Presentation Details
| Correlation Between ABO Blood Types and Disease Severity in Sickle Cell Anemia: Implications for Thrombosis and Hemostasis. George M Bassey1, Titilope A Adeyemo1, 2, Ann A Ogbenna1, 2, Abiola B Bolarinwa1, Ademola S Adewoyin2, Emmanuel Iyere1. 1Lagos University Teaching Hospital, Lagos, Nigeria.2College of Medicine University of Lagos, Lagos, Nigeria |
Abstract
Background: Hemoglobin S (HbS), arising from a single nucleotide substitution in the gene encoding β-globin, leads to pathological hemolysis and concurrent endothelial dysfunction. This process induces a prothrombotic state characterized by elevated markers such as VCAM and VWF. Hemolysis, along with other mechanisms also contributes to an increased platelet count, exacerbating adhesion molecule expression, thus intensifying the prothrombotic state and worsening the vaso-occlusive complications associated with sickle cell disease (SCD) e.g. pulmonary hypertension, non-hemorrhagic stroke, priapism, and cutaneous leg ulcers. While the scientific relevance of ABO blood types in various diseases, including thrombosis, is well-established in non-SCD populations, this is yet to be examined in SCD population.
Aim: Our study seeks to explore the correlation between disease severity, markers of endothelial dysfunction, thrombosis, and ABO phenotypes in individuals with sickle cell anemia. Materials and Methods: We enrolled seventy-three participants with SCD in this investigation. We evaluated their clinical attributes, disease severity, ABO blood phenotypes, markers of hemolysis (Hbfree, lactate dehydrogenase - LDH, total and conjugated bilirubin, corrected reticulocyte count, and reticulocyte production index), as well as markers for endothelial dysfunction and thrombosis (VCAM, von Willebrand Factor - vWF, platelet count, and nitric oxide - NO). Hbfree, VCAM, vWF, and NO levels were quantified using enzyme-linked immunoassay techniques. LDH and bilirubin (total, conjugated, and unconjugated) were assessed using a COBAS C311 chemistry auto-analyzer. Full blood count and reticulocyte count were determined through automated procedures. Blood group phenotypes were determined using the tile method. Our analyses involved ANOVA and logistic regression to establish associations between hemolysis markers, blood group phenotypes, and disease severity, with a statistical significance level set at 5%. Results: Our findings indicated that individuals with sickle cell anemia (SCA) and non-group O blood phenotypes demonstrated elevated levels of VCAM, vWF, platelet count, and reduced levels of nitric oxide compared to SCA individuals with group O blood types (P <0.05 in all cases). Disease severity was notably higher in SCA individuals with non-group O blood types. Conclusion: The combined effects of non-group O blood type and SCA appear to independently contribute to a prothrombotic state, heightening the severity of the disease and increasing the risk of developing severe complications associated with sickle cell disease. These findings have significant implications for understanding the pathophysiology of thrombosis and hemostasis in individuals with SCD.
No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.
Aim: Our study seeks to explore the correlation between disease severity, markers of endothelial dysfunction, thrombosis, and ABO phenotypes in individuals with sickle cell anemia. Materials and Methods: We enrolled seventy-three participants with SCD in this investigation. We evaluated their clinical attributes, disease severity, ABO blood phenotypes, markers of hemolysis (Hbfree, lactate dehydrogenase - LDH, total and conjugated bilirubin, corrected reticulocyte count, and reticulocyte production index), as well as markers for endothelial dysfunction and thrombosis (VCAM, von Willebrand Factor - vWF, platelet count, and nitric oxide - NO). Hbfree, VCAM, vWF, and NO levels were quantified using enzyme-linked immunoassay techniques. LDH and bilirubin (total, conjugated, and unconjugated) were assessed using a COBAS C311 chemistry auto-analyzer. Full blood count and reticulocyte count were determined through automated procedures. Blood group phenotypes were determined using the tile method. Our analyses involved ANOVA and logistic regression to establish associations between hemolysis markers, blood group phenotypes, and disease severity, with a statistical significance level set at 5%. Results: Our findings indicated that individuals with sickle cell anemia (SCA) and non-group O blood phenotypes demonstrated elevated levels of VCAM, vWF, platelet count, and reduced levels of nitric oxide compared to SCA individuals with group O blood types (P <0.05 in all cases). Disease severity was notably higher in SCA individuals with non-group O blood types. Conclusion: The combined effects of non-group O blood type and SCA appear to independently contribute to a prothrombotic state, heightening the severity of the disease and increasing the risk of developing severe complications associated with sickle cell disease. These findings have significant implications for understanding the pathophysiology of thrombosis and hemostasis in individuals with SCD.
No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.
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