Phosphatidylserine and the thrombin–antithrombin complex as markers for hypercoagulability in Egyptian beta-thalassemia patients

Abstract

Background Hypercoagulability is a known complication of thalassemia, in particular, thalassemia intermedia. Several factors contribute to this hypercoagulability, including chronic platelet activation and the presence of other comorbid conditions. In addition, the oxidation of globin subunits in thalassemic red blood cells (RBCs) triggers the formation of reactive oxygen species. These factors lead to the exposure of negatively charged phospholipids like phosphatidylserine (PS), which ultimately causes increased thrombin generation, particularly in splenectomized patients. Aim This study aimed to assess the risk for hypercoagulability in thalassemic patients using PS expression on RBCs and the thrombin–antithrombin (TAT) complex in plasma. Patients and methods This study included 50 thalassemic patients (19 patients with splenectomy and 31 patients without splenectomy) and 30 apparently healthy individuals as a control group. Patients were subjected to assessment of history for deep venous thrombosis or pulmonary hypertension by echocardiography. Annexin V was used to detect PS expression on RBCs by flow cytometry, while the enzyme-linked immunosorbent assay was used to detect the TAT complex in plasma. Results Erythrocyte PS expression was significantly higher (P<0.001) in thalassemic patients than in the control group. The TAT complex level revealed no significant difference between thalassemia patients and the control group (P=0.468). Patients with pulmonary hypertension showed a statistically significant higher PS expression and TAT complex level. However, there was no significant increase in PS expression or TAT level in patients with a history of deep venous thrombosis only. Conclusion Increased PS expression and TAT complex level may be a risk factor for pulmonary hypertension in thalassemia patients with splenectomy.