Thromboembolic events are potentially life-threatening clinical complications found in β-thalassemia patients. The pathogenesis of the hypercoagulable state in β-thalassemia patients results from the degradation of excess α-globin chains in red blood cells, leading to intracellular labile iron accumulation, oxidative stress, and more rigid, deformed, and eventually prematurely damaged red blood cells. This process is associated with the loss of the normal asymmetrical distribution of membrane phosphatidylserine and its exposure to the outer surface of the blood cell membrane resulting in the formation of tenase complexes, prothrombinase, and thrombin complexes. Increased thrombins lead to platelet activation and platelet-derived microparticles synthesis, which in turn contributes to thrombus formation. This study aimed to determine the increase in the platelet-derived microparticle count by direct labeling of CD62P and CD41 monoclonal antibodies in β-thalassemia patients when compared with normal subjects. This was a cross-sectional analytical quantitative study conducted in Dr.
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