Importance of CD71+ Erythrocyte Cell Levels in Prognosis in Patients With β‐Thalassemia

Author:

Görgülügil Gizem Zorlu1,Uğur Kurtoğlu Ayşegül2ORCID,Uğur Sevcan3,Kurtoğlu Erdal4

Affiliation:

1. Department of Internal Medicine Antalya İl Sağlık Müdürlüğü Antalya Turkey

2. Department of Biochemistry Sağlık Bilimleri University Antalya Turkey

3. Department of Rheumatology Antalya City Hospital Antalya Turkey

4. Department of Hematology Sağlık Bilimleri University Antalya Turkey

Abstract

ABSTRACTBackground/ObjectivesCD71+ erythroid cells (CECs) are immature red blood cells (proerythroblasts, erythroblasts, and reticulocytes). CECs play an important role in the development of sepsis and cancer by causing immunosuppression. We examined the CEC levels in the peripheral blood of beta thalassemia (βThal) patients and investigated the relationship between CECs and the clinical status of the patients, especially splenectomy.MethodsSixty‐eight patients with βThal (46 splenectomized and 22 nonsplenectomized) and 15 healthy controls were included in this study. The hemogram parameters, ferritin, and CECs (flow cytometry method) were measured.ResultsIt was observed that the CEC level in the patient group was significantly higher than the control group (p < 0.05). CEC levels were found to be significantly higher in patients with splenectomy than in patients with nonsplenectomy (p < 0.05). CEC levels were higher in patients with nontransfusion‐dependent βT (NTD‐βThal) than in patients with transfusion‐dependent βT (TD‐βThal) (p < 0.05). CEC levels were found to be significantly higher in patients with splenectomy than in patients with nonsplenectomy in both TD‐βThal and NTD‐βThal groups (p < 0.05). There was a moderate‐negative correlation was detected between CECs and Hb levels (r = −0.467; p < 0.05).ConclusionsHigh CEC levels in βThal patients develop as a result of ineffective erythropoiesis. We think that keeping CEC levels under control is important for prognosis, especially in patients with splenectomy.

Publisher

Wiley

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