• pomegranates, bananas, rowan berries, rosehip juice.

In this case, you should reduce or completely eliminate the consumption of ginger, citrus fruits, and garlic.

Traditional treatment

In advanced cases, treatment is carried out only in a hospital setting. The patient is prescribed:

1. Aminocaproic acid solution 5% intravenously.
2. Sodium adenosine triphosphate intramuscularly or subcutaneously.
3. Preparations: Emosint, Dicynone, Tranexamic acid.

In case of severe bleeding, a transfusion of donor platelet mass is performed.

Patients should avoid taking medications that thin the blood:

• Troxevasin;
• Aspirin;
• Paracetamol;
• Ibuprofen;
• Eufillin;
• Antidepressants.

Drugs for the treatment of hypoaggregation - gallery

Hypoaggregation

A decrease in aggregation capacity is no less dangerous for the health of a pregnant woman and the fetus than hyperaggregation. In this condition, the vessels become fragile, bruises appear on the body, and the gums begin to bleed. This occurs due to a violation of the qualitative composition of blood cells or their insufficient production. Hypoaggregation can cause uterine bleeding during and after childbirth.

A decrease in platelet levels is provoked by the following factors:

• taking medications - diuretics, antibacterials;
• autoimmune and endocrine diseases;
• allergy;
• severe toxicosis;
• poor nutrition;
• lack of vitamins B12 and C.

To improve the synthesis of blood cells, a woman is recommended to consume foods rich in vitamins B and C:

• black currant;
• apples;
• Bell pepper;
• cabbage;
• lemons;
• rosehip tincture.

The doctor prescribes special medications that have a beneficial effect on the hematopoietic system without having a negative effect on the baby.

To avoid the negative consequences and risks associated with hyper- or hypoaggregation, doctors recommend conducting a study on platelet aggregation ability even when planning pregnancy.

Features in children

Despite the fact that increased aggregation capacity is usually found in the adult population, recently there has been an increase in cases of the disease in children.

Hyperaggregation can be either hereditary or acquired. The causes of elevated platelet levels are not much different in adults. Mainly:

• diseases of the circulatory system;
• infectious and viral diseases;
• surgical intervention.

1. In children under one year of age, hyperaggregation can be caused by dehydration and anemia. In adolescence, stressful situations and physiological growth of the body play an important role.
2. Hypoaggregation in children manifests itself in the form of nosebleeds and bruises. Girls in adolescence may experience heavy periods. In 100% of cases, pinpoint rashes are observed on the skin, and 20% of children experience bleeding gums.

Treatment begins with finding out the cause of the deviation from the norm in platelet aggregation ability. Sometimes adjusting your diet and drinking regime is enough. In some cases, treatment of the disease that caused the abnormality is required.

If necessary, a hematologist will conduct an additional examination and prescribe medication according to the patient’s age and severity of the disease.

Why platelet levels drop - video

A study of the level of platelet aggregation is an important diagnostic procedure that allows you to identify serious diseases, reduce the risk of complications and carry out timely therapy.

Such “help” for injuries helps preserve a person’s life and prevents heavy blood loss. Regular blood testing for the content and average volume of platelets, as well as the level of aggregation, is an important need for every person.

Aggregation, its forms, types and role in the body

The aggregation process is one of the final stages of the blood coagulation mechanism. In this case, crowding or sticking of platelets occurs. When the integrity of a blood vessel is damaged, a special substance is released from its tissues - adenosine diphosphate (ADP). It is the most important stimulator of platelet aggregation at the site of injury. ADP is also produced and released by blood cells such as red blood cells and platelets.

Platelet aggregation always follows adhesion, when single cells adhere to the site of vessel injury. Further sticking of platelets is called aggregation - the formation of a stable and dense clot, a plug that can clog the damaged area.

Depending on the type of clot formed during the crowding process, two forms of aggregation are distinguished:

1. Reversible. The plug is loose and allows plasma to pass through.
2. Irreversible. It is formed with the participation of thrombostenin, a protein that promotes compaction and fastening of the plug in the vessel.

Platelet aggregation allows bleeding to stop within 15 seconds.

There are several types of platelet crowding:

• decreased - hypoaggregation;
• increased - hyperaggregation;
• moderately elevated. This type is typical for pregnant women;
• normal induced. It develops according to a standard mechanism with the participation of activators - ADP and other substances;
• normal spontaneous. It occurs without the participation of stimulants under the influence of external factors, especially heating above body temperature. Often used in the process of performing a blood test.

Role of platelet crowding:

• clogging of the wound;
• stopping any type of bleeding;
• protection against anemia caused by blood loss;
• preventing the development of excessive physiological bleeding. An example is menstruation in women.

Aggregation study, normal values

Reasons to consult a doctor and examine the condition of the coagulation system are:

• frequent bleeding, even minor, increased bleeding of the gums, periodic nosebleeds;
• heavy menstruation;
• hematomas from minor blows;

• long-term non-healing wounds;
• swelling;
• autoimmune diseases;
• bone marrow pathologies;
• oncological diseases;
• spleen diseases;
• circulatory and heart problems;
• frequent surgical interventions;
• the need to select a dose of a blood thinner;
• before surgery.

When performing a blood test for platelet aggregation, it is important to understand that this is a test that requires preliminary mandatory preparation.

• following a special diet during the day before blood sampling. It is important to avoid eating fatty foods;
• 6-8 hours before giving up coffee and alcohol;
• no smoking 4 hours before;
• do not eat spicy foods, onions and garlic 6 hours before;
• If possible, avoid taking medications for 5-7 days, especially those that affect the blood clotting process. If the study is carried out on people with chronic pathologies, then it is important to inform the doctor about the medications being taken;
• exclude the presence of acute inflammation in the body;
• in one day, eliminate heavy loads and exhausting work, relax and get enough sleep.

For analysis, venous blood taken on an empty stomach is used, preferably within three hours after waking up. Aggregation stimulants are added to the resulting sample in the required volume. Different laboratories use such substances to choose from - ADP, adrenaline, collagen, serotonin. Further analysis is to study the changes in the wavelength of light passed through the blood sample before and after clotting.

The norm of platelet crowding indicators depends on which stimulating substance is taken for analysis:

• ADP - platelet aggregation from 31 to 78%;
• collagen - norm from 46.5 to 93%;
• adrenaline - 35-92%.

Increased aggregation: causes, complications and treatment

This condition is called hyperaggregation. It consists of increased blood clotting in the vessels, which can lead to an increased risk of blood clots, as well as death.

Causes and diseases that are accompanied by hyperaggregation:

• oncological diseases of the blood;
• stomach cancer;
• kidney cancer;
• hypertonic disease;
• circulatory disorders;
• arrhythmia;
• bradycardia.

• strokes;
• heart attacks;
• sudden death due to blockage of large blood vessels by a thrombus;
• insufficient blood supply to organs due to narrowing of the lumen of blood vessels, mainly the brain;
• vein thrombosis in the lower extremities.

Principles of drug treatment of hyperaggregation:

1. Taking medications based on acetylsalicylic acid (Cardiomagnyl). Taking such drugs is justified from the age of 40 to maintain normal blood consistency and reduce the risk of blood clots.
2. Taking antiplatelet agents (Clopidogrel), which reduce platelet aggregation and normalize blood viscosity.
3. Taking anticoagulants (Heparin, Fraxiparine, Streptokinase) to prevent the formation of blood clots.
4. The use of agents that dilate the lumen of blood vessels - vasodilators and antispasmodics.
5. Treatment of the underlying pathology that causes hyperaggregation.

Principles of non-drug treatment of hyperaggregation:

1. A diet rich in plant foods - greens, citrus fruits, vegetables. For protein products, give preference to dairy products. Seafood will also help maintain normal blood properties. Limit the consumption of buckwheat, pomegranates and chokeberries.
2. Compliance with drinking regime. Lack of fluid in the body is often accompanied by hyperaggregation and thrombus formation. You should drink at least 2 liters of clean water per day.
3. Traditional medicine cannot be considered as an alternative to drug treatment. The main medicinal plants that reduce blood clotting are sweet clover, peony root, and green tea.

Reduced aggregation: causes, complications and treatment

This condition is called hypoaggregation in medicine. This is a dangerous disorder that leads to poor blood clotting, the threat of serious blood loss and possible death of the patient.

• infectious diseases;
• renal failure;
• leukemia;
• hypothyroidism;
• anemia;
• irrational use of blood thinning drugs;
• intoxication;
• thrombocytopenia;
• dehydration;
• chemotherapy.

Drug treatment is based on the use of drugs with hemostatic properties, as well as treatment of the underlying disease:

In severe cases, the patient is transfused with donor blood.

Non-drug methods of helping the patient:

1. Diet. Enrich the diet with foods that stimulate hematopoiesis - buckwheat, liver, meat, pomegranates, red fish.
2. Herbal medicine with nettle leaves, beet juice, chokeberry, sesame seeds.

Aggregation in children and pregnant women: main features

Bleeding disorders are rare in childhood. They can be hereditary, and also be the result of viral and bacterial infections, anemia and severe dehydration. The main measure of assistance is the normalization of nutrition, drinking regime, as well as the treatment of diseases that have caused clotting disorders. During adolescence, the role of stress in the development of platelet aggregation disorders increases.

Particular attention should be paid to issues of blood clotting in pregnant women. This is important both for the process of gestation and for the normal course of labor.

In expectant mothers, platelet aggregation is slightly increased, which is caused by a physiological increase in circulating blood volume.

• miscarriage;
• premature onset of labor;
• miscarriage.

• bleeding during pregnancy;
• heavy and dangerous bleeding during childbirth;
• death from massive blood loss.

Timely provision of assistance and the prescription of effective medications will help prevent life-threatening complications for the mother and child.

What is platelet aggregation?

Platelet aggregation is the process of gluing the presented blood cells together, as well as their attachment to the vascular walls. Aggregation is inherently the initial stage of the formation of a blood clot, which prevents blood loss.

What are platelets?

Platelets are formed blood cells that help normalize the process of blood clotting. This happens as follows. In the event of a violation of the integrity of the vascular walls, platelets, through a chain of biochemical reactions, receive a certain signal, gather at the site of the breakthrough and, sticking together, ensure the blockage process. This is how the aggregation process occurs.

However, an excessively intense aggregation process is pathological. Platelet hyperaggregation leads to increased thrombus formation, which significantly increases the risk of developing diseases such as stroke and myocardial infarction.

Low aggregation rates are no less dangerous and pose a potential threat not only to the health, but also to the life of the patient. Insufficient platelet adhesion leads to the formation of a disease such as thrombocytopenia (reduced blood clotting). At the same time, there is a high probability of developing internal and external bleeding, which not only contributes to the development of severe forms of anemia, but can also cause death.

Therefore, it is extremely important to monitor the platelet content in the blood, as well as their ability to aggregate.

Platelet aggregation is especially important during pregnancy. The fact is that violations of this process can lead to a number of quite serious consequences. Hypoaggregation (reduced platelet aggregation) can provoke uterine bleeding during the birth process or after the birth period. Excessively active aggregation is also dangerous for the expectant mother and her baby, as it can lead to the formation of blood clots, which is one of the most common causes of miscarriages and spontaneous termination of pregnancy in the early stages.

In order to avoid such adverse consequences and minimize risks, experts recommend conducting a study on the level of platelets in the blood and identifying their ability to regenerate before conception, when planning pregnancy.

Studies to control aggregation

Laboratory testing of platelets is carried out using a diagnostic technique called induced aggregation. To carry out this procedure, specific substances are added to the venous blood taken from the patient, the chemical composition of which is similar to the cells of the human body, promoting the process of thrombus formation, resulting in platelet agglutination. Substances that make up the walls of blood vessels are usually used as inducers. These include:

A special device is used for analysis - a platelet aggregation analyzer. During the study, light waves are passed through blood plasma filled with platelets. The analysis is carried out in two stages. Indicators of the degree of aggregation represent the difference in the light density of the plasma before the start of the coagulation process and after its completion. In addition, experts pay attention to factors such as the shape, nature and specificity of the light wave.

Induced platelet aggregation is a method of blood testing that is characterized by extremely high accuracy and is therefore widely used in modern diagnostics when certain diseases are suspected.

Not all clinics have the necessary equipment to carry out this type of diagnostic procedure. To date, platelet aggregation studies have been successfully carried out in Invitro laboratories.

Why is the research being conducted?

A blood test to study platelets allows a specialist to determine the ability of these blood cells to aggregate and makes it possible to identify certain hemostasis disorders, which can be both congenital and acquired. In addition, by studying platelet aggregation, it is possible to diagnose not only pathologies of the hematopoietic system, but also diseases of the cardiovascular system. This procedure is necessary to monitor the dynamics of a number of certain diseases, determine the necessary therapeutic techniques, and control the treatment process.

Indications for the study

Induced aggregation can be prescribed by a specialist in the following cases:

1. Thrombocytopenia.
2. Increased blood clotting.
3. Tendency to thrombosis.
4. Bleeding gums.
5. Increased swelling.
6. Tendency to bleeding, uterine bleeding.
7. Poorly healing wounds.
8. Long-term treatment with acetylsalicylic acid preparations.
9. Von Willebrand's and Glanzmann's diseases.
10. Thrombophilia.
11. Complicated pregnancy.
12. Cerebrovascular accident, coronary heart disease.
13. Thrombocytopenia of congenital or acquired nature.
14. Varicose veins.
15. Monitoring the dynamics of treatment with antiplatelet drugs.
16. Autoimmune diseases.
17. Study of the functionality of platelet cells before surgery.
18. Infertility.
19. Several unsuccessful IVF attempts in a row.
20. Frozen pregnancy.
21. Determining the degree of sensitivity of the patient to the effects of antiplatelet agents.
22. Glanzmann's thrombasthenia.
23. Bernard-Soulier disease.
24. Before and while taking hormonal contraceptives.

How to prepare for research?

A blood test for the ability of platelets to undergo the aggregation process requires strict adherence to the preparation rules. In order for the study to be extremely correct and effective, patients must follow the following recommendations:

1. A week before taking blood for testing, you must stop taking medications that suppress thrombus formation. These include the following medications: acetylsalicylic acid preparations, antidepressants, Sulfapyridazine, Dipyridamole, Indomethacin, antiplatelet agents, hormonal drugs, contraceptives.
2. The day before the study, you must refrain from drinking caffeine-containing and alcoholic beverages.
3. Eliminate fatty, hot, spicy foods, spices and garlic from your diet.
4. Smoking is prohibited on the day of the procedure.
5. Extremely limit physical and psycho-emotional stress.
6. The last meal should be no later than 12 hours before blood sampling for analysis.

A contraindication to induced platelet aggregation is considered to be the presence of acute or chronic inflammatory processes in the body.

Compliance with the above rules is necessary to obtain the most accurate and objective results of the study!

Carrying out analysis

A blood test to determine the ability of platelet cells to regenerate is carried out exclusively in the morning. The ideal time for blood collection is considered to be from 7 to 10 am.

The study is carried out on an empty stomach; on this day the patient should not drink anything other than pure still water.

Venous blood is used to conduct a test to determine the degree of platelet aggregation. It is collected from the patient’s ulnar vein using a disposable syringe. Next, the material is placed in a test tube with a four percent sodium citrate solution. After this, the container is turned over several times so that the blood is completely mixed with this active substance. At the next stage, the tube with the collected blood is sent to the laboratory for further research.

Interpretation of results

Interpretation of the research results is carried out by a qualified specialist in laboratory conditions.

The norm in the case of this analysis is determined depending on the substance used - an inducer that reacts with the patient’s blood.

Let's look at this issue in more detail:

1. Normal levels for reaction with collagen range from 46 to 93%.
2. Normal values ​​for the reaction with adenosine diphosphate range from 30 to 77%.
3. Normal levels for reactions with ristomycin range from 35 to 92.5%.

A decrease in platelet aggregation can be caused by the following factors:

1. Pathologies of the hematopoietic system.
2. Positive effect of antiplatelet therapy.
3. Thrombocytopathy.

An increase in platelet aggregation may indicate the presence of the following pathologies:

1. Hypertension.
2. Stroke.
3. Diabetes.
4. Heart attack.
5. Vascular atherosclerosis.
6. Thrombosis of the abdominal arteries.

The study of platelet aggregation properties is an important diagnostic procedure, which makes it possible to diagnose a number of diseases at an early stage of their development, predict possible complications, and prescribe the optimal course of treatment.

• Hemoglobin
• Glucose (sugar)
• Blood type
• Leukocytes
• Platelets
• Red blood cells

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Platelet aggregation. What is it, how to get tested, what to do if there are deviations from the norm

A specific stimulated process during which gluing, or more precisely, platelet clumping, occurs is called aggregation. It occurs in two stages. At the first stage, platelets stick together, at the second they attach to the walls of blood vessels. Thus, these cells form a kind of plug. In medicine it is called a blood clot. Using this reaction, it is possible to determine disturbances in the functioning of the cardiovascular system. A blood test, which is taken to study platelets, is prescribed in cases of: decreased/increased coagulability (in the first case, this is evidenced by bruises from minor blows, poor wound healing, etc., in the second - swelling), pregnancy with some complications.

Why does the human body need platelet aggregation?

This reaction is defensive. With various damage to blood vessels, platelets stick together, reach the diameter of the blood flow and block the problem area. Deviation from the norm in aggregation indicators requires immediate medical intervention. Increased platelet adhesive properties can lead to heart attack and stroke. Reduced aggregation indicates that a minor cut will result in a large loss of blood, subsequently causing anemia, exhaustion, etc. Platelet aggregation, the norm of which is 0–20%, is very important for the normal functioning of the body.

Procedure for taking a blood clotting test

Before the analysis, the attending physician must conduct a specialized consultation with the patient. During the conversation, he must indicate: the purpose of donating blood, what coagulation means, the dependence of treatment on the test result, how, when, under what circumstances the procedure will take place. Also, during the consultation, the doctor is obliged to talk about the possibility of discomfort for the patient during the test. Platelet aggregation is examined after the patient has followed a diet prepared by a specialist for 1-3 days, and 8 hours before the procedure he has given up foods that contain large amounts of fat. Also, to ensure the reliability of the results, the patient is forced to refrain from taking medications for some time. If this is not possible, then this should be taken into account when testing blood for coagulation.

Platelet aggregation during pregnancy

During this period, for women there is some likelihood of increased blood clotting. This deviation from the norm occurs during pregnancy pathology. Platelet aggregation in women in an “interesting” position should be constantly monitored by a hematologist, who gives a referral for the necessary tests. In case of an increase, or in some cases a decrease in blood clotting, the specialist prescribes medication. Doctors strongly recommend checking platelet aggregation at the planning stage of pregnancy, as this can help avoid significant problems with the health of the mother and child in the future.

Deviations from the norm. What to do?

If blood clotting is reduced or increased, in any case you need to consult an experienced specialist. He will prescribe additional tests, conduct a survey, examination and make a diagnosis. Often, platelet aggregation that does not correspond to the norm is secondary. It should also be taken into account that women may experience decreased blood clotting during menstruation. This protects them temporarily from blood clots. A fatal outcome can occur with an increased tendency to blood clotting, therefore, at the slightest suspicion of this (numbness of the limbs, swelling), immediate treatment is necessary. Ignoring symptoms is life-threatening.

What can not the result of a blood test affect clotting?

If the patient does not take into account the recommendations of the attending physician before undergoing the test, this may lead to incorrect treatment. As a result, irreparable harm will be caused to the general condition of the patient. Distortion of the results of the platelet aggregation test may be due to the fault of the laboratory technician who performed it. This occurs when the inductors that stimulate the required process are incorrectly selected or when the component reactions interact poorly with each other. Impaired platelet aggregation occurs in people suffering from obesity, hemolysis, and tobacco smokers.

Platelet aggregation

Platelets are small blood cells that are responsible for blood clotting. They help stop blood loss if bleeding occurs.

When a wound occurs, platelets move to the injured area. Here they are attached to the wall of the damaged vessel, as a result of which the bleeding stops. This process is called platelet aggregation.

What is platelet aggregation

Platelet aggregation is a process in which blood cells adhere to each other and fix them on the wall of the injured vessel. This stops the bleeding. However, such a process can also be dangerous for the body. In this case, a blood clot forms, which under some circumstances can cause a heart attack and stroke. This can happen if platelets are overactive and aggregation occurs too quickly.

In addition, the slow process also does not promise anything good for the body. In this case, poor blood clotting may occur due to slow platelet adhesion. This pathology causes anemia. If blood clotting is poor, it is difficult to stop bleeding, which can lead to health problems and even death. To prevent this from happening, it is necessary to monitor the level of platelets in the blood and their ability to stick together.

The process of platelet aggregation during pregnancy

It is extremely important that platelet aggregation proceeds normally during pregnancy. If the process occurs too slowly, then during childbirth or in the postpartum period, bleeding from the uterus may occur, which can lead to the death of the woman. In addition, if platelet aggregation occurs quickly during pregnancy, blood clots may form, which during pregnancy can lead to its interruption at any stage.

You can avoid this situation if you plan your pregnancy and take care of your health in advance. It is necessary, even before conception, to find out what state the platelets are in and, if necessary, take measures to correct the situation. If pregnancy was not planned, then the pathology of aggregation can be avoided by registering at an early stage. Then the doctor will prescribe the necessary tests and help get rid of the pathological state of platelets if one is detected.

Normal platelet count in blood

To know the state of platelet levels, you need to have an idea of ​​their normal level.

If we talk about the aggregation rate, then it is 25-75%. In this case, the process of platelet gluing occurs well and does not pose any health hazard.

Blood test for platelet aggregation

A blood test called induced aggregation helps to study the state of platelets. In this case, blood is taken from the patient’s vein and mixed with special substances. Such agents have a composition that is similar to the composition of the body cells that take part in the aggregation process. The following substances are most often taken as inductors:

The most commonly performed procedure is platelet aggregation with ADP. To perform the study, a special device is taken. It's called a platelet aggregation analyzer. With its help, light waves are passed through the blood before it begins to clot and after this process is completed. Then the result is evaluated.

Preparing for tests

To ensure that the result is as accurate as possible, you must follow the following rules for taking a blood test:

• The study is performed on an empty stomach. In this case, you need to stop eating 12 hours before the test. In this case, you can drink clean still water.
• 7 days before the test, you need to stop drug treatment with certain medications. If this is not possible, then you need to inform the doctor who is conducting the analysis.
• A few days before the analysis, you should avoid stressful situations and physical activity.
• You must stop drinking coffee, smoking, drinking alcohol and garlic 24 hours in advance.
• Research cannot be carried out if an inflammatory process occurs in the body.

Indications for analysis

• increased blood clotting;
• predisposition to blood clots;
• thrombocytopenia and thrombophlibia;
• predisposition to bleeding of various types, including uterine;
• constant swelling;
• bleeding from the gums;
• long wound healing process;

Interpretation of the result of the analysis of induced aggregation

The interpretation of indicators depends on the means by which the study was conducted. To do this, the data is compared with the norm.

If the results deviate from the norm upward, then increased platelet aggregation is diagnosed. This condition occurs when:

• high blood pressure;
• atherosclerosis;
• leukemia;
• diabetes mellitus;
• oncological diseases of the gastrointestinal tract or kidneys;
• lymphogranulomatosis;
• sepsis;
• surgical removal of the spleen.

Increased platelet aggregation can lead to heart attack, stroke, thrombosis and death due to blockage of a vessel by a blood clot.

If the results deviate from the norm towards a decrease, then a reduced aggregation of thrombosis is diagnosed. This is due to:

• blood diseases;
• thrombocytopathy;
• use of antiplatelet agents.

With reduced aggregation, vessels become fragile. In addition, the process of stopping bleeding is difficult, which can cause death.

Means that reduce the aggregation process

Some agents inhibit the aggregation process. These drugs include antiplatelet agents. Platelet aggregation inhibitors include drugs such as acetylsalicylic acid, ibustrin, micristin and others. Such drugs are prescribed for the treatment of certain diseases. However, if the aggregation process sharply deviates from the norm, then inhibitor drugs should be replaced with other agents that do not lead to such consequences. If this is not possible, then the doctor may prescribe special drugs that promote aggregation.