Thrombocytosis is a pathological condition characterized by an increase in the content of platelets in the blood. The cause of this phenomenon is infectious, inflammatory or autoimmune pathologies, as well as malignant tumors of the hematopoietic system. In children, it often occurs against the background of iron deficiency anemia. The clinical picture may be different and is determined by the underlying disease. The level of platelets, as part of a complete blood count, is examined in venous or capillary blood. To correct thrombocytosis, the disease against which it developed is treated.
The upper limit of the normal value of platelets varies from 3500 to 4000 in 1 µl, depending on the reference intervals of the particular laboratory performing the analysis. According to the degree of increase, the following types of thrombocytosis are distinguished:
The cause of extreme and severe thrombocytosis is oncohematological pathologies. According to the origin of thrombocytosis are:
An elevated platelet count does not always indicate pathology. There is physiological (short-term, transient) thrombocytosis due to various circumstances, for example, stress, intense physical activity. The reason is the mobilization of platelets, or rather their transition from marginal standing to central blood flow in the vessels of the spleen and lungs.
In addition, slight physiological thrombocytosis is observed in children from the neonatal period to 11 years of age. There is also the so-called hemoconcentration thrombocytosis, which is caused by dehydration. This phenomenon is due to a decrease in the volume of the liquid part of the blood (plasma) and a relative increase in formed elements (platelets, erythrocytes, leukocytes). In this situation, it is necessary to focus on the hematocrit - with dehydration, it is increased.
It is the most common cause of thrombocytosis (about 40%). An increase in the level of platelets develops when:
There are two pathogenetic mechanisms for the development of thrombocytosis in response to an infectious disease. First, during the fight against pathogens, leukocytes produce a large number of inflammatory mediators, including interleukin-6, which stimulates bone marrow megacarycytopoiesis (formation of platelet precursors). Secondly, platelets themselves are part of anti-infective immunity - they are able to produce bactericidal substances, capture, neutralize, even phagocytose some types of bacteria, viruses, foreign particles.
Platelets facilitate the migration of leukocytes to the focus of infectious inflammation by interacting with the endothelial cells of the vascular wall. Thrombocytosis during infections occurs abruptly, correlates with the severity of the disease, quickly resolves after the pathogen is eliminated from the body and the inflammatory process subsides. Thrombocytosis is usually mild or moderate, with a septic condition it can reach a severe degree, in children it is somewhat more pronounced than in adults.
Another common cause of thrombocytosis is considered to be chronic rheumatological pathologies that occur with autoimmune inflammation. The mechanism for increasing the content of platelets is the hyperproduction of substances such as interleukin-6, colony-stimulating factors that activate bone marrow platelet formation. The degree of thrombocytosis corresponds to the activity of inflammation (minimum during remission, maximum during relapse).
In diseases such as rheumatoid arthritis, systemic lupus erythematosus (SLE), inflammatory bowel disease (Crohn's disease, ulcerative colitis), there is a mild or moderate degree. In systemic vasculitis with necrotizing destruction of vessel walls, severe thrombocytosis occurs, since in vasculitis, in addition to other inflammatory mediators, tumor necrosis factor is synthesized in large quantities, which also has a stimulating effect on platelet formation. Especially often high numbers of platelets are observed in children.
Often the cause of thrombocytosis, especially in children, is iron deficiency anemia. The exact mechanisms of this phenomenon have not yet been elucidated, however, an inverse relationship has been established between reduced iron metabolism (ferritin, serum iron-binding capacity) and elevated platelet levels. It is assumed that iron has an inhibitory effect on the maturation of megakaryocytes (progenitor cells).
In addition, part of the pluripotent stem cells of the bone marrow in conditions of iron deficiency is not able to turn into erythrocytes. As a result, a kind of “shunting” occurs and a greater percentage of stem cells begin to mature along the megakaryocytic pathway. Thrombocytosis in iron deficiency anemia is mild, sometimes moderate. Platelets quickly return to normal after correction of iron deficiency, an increase in hemoglobin.
However, as the anemia worsens, the platelet count drops to a state of thrombocytopenia. The cause of iron deficiency can be a lack of iron in food, increased iron consumption (growth period in children, pregnancy, lactation) or chronic blood loss (prolonged menstruation, bleeding from the gastrointestinal tract with stomach ulcers).
The cause of approximately 15% of all thrombocytosis are hemoblastoses - chronic myeloid leukemia, Ph-negative myeloproliferative pathologies (essential thrombocythemia, polycythemia vera, and also primary myelofibrosis). An increase in the number of platelets in these diseases is due to clonal (tumor) transformation of the bone marrow megakaryocytic germ due to various mutations, which leads to overproduction of platelets.
These diseases are more common in adults and the elderly, in children - only in exceptional cases. Initially, thrombocytosis is moderate, as it progresses, it increases, reaching a severe or extreme degree, which often causes microcirculation disorders, arterial, venous thrombosis of various localization. The concentration of platelets normalizes very slowly, only after courses of specific myelosuppressive treatment.
The spleen, being an organ that deposits blood, retains a large number of formed elements, including platelets. Also, the spleen is directly involved in thrombocytopenia, secreting the hormones thrombocytopenin, splenin, which suppress the bone marrow maturation of megakaryocytes. Therefore, thrombocytosis after splenectomy is due to two mechanisms: the release of platelets into the circulating blood, which are normally located in the splenic depot, and the phenomenon of "disinhibition of the bone marrow", i.e. increased production of platelets.
An increase in the number of platelets does not occur immediately, but approximately a week after splenectomy, reaches a maximum by day 13-14 (up to 700-80 thousand), often causing venous thrombosis of the portal vein, and then slowly returns to normal over several weeks or months.
Massive tissue damage (wound during abdominal surgery, fracture, extensive burns) causes activation of the blood coagulation system, namely the vascular-platelet link, which is the first stage of hemostasis. It implies vasospasm, as well as adhesion and aggregation of platelets at the site of damage to the vascular wall. The consumption of platelets stimulates their active release from the depot and a compensatory increase in their bone marrow production. The amount of damage correlates with the degree of thrombocytosis. This type of thrombocytosis usually does not require treatment.
The cause of thrombocytosis in solid (non-hematopoietic) tumors is the ability of cancer cells to produce interleukin-6, which stimulates thrombopoiesis. This feature is found in small cell lung cancer, colon adenocarcinoma, malignant mesothelioma. In addition, the collapse of the tumor often causes bleeding, leading to iron deficiency anemia. The degree of thrombocytosis is usually moderate, may be severe in children, regresses after long-term treatment with chemotherapeutic agents.
Thrombocytosis is detected in a clinical blood test. Although very high platelet counts are more common in hematological disorders, platelet count alone cannot determine the cause of thrombocytosis. Therefore, if it is detected, you should visit a therapist. The doctor carefully asks about the patient's complaints, the duration of the onset of symptoms, and conducts a general examination of the patient. Then, based on the data obtained, an additional examination is assigned, including:
Fonio platelet count
In most cases, to correct thrombocytosis, it is enough to eradicate the cause, i.e. treatment of the underlying disease. Short-term thrombocytosis, which developed on the background of stress or the introduction of drugs, does not require intervention. With persistent long-term thrombocytosis, a consultation with a hematologist is necessary to identify the cause and prescribe the appropriate treatment. Therapy for thrombocytosis has several directions, including:
The only method that allows to achieve complete healing from a malignant hematological disease is allogeneic bone marrow transplantation. This requires HLA typing to select a compatible donor. However, due to the high risk of life-threatening complications, this method is used only when conservative treatment is ineffective.
The outcome depends on both the underlying pathology and the degree of thrombocytosis. For example, acute viral infection, iron deficiency anemia are characterized by a benign course. Patients with essential thrombocythemia with proper selection of pathogenetic and symptomatic treatment can live more than 8 years. In contrast, people with chronic myelogenous leukemia live about 5 to 1 years from the time of diagnosis.
Since children almost always have reactive thrombocytosis, they have a favorable prognosis. For mild and moderate thrombocytosis, thrombosis is atypical. With an extreme or severe degree, there is a very high probability of fatal thrombosis, leading to myocardial infarction, lung, ischemic stroke.