Thrombocytosis is an increase in the number of platelets in the blood. With thrombocytosis, the platelet count can reach about 500,000 per cubic meter. mm. The causes of the development of this disease can be: too rapid production of platelets in the bone marrow, slowing down their decay, changing their distribution in the blood stream, etc.
Thrombocytosis of blood is a provoking factor in the formation of thrombi. In certain cases, thrombocytosis can lead to bleeding due to platelet defects and due to impaired microcirculation. Therapy of thrombocytosis consists in the prevention of thrombosis and the treatment of the underlying disease, which causes an increase in the level of platelets.
Clarification of the type of thrombocytosis is considered extremely important, because clonal thrombocytosis of blood is often accompanied by the formation of complications of thrombotic nature and requires careful therapeutic examination.
In other myeloproliferative pathologies (true polycythemia, chronic leukemia , essential thrombocythemia, etc.), thrombocytosis acts as a major complication, which affects the nature of the underlying disease and leads to complications with the formation of thrombi.
Thrombocytosis is of several types: clonal thrombocytosis, primary thrombocytosis, secondary thrombocytosis. At its core clonal and primary thrombocytosis have a similar developmental pattern.
With clonal thrombocytosis, the cause of development is the defect of stem hemopoietic cells. These stem cells have a tumor character in the case of myeloproliferative states with chronic course. They also have a high sensitivity to thrombopoietin and do not have a particular dependence on stimulation of the exocrine system. The production of platelets in this case is an uncontrolled process, while the platelets themselves are functionally defective, as a result of which their interaction with other substances and cells stimulating thrombus formation is disturbed.
Primary thrombocytosis is referred to as the so-called myeloproliferative syndrome, in which the work in the bone marrow of stem cells is disrupted and several areas of hematopoiesis in the given organ are proliferating. Therefore, a large number of platelets is released into the peripheral blood.
Secondary thrombocytosis develops due to an increase in the amount of platelet level in a chronic disease. Currently, there are several reasons for its development.
The most common cause of secondary thrombocytosis is infection. Infectious factors include: meningococcal infection, viruses, fungi, parasites.
In addition to infectious agents, there are other factors: hematologic (iron deficiency in anemia, the use of chemotherapy for oncological conditions); removal of the spleen (1/3 of the total platelet counts accumulate in this organ, after removal of which the volume of blood with artificial growth of platelets decreases); surgical operations and trauma; inflammatory processes provoke an increase in platelets (increases the level of interleukin, which provokes increased production of thrombopoietin); oncological conditions; medicinal preparations (corticosteroids, sympathomimetics, antimitotics, contraceptives).
Thrombocytosis in pregnancy is in most cases a reversible condition and is explained by the physiological processes when carrying a child. These include: slowing the metabolism, increasing blood volume, iron deficiency anemia of pregnant women, etc.
Primary thrombocytosis is classified as a myeloproliferative disease, which is manifested by a significant increase in the number of platelets in the blood. In connection with these patients, thrombohemorrhagic syndrome develops. The basis of this thrombocytosis is the development of intravascular disseminated blood clotting and microcirculation disorders. The aggregation capacity of platelets is also impaired. The frequency of morbidity in men and women is the same. The first signs of blood thrombocytosis appear more often at the age of 50 years.
Patients complain of bleeding (uterine, nasal, intestinal, renal, etc.), ecchymosis, hemorrhages of subcutaneous localization, cyanosis of the skin and mucous membranes, itching of the skin , tingling in the fingers and toes. In some cases, gangrene develops. In addition to bleeding, patients with thrombocytosis may have diseases such as vegetative-vascular dystonia (cold extremities, migraine headaches, blood pressure instability, tachycardia , dyspnea, etc.), vein thrombosis (splenic, portal, hepatic, uterine (up to 15 mm)).
But the appearance of thrombi can be not only in the veins, but also in the arteries (carotid, mesenteric, pulmonary, cerebral, etc.). The content of platelets in the blood reaches 800 to 1250. In microscopic blood tests, platelets are presented in the form of large aggregates. In some cases, platelets reach gigantic sizes, with altered vacuolization and shape, with the detection of megakaryocytes or fragments thereof. The content of leukocytes usually does not reach high values (10-15), the leukocyte formula is not changed. The content of hemoglobin and erythrocytes can be increased.
With recurrent bleeding, iron deficiency anemia may develop. During the study in bone marrow trephanobioptate there is no three-sided pronounced hyperplasia, an increase in the level of megakaryocytes (more than 5 in the field of vision) is revealed. In some cases, myelofibrosis is observed, as well as an increase in the spleen to not expressed indices.
Secondary thrombocytosis develops, both in pathological and in physiological states. It is characterized by the same symptomatology as for the primary one.
Thrombocytosis is detected during a full-time examination by a doctor, a laboratory blood test, aspiration biopsy and bone marrow biopsy (trepanobiopsy).
Reactive thrombocytosis is characterized by an increase in platelet count due to non-specific activation of thrombopoietin (a hormone regulating ripening, division and platelet entry into the blood). Such a process stimulates the formation of a large number of platelets without pathological changes in their functional properties.
For reactive thrombocytosis, the cause of their appearance may be acute and chronic processes. Acute processes include: blood loss, acute inflammatory or infectious diseases, excessive physical activity, platelet recovery after thrombocytopenia. Chronic processes include: iron deficiency anemia, hemolytic anemia, aspiration, oncological process, rheumatism, intestinal inflammation, tuberculosis , lung diseases, reaction to certain medications (Vincristine, Cytokines, etc.).
Under certain conditions, the disease occurs due to ethanol poisoning (chronic alcoholism). It is very important to correctly differentiate reactive thrombocytosis, because it is often confused with clonal thrombocytosis. If clonal thrombocytosis causes the disease to be difficult to diagnose, then for the reactive it is not particularly difficult, although clinically they are poorly expressed. Clonal thrombocytosis is also characterized by: peripheral or central ischemia, large artery thrombosis and / or veins, bleeding, splenomegaly, giant platelet sizes and impaired function, increased megakaryocytes. Also, clonal thrombocytosis is characterized by the detection of giant dysplastic polyploid forms with a huge content of traces of platelets in the study of their morphology.
Reactive thrombocytosis is characterized by: normal morphological pattern, absence of central or peripheral ischemia, absence of bleeding and splenomegaly, an increase in megakaryocytes in the bone marrow biopsy, there is no risk of developing venous thrombosis and arteries.
Dynamic observation may allow the establishment of reactive thrombocytosis with normal platelet levels during treatment of the disease that caused thrombocytosis. For example, with injuries and neurological pathologies, thrombocytosis forms during the first days of the disease and, thanks to correct treatment for two weeks, passes quickly.
There are cases of reactive thrombocytosis due to the use of medications, which, despite significant platelet counts (about 500), does not pose a threat for the occurrence of thrombotic complications and disappears after treatment.
Therefore, in the treatment of reactive thrombocytosis, it is necessary to identify the causative disease. To do this, it is necessary to collect an anamnesis with the detection of episodes of disorders of microcirculation and thrombosis in the past; laboratory blood tests, biochemical studies on markers of inflammatory processes (C-reactive protein, seromucoid, thymol test, fibrinogen); US - examination of internal organs.
Relying on the results obtained with diagnostic data, form the treatment tactics. If there is no clearly expressed thrombocytosis (up to 600), with no risk of thrombosis, the patient is prescribed therapy of the underlying disease with constant monitoring of the number of platelets.
Essential thrombocytosis is characterized by a marked increase in platelets, whose function and morphology are often altered, which seems to be the cause of such manifestations as thrombosis and bleeding.
Essential thrombocytosis occurs in the elderly and in the elderly. Clinical manifestations of the disease are very nonspecific, sometimes essential thrombocytosis is detected accidentally in those persons who do not make complaints. However, the first clinical symptoms of the disease are the various severities of spontaneous bleeding, which often occur in the gastrointestinal tract and are often repeated for several years. There may also be hemorrhages beneath the skin, thromboses that affect small vessels may be accompanied by the appearance of gangrene or peripheral ulcers, areas of erythromelalgia and chilblains. In some patients, splenomegaly is observed - sometimes very severe and associated with hepatomegaly. There may be a spleen infarction.
Laboratory diagnosis indicates an increase in platelets to 3000, and the platelets themselves are caused by morphological and functional disorders. These disorders explain the paradoxical combination of bleeding and thrombosis. The parameters of hemoglobin and the morphological picture of platelets are within the limits of the norm, provided that shortly before the diagnosis there was no bleeding. The number of white blood cells is also within normal limits. The duration of bleeding can be pronounced, but the clotting time does not exceed the limits of normal indices. A biopsy of the bone marrow reveals a pronounced change in the size and number of megakaryocytes, in addition, hyperplasia of the erythroid and myeloid sprouts.
In essential thrombocytosis, there is a tendency to chronic flow with a gradual increase in platelets in those patients who do not receive treatment. Lethal outcome is caused by bleeding or thromboembolism. Treatment is to achieve normal platelet count. As a rule, Mulfalan in a dose of 375-450 MBq is used for this. To reduce the risk of bleeding, therapy should also be started in patients without severe symptoms. With thrombotic pathologies, the use of Aspirin or acetylsalicylic acid may help.
Thrombocytosis in the child
It is known that platelets are a constituent element of the blood or cells produced by the bone marrow and serving for blood clotting. The existence of individual platelets persists for up to 8 days, after which they enter the spleen, where they are destroyed. Depending on the age, the number of platelets that form in the bone marrow can have significant differences. In newborns, their number is about 100-400, for children up to a year - 150-360, for children older than a year - 200-300.
The cause of the development of primary thrombocytosis in children may be leukemia or leukemia. The causes of secondary thrombocytosis, which are not associated with hematopoietic function, are pneumonia (inflammation of the lungs), osteomyelitis (inflammatory process of the bone marrow, followed by destruction of bones), anemia (low hemoglobin content in the blood).
In addition, thrombocytosis in children may indicate the presence of a bacterial or viral infection. It can be viral hepatitis or influenza , tick-borne encephalitis or the varicella-zoster virus. Any infectious disease can increase the number of platelets.
Thrombocytosis in a child can be caused by a fracture of the tubular bones. This condition is noted in such patients who have undergone an operation to remove the spleen. The spleen takes a lasting part in the metabolism of erythrocytes, and its removal can be carried out only in those diseases that interfere with normal blood coagulability. Such diseases include hemophilia , which occurs mainly in males, and is still incurable. At a hemophilia there is an insufficient development of thrombocytes.
Treatment of thrombocytosis in children should be carried out by the treatment of a disease that caused an increase in the level of platelets, therefore the main role is played by qualitative diagnostics.
If there is clonal thrombocytosis, then treatment should be carried out by prescribing antiplatelet agents. These include: Acetylsalicylic acid 500 mg 3 times a day for 7 days; Clobidogrel or Ticlopidine, where the dosage is taken into account with age and body weight of the patient. It should be borne in mind that the short-term use of Aspirin can determine in it the ulcerogenic effect that occurs when the drug is administered in minimal doses. It is necessary to exclude the presence of erosive-ulcerative gastrointestinal lesions before the appointment of Aspirin (acetylsalicylic acid), because its reception can provoke bleeding.
If there are thromboses or ischemia due to the development of thrombocytosis, then it is necessary to carry out a pronounced antiplatelet therapy with the use of anticoagulants directed (Heparin, Bivalirudin, Livarudin, Argotoban) and a daily laboratory study of the level of platelets. In severe thrombocytosis resort to cytostatic therapy and thrombocytopheresis (removal of platelets from the blood by separation). For successful treatment of thrombocytosis, a comprehensive examination of the patient is necessary to identify concomitant and causative diseases.
In pregnancy, thrombocytosis is corrected with Dipiridamol 1 tab. 2 times a day, which, in addition to antithrombotic action, has an immunomodulating and improving utero-placental blood flow. But it is worth remembering that thrombocytosis in pregnancy is a physiological phenomenon and rarely requires correction.
In addition to drug therapy for thrombocytosis, it is important to follow a diet that is determined by a balanced diet, and follow the principles of a healthy lifestyle. An important condition in this case is the refusal to smoke and use of ethanol (alcohol).
It is necessary to eat foods rich in iodine (kelp, nuts, seafood), calcium (dairy products), iron (red meat and offal), B vitamins (green vegetables). It will not be superfluous to use freshly squeezed juices with a high content of vitamin C (lemon, orange, pomegranate, cowberry, etc.). Such juices must be diluted with water in a ratio of 1: 1.
From traditional medicine for the treatment of thrombocytosis, it is recommended to use tincture of garlic, cocoa, ginger and hirudotherapy (treatment with leeches).