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Thrombocytopathies
Last reviewed: 05.07.2025
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Thrombocytopathies are hemostasis disorders caused by qualitative inferiority of blood platelets with their normal quantity. A distinction is made between hereditary and acquired. Among the primary hereditary platelet dysfunctions, the most common are athrombia, thrombocytopathy with a defect in the platelet release reaction, and thrombasthenia. Secondary hereditary thrombocytopathies are typical for von Willebrand disease, afibrinogenemia, albinism (Herzmansky-Pudlak syndrome), hyperelastic skin syndromes (Ehlers-Danlos), Marfan and other connective tissue dysplasias, and many metabolic anomalies. Acquired thrombocytopathy with or without hemorrhagic syndrome is characteristic of many blood diseases (leukemia, hypoplastic and megaloblastic anemia), uremia, disseminated intravascular coagulation syndrome, immunopathological diseases (hemorrhagic vasculitis, lupus erythematosus, diffuse glomerulonephritis, etc.), radiation sickness, drug sickness when taking salicylates, xanthines, carbenicillin, neurocirculatory dysfunctions.
The prevalence of primary hereditary thrombocytopathy in children has not been established, but it is undoubtedly the most common genetically determined pathology of the hemostasis system. In most cases of so-called familial bleeding of unknown genesis, hereditary thrombocytopathy can be diagnosed. Their frequency in the population reaches 5%.
Causes of thrombocytopathy in children
Hereditary thrombocytopathy
There are primary hereditary thrombocytopathies (thrombocytopathy with a defect in the release reaction, Glanzmann thrombasthenia, etc.) and secondary ones, which are part of the symptom complex of the underlying disease (for example, thrombocytopathy in von Willebrand disease, albinism, Ehlers-Danlos syndrome, etc.).
Acquired thrombocytopathy
They are widespread, since the functional state of platelets suffers in the overwhelming majority of severe pathological conditions of newborns (hypoxia, acidosis, infections, shock, etc.).
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Medicines
Platelet function can be impaired by medications that affect the arachidonic acid cascade, increase the level of cAMP in platelets, inhibit thrombin formation, as well as sodium heparin and other medications: carbenicillin, nitrofuran derivatives, antihistamines, phenobarbital, antioxidants, chlorpromazine, dextrans, povidone, beta-blockers, sulfonamides, cytostatics, B vitamins and other drugs. In newborns, bleeding is most often caused by carbenicillin, aminophylline, high doses of ascorbic acid, furosemide.
Symptoms of thrombocytopathy in children
In the neonatal period, hereditary thrombocytopathy clinically manifests itself under additional influences (hypovitaminosis and other nutritional deficiencies in the mother, perinatal pathology, in particular acidosis, hypoxia, sepsis). However, drug-induced acquired thrombocytopathy predominates. Clinical manifestations of bleeding can be both general (generalized cutaneous hemorrhagic syndrome, bleeding of the mucous membranes) and local (hemorrhages into internal organs, as well as intraventricular and other intracranial hemorrhages, hematuria).
The child's relatives have a history of increased bleeding. Thrombocytopathy is characterized by positive endothelial tests (tourniquet, pinch, etc.) with a normal number of platelets in the blood and normal coagulation system parameters. Bleeding time is increased.
The diagnosis is established based on the study of the aggregation function of platelets with aggregates (ADP in different doses, collagen, adrenaline, ristocetin).
What tests are needed?
Treatment of thrombocytopathy in children
In thrombocytopathy, drugs are prescribed that increase the functional activity of platelets. In mild cases, sodium etamsylate is prescribed at a dose of 0.05 g 3-4 times a day for 7-10 days; in more severe cases, it is administered intramuscularly or intravenously at a dose of 0.5-1.0 ml of a 12.5% solution once a day for 7-10 days. Calcium pantothenate, aminocaproic acid, carbazochrome, and triphosadenine have a stimulating effect on platelet function (in addition to sodium etamsylate).
How are thrombocytopathy prevented in children?
Primary prevention of the disease has not been developed, secondary prevention of relapses includes: planned sanitation of foci of infection prevention of contacts with patients with infectious diseases (especially acute respiratory viral infections) deworming individual decision on the issue of preventive vaccinations exclusion of insolation, ultraviolet irradiation and UHF physical education classes in the preparatory group mandatory blood testing after any illness.
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