The effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major

Introduction Hemolysis 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 regula...

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Autores principales:	Ayşegül Uğur Kurtoğllu, Belkıs Koçtekin, Erdal Kurtoğlu, Mustafa Yildiz
Formato:	article
Lenguaje:	EN
Publicado:	Termedia Publishing House 2018
Materias:	splenectomy beta thalassemia complement regulatory proteins β-thalassemia Medicine R
Acceso en línea:	https://doaj.org/article/8ec41884189145289d8e7e8e52d5a033
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spelling	oai:doaj.org-article:8ec41884189145289d8e7e8e52d5a0332021-12-02T16:58:24ZThe effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major1734-19221896-915110.5114/aoms.2018.81036https://doaj.org/article/8ec41884189145289d8e7e8e52d5a0332018-12-01T00:00:00Zhttps://www.archivesofmedicalscience.com/The-effect-of-splenectomy-on-complement-regulatory-proteins-in-erythrocytes-in-thalassemia,66492,0,2.htmlhttps://doaj.org/toc/1734-1922https://doaj.org/toc/1896-9151Introduction Hemolysis 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 methods In 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. Results The 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). Conclusions Increased 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.Ayşegül Uğur KurtoğlluBelkıs KoçtekinErdal KurtoğluMustafa YildizTermedia Publishing Housearticlesplenectomybeta thalassemiacomplement regulatory proteinsβ-thalassemiacomplement regulatory proteinsMedicineRENArchives of Medical Science, Vol 15, Iss 1, Pp 191-195 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	splenectomy beta thalassemia complement regulatory proteins β-thalassemia complement regulatory proteins Medicine R
spellingShingle	splenectomy beta thalassemia complement regulatory proteins β-thalassemia complement regulatory proteins Medicine R Ayşegül Uğur Kurtoğllu Belkıs Koçtekin Erdal Kurtoğlu Mustafa Yildiz The effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major
description	Introduction Hemolysis 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 methods In 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. Results The 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). Conclusions Increased 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.
format	article
author	Ayşegül Uğur Kurtoğllu Belkıs Koçtekin Erdal Kurtoğlu Mustafa Yildiz
author_facet	Ayşegül Uğur Kurtoğllu Belkıs Koçtekin Erdal Kurtoğlu Mustafa Yildiz
author_sort	Ayşegül Uğur Kurtoğllu
title	The effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major
title_short	The effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major
title_full	The effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major
title_fullStr	The effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major
title_full_unstemmed	The effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major
title_sort	effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major
publisher	Termedia Publishing House
publishDate	2018
url	https://doaj.org/article/8ec41884189145289d8e7e8e52d5a033
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The effect of splenectomy on complement regulatory proteins in erythrocytes in β-thalassemia major

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