Circulating microparticles and the risk of thromboembolic events in Egyptian beta thalassemia patients

Abstract

The presence of elevated numbers of circulating microparticles (MPs) has been hypothesized to be responsible for the occurrence of thromboembolic events (TEEs) in thalassemic patients. Our aim is to evaluate the presence and the thrombotic risk of circulating MPs in thalassemia patients and to determine the difference in MPs between β-thalassemia major (β-TM) and thalassemia intermedia (TI). The percentage of the annexin-labeled MPs, platelet-derived MPs (PMPs), erythrocyte-derived MPs (RMPs), and endothelial-derived MPs (EMPs) was measured by flow cytometry, in 87 thalassemia patients (39 β-TM and 48 TI). By multiple regression analysis, we then assessed the various independent risk factors for the occurrence of TEE. The thalassemic patients who experienced TEE had a significantly higher platelet count, higher percentage of annexin-labeled MPs, and higher percentage of PMPs (p value = 0.014, 0.003, and 0.014, respectively). There was no significant difference between β-TM and TI patients at the level of any of the studied MPs. The predictive risk factors for TEE in thalassemic patients were splenectomy, total and direct bilirubin, the RMPs, and the EMPs (OR = 10.07 (CI = 3.7-27.1), 4.3 (CI = 2.1-8.7), 1.4 (CI = 1.5-6.2), 1.6 (CI = 1.1-2.2), 3.0 (CI = 1.9-4.9), respectively). In conclusion, the elevated numbers of circulating MPs is a risk factor for the TEE in thalassemia patients.

Thromboembolism in Beta-Thalassemia Disease

“…Increased endothelial activation caused by the activation of monocytes and granulocytes leads to endothelial injury and increased level of endothelial adhesion proteins and tissue factor contributing to hypercoaguable state. Moreover, the elevation of endothelial cell, platelet and white blood cell (WBC) and RBC microparticles, which are the shedded fragments containing high PS with the size of 0.1-2 μm from activated and apoptotic cells, leads to increased activation of hemostatic system [17][18][19].…”

Proteomic profiling of circulating β‐thalassaemia/haemoglobin E extra‐cellular vesicles reveals that association with immunoglobulin induces membrane vesiculation

“…3 Notably, mEVs are associated with vascular dysfunction and thrombotic events in various diseases, including βthalassaemia. 4 mEVs from splenectomised βthalassaemia/HbE patients have increased coagulation activity and can induce platelet activation and aggregation. 2,5 In addition, mEVs from splenectomised βthalassaemia/HbE patients can induce endothelial cell (EC) expression of coagulation protein, inflammatory cytokines and adhesion molecules, which ultimately leads to increased monocyte-EC adhesion.…”

The in vitro red blood cell microvesiculation exerts procoagulant activity of blood cell storage in Southeast Asian ovalocytosis

“…Outward blebbing and shedding of RBC membranes have been observed during the genesis of RBC-derived extracellular vesicles (REVs), under both normal and pathological conditions [ 9 ]. For instance, increased shedding of the small sizes of phospholipid-containing particles has been reported in thalassemia patients [ 10 – 12 ] and RBC membrane disorders, such as hereditary spherocytosis, hereditary elliptocytosis, and G-6PD deficiency [ 9 , 13 ].…”