Platelet-Derived Microparticle Count In Beta-Thalassemia Patients With Direct Labeling Monoclonal Antibody Cd62p And Cd41

Thromboembolic events are potentially life-threatening clinical complications found in beta-thalassemia patients. The pathogenesis of the hypercoagulable state in beta-thalassemia patients results from the degradation of excess a-glohin 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 beta-thalassemia patients when compared with normal subjects. This was a cross-sectional analytical quantitative study conducted in Di: Hasan Sadikin General Hospital Bandung and Dharmais Cancer Hospital Jakarta Indonesia between August and September 2019. Sixty patients, divided evenly into beta-thalassemia group and control group, were labeled by CD62P and CD41 monoclonal antibodies. Results showed that the beta-thalassemia group had a platelet count of 197x103/uL (58-1,261) with a median count for platelet-derived microparticles of 10,553 events/uL (779-90,971) as opposed to 1,861 events/uL (1,244-3,174) in the normal group (p<0.05). Therefore, the plateletderived microparticle count in the beta-thalassemia patients is 5.7 times greater than in the normal subjects.