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Transfusion safety and immune response to red blood cell antigens in patients with sickle cell disease

Abstract

Antibody production is a serious complication in patients with SCD on long-term transfusion therapy. From 33 to 60 percent of chronically transfused patients with SCD become immunized, and transfusion is further complicated by the presence of multiple alloantibodies. Alloimmunization can have severe clinical consequences including delay in obtaining matched blood as well as potentially life-threatening delayed hemolytic transfusion reactions (DHTRs), autoantibody formation, and hyperhemolysis syndrome. In an effort to reduce alloimmunization, some programs have been designed and implemented to provide antigen-matched RBC transfusions to patients with SCD particularly those who are in need of chronic transfusion support but, despite antigen matching, some patients still become alloimmunized. In contrast to prophylactic antigen matching, some institutions argue that the data supporting a reduction in DHTRs are insufficient to offset the cost of labor and resources required to perform extended matching for SCD patients. Several factors are predicted to influence the recipient's immune system to react to alloantigens including the dose, and the immunogenicity of the antigen as well as genetic or acquired patient-related factors. However, possible differences in the immune makeup of transfused patients who make alloantibodies (responders) and those who do not (non-responders) are not known. By identifying such markers, it may be possible to predict in advance responders and non-responders, thereby avoiding the use of costly antigen-matched units for non-responders, and only selecting phenotyped/genotyped-matched units for responders to reduce alloimmunization-associated morbidity and mortality. We believe that this information will enable us to predict which transfused patients are likely to progress to alloimmunization which in turn would help in preselecting better matched units for such patients and reducing transfusion-associated morbidity. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
GUELSIN, GLAUCIA A. S.; RODRIGUES, CAMILA; VISENTAINER, JEANE E. L.; CAMPOS, PAULA DE MELO; TRAINA, FABIOLA; GILLI, SIMONE C. O.; SAAD, SARA T. O.; CASTILHO, LILIAN. Molecular matching for Rh and K reduces red blood cell alloimmunisation in patients with myelodysplastic syndrome. BLOOD TRANSFUSION, v. 13, n. 1, p. 53-58, JAN 2015. Web of Science Citations: 7.
SIPPERT, EMILIA; FUJITA, CLAUDIA R.; MACHADO, DEBORA; GUELSIN, GLAUCIA; GASPARDI, ANE C.; PELLEGRINO, JR., JORDAO; GILLI, SIMONE; SAAD, SARA S. T. O.; CASTILHO, LILIAN. Variant RH alleles and Rh immunisation in patients with sickle cell disease. BLOOD TRANSFUSION, v. 13, n. 1, p. 72-77, JAN 2015. Web of Science Citations: 21.

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