Platelet-Derived Microparticle Count in β-Thalassemia Patients with Direct Labeling Monoclonal Antibody CD62P and CD41

Abstract

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.

Hemostatic changes in patients undergoing hemodialysis: Differences between central venous catheters and arterio‐venous fistulas

“…Other experimental studies, despite not portraying the theme of the present study, and focusing on certain pathological and clinical conditions of patients, stated in their results that the high rate of p‐selectin can lead to a state of hypercoagulability and a consequent facilitator for thrombus formation 15,16 . Such analyzes corroborate the results of this study, since invasive procedures that remain a long time inside the patients, regardless of the clinical condition, can also lead to a state of hypercoagulability.…”

“…It is noteworthy that the recruitment of monocytes from the formation of MPAs can amplify the production of procoagulants, especially TF 15,16 . TF expression in monocytes is regulated by proinflammatory cytokines and p‐selectin.…”

“…15 Associated with this factor, platelet-bound neutrophils (platelet-neutrophil-APN aggregates) secrete endothelial activators, facilitate their stagnation in small vessels, initiate the production of inflammatory cytokines and release the content of protease-rich granules triggering inflammatory and thrombotic processes. 15,16 In addition, APNs can cause embolization due to the adhesion of microcirculatory structures, resulting in vascular injury, possibly due to increased synthesis and diffusion of free radicals. This can increase the risk of thrombus formation in patients undergoing hemodialysis, especially with CVC.…”

“…It cross-links platelets and leukocytes and is the main mediator of the formation of platelet-leukocyte aggregates, thus regulating the release of pro-inflammatory cytokines and adhesion to the endothelium. [11][12][13][14] Despite the diversity of studies that evaluated platelet activation and the intrinsic and extrinsic pathways during thrombus formation, [15][16][17] none of them compared the potential for thrombus formation in patients using CVCs with patients using AVF. Furthermore, although the endothelium generally shows expression of several anticoagulants, including TM, tissue factor (TF) pathway inhibitor, and protein C, the venous endothelium can be activated by oxidative stress.…”

“…Despite the diversity of studies that evaluated platelet activation and the intrinsic and extrinsic pathways during thrombus formation, 15–17 none of them compared the potential for thrombus formation in patients using CVCs with patients using AVF. Furthermore, although the endothelium generally shows expression of several anticoagulants, including TM, tissue factor (TF) pathway inhibitor, and protein C, the venous endothelium can be activated by oxidative stress.…”