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Subject Area

Clinical Pathology

Article Type

Original Study

Abstract

Background Beta-thalassemia is a hereditary disease that is characterized by ineffective erythropoiesis and shortened red blood cell survival. In severe cases, blood transfusion is a mainstay therapy; however, regular blood transfusions result in iron overload with serious complications. Complement-mediated erythrocyte destruction is one of the pathological causes of hemolysis in beta-thalassemia. Membrane-bound complement regulatory proteins such as CD55 and CD35 ensure that the complement system does not become overactivated, thus causing harm to self-tissues. Objectives To assess the expression of CD55 and CD35 on erythrocytes of β-thalassemia patients and its correlation with hemoglobin (Hb) levels and other markers of hemolysis. Patients and methods Flow cytometry was used to evaluate the expression of CD55 and CD35 on erythrocytes of 50 patients with β-thalassemia and 50 age-matched and sex-matched controls. Results CD55 and CD35 expression on erythrocytes were significantly reduced in thalassemia patients as compared with controls (P < 0.001). Correlation analysis revealed a significant positive correlation between CD55% expression and Hb concentration (r = 0.347, P = 0.013). However, a significant negative correlation was demonstrated between CD55% and lactate dehydrogenase (r=−0.358, P = 0.011). A statistically significant positive correlation was observed between CD35% expression and Hb concentration (r = 0.302, P = 0.033). Moreover, a significant negative correlation was found between CD35% and reticulocyte % (r=−0.304, P = 0.032). Conclusions Low expression levels of CD55 and CD35 on erythrocytes of patients with β-thalassemia demonstrate the important role of these complement regulatory molecules in the pathogenesis of hemolysis and anemia in β-thalassemia.

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