• Ayşegül Uğur Kurtoğllu, Belkıs Koçtekin, Erdal Kurtoğlu, and Mustafa Yildiz.
• Department of Biochemistry, Antalya Education and Research Hospital, Antalya, Turkey.
• Arch Med Sci. 2019 Jan 1; 15 (1): 191-195.

IntroductionHemolysis due to ineffective erythropoiesis is a serious problem β-thalassemia major (β-TM) patients. The role of complement system in the etiopathogenesis of hemolysis observed in β-TM were released. Hemolysis induced by activation of complement system is prevented by complement regulatory proteins. Decay accelerating factor (CD55), membrane inhibitor of reactive lysis (CD59), and complement reception 1 (CR1, CD35) are among these proteins. The absence of these proteins thus accounts for the increased susceptibility of erythrocytes to complement lysis. Splenomegaly and hypersplenism are common complications among thalassemia major patients necessitating splenectomy.Material And MethodsIn this study we investigated how splenectomy effects complement regulatory system in erythrocytes. We analysed CD35, CD55, and CD59 levels on erythrocytes in β-TM by flow cytometry.ResultsThe overall mean percentage of CD55 and CD35 positive RBCs of group 1 (22 β-TM with splenectomy) was significantly lower than group 2 (23 β-TM without splenectomy) and group 3 (healthy controls) (p < 0.05). The overall mean percentage CD59 positive RBCs of patients was no significantly different in all groups. The levels of CD35 and CD55 expression on the erythrocytes of splenectomized patients was significantly lower than non-splenectomized patients (p < 0.05).ConclusionsIncreased erythrocyte destruction and iron deposition in organs due to deficiency of these regulatory proteins may be the underlying mechanism of organ damage developing in β-TM patients.

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