Abstract
Chronic immune thrombocytopenic purpura (ITP) is a condition based on an immune-mediated mechanism that determines the premature hyperdestruction of the thrombocytes in peripheral blood, as well as their deficient synthesis at the level of the bone marrow. The chronic immune purpura could be of primary, idiopathic cause, as well as of secondary cause, occurring in the context of other pathologies. The characteristic of the primary form of the disease is the presence of isolated thrombocytopenia, defined by a platelet count under 100,000/mm3 in peripheral blood, in the absence of supporting causes for thrombocytopenia. In the secondary form of the disease, the decreased platelet count is due to associated pathologies involving an immune mechanism, responsible for the occurrence of thrombocytopenia. This study aims to emphasize the involvement of autoimmune diseases, such as systemic lupus erythematosus (SLE), dermatomyositis, rheumatoid polyarthritis or antiphospholipid syndrome in the pathogenesis of secondary thrombocytopenia. Furthermore, the study was conducted on a sample of 40 patients, divided into two groups: The first group comprising asymptomatic patients diagnosed with thrombocytopenia following routine tests, and the second group comprising patients with hemorrhagiparous symptomatology (petechiae, ecchymoses, epistaxis, gingivorrhagia), who went to the doctor in order to determine the etiology of the hemorrhagiparous syndrome. The average value of the thrombocytopenia of the patients included in the study was of 60.20 ± 19.75 × 103/μL. Laboratory investigations performed in order to establish the etiology of thrombocytopenia showed that 80% of patients presented positive antiplatelet antibodies. Moreover, 20% of the patients in the study showed positive anti-double-stranded DNA, 20% were identified with IgG anticardiolipin antibodies, while antinuclear antibodies were present in 10% of the patients.
Highlights
Immune thrombocytopenic purpura (ITP) is a condition characterized by peripheral platelet hyperdestruction exceeding the capacity of compensatory thrombopoiesis of the bone marrow [1] [2]
None of the patients included in the study, prior to the occurrence of thrombocytopenia, used medication involved in its production, nor were they diagnosed with other active pathologies that would justify the decreased platelet count
Their involvement in the etiopathogenesis of primary immune purpura is explained by the property of these autoantibodies to act directly on glycoprotein (GP) complexes from the level of the platelet membrane, of GP IIb/IIIa or GP Ib/IX type
Summary
Immune thrombocytopenic purpura (ITP) is a condition characterized by peripheral platelet hyperdestruction exceeding the capacity of compensatory thrombopoiesis of the bone marrow [1] [2]. Peripheral thrombocytopenia occurs secondary to the fixation of antiplatelet autoantibodies or immune complexes on the platelet membrane, a process that will lead to the phagocytosis of the thrombocytes by the macrophages. Recent studies show that the disorder of the humoral immune response is based on the complex interaction between antigen-presenting cells and T and B lymphocytes. The role of antigen-presenting cell lies with the thrombocyte. The activation of the immune system that will produce antibodies, the main target of which are membrane glycoproteins, takes place. The platelets on which antibodies are fixed are sequestrated and destroyed in great majority, in the spleen, but the liver and the reticuloendothelial system of the marrow can play an important role in platelet sequestration. The median survival time is between 2 - 3 days with the possibility of dropping to a few minutes
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