| Autor: |
Costa Neto, Abel, Santos, Flávia Leite, Ribeiro, Ingrid Helena, Oliveira, Valeria Brito, Dezan, Marcia Regina, Kashima, Simone, Covas, Dimas Tadeu, Pereira, Alexandre Costa, Fonseca, Guilherme Henrique Hencklain, Moreira, Frederico, Krieger, José Eduardo, Gualandro, Sandra Fatima Menosi, Rocha, Vanderson, Mendrone, Alfredo, Dinardo, Carla Luana |
| Zdroj: |
Blood; November 2018, Vol. 132 Issue: 1, Number 1 Supplement 1 p1255-1255, 1p |
| Abstrakt: |
Introduction:Red blood cell (RBC) alloimmunization is an important transfusion complication which is very prevalent among patients with sickle cell disease (SCD). Only part of patients is able to develop alloantibodies following antigen-mismatched transfusions, named the ‘immune responders’, who should be prospectively transfused with antigen-matched RBC units, comprising the most immunogenic erythrocyte antigens. Auto-immune diseases are a known risk factor for RBC alloimmunization, suggesting that auto-immunity and post-transfusion alloantibody development happen through similar physiopathological pathways. In this context, polymorphisms in FCGR2Bgene have already been associated with several auto-immune disorders and, hypothetically, could be associated with RBC alloimmunization and help to identify the ‘immune responders’ in transfusion practice. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
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