Department of Hematology, Medical Research Institute, Alexandria University
Abstract
βeta-Thalassemia is a worldwide single gene autosomal recessive genetic disorder characterized by excess unpaired alpha globulin chains and deficient or absent beta globulin chains. Excessive increase of unpaired α-globin chains in red blood cells causes hemolysis and ineffective erythropoiesis leading to chronic anemia and hypoxia, that triggers most of the symptoms that the patients exhibit. Recently patients with thalassemia disease are described according to their transfusion requirements into transfusion-dependent thalassemia andnon-transfusion-dependent thalassemia. Thromboembolic events (TEE) are a known complication observed in thalassemic patients. Multifactorial mechanisms are tangled in the pathogenesis of TEE in thalassemia, including the combination of the classical components of the hemostatic process together with the disease-specific features. Glycoprotein IIb/IIIa is an integrin complex found on surface of platelets. It is a receptor for fibronectin, fibrinogen, plasminogen, prothrombin, thrombospondin and vitronectin. Its activation leads to platelet/platelet interaction via binding of soluble fibrinogen consequently causing prompt platelet aggregation. Aim of the work Estimate the plasma level of soluble GpIIb/IIIa in β- thalassemia major patients.
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