Abstract
Background: Red blood cell (RBC) transfusion remains an essential part of the management of patients with sickle cell disease (SCD). Alloimmunization is a major complication of transfusions. Extended RBC typing is advocated as a means to reduce alloimmunization in SCD. Our goal was to assess alloimmunization among individuals with SCD at our center since implementing extended RBC typing. Materials and Methods: We reviewed electronic medical records of all patients with SCD (N=641) in our comprehensive SCD Program to determine transfusion histories. Cross-referencing with our blood bank database, we extracted data such as antibodies identified, detection date and genotyping in specific cases. Transfusion sources were determined for those with C, E, and Kell antibodies. Results: Of 180 patients transfused from 2002 to 2011, 26 developed at least one new antibody. The majority of alloimmunized patients (14/26) received episodic transfusions only. The most common antibodies formed were against C and E antigens. Of the 16 patients who developed C, E, Kell antibodies, nine had one or more documented transfusions at an outside hospital. Five patients had Rh variants undetectable on routine phenotyping including two novel e alleles related to ceAR and ceS(733G). Conclusion: Despite extended RBC typing, alloimmunization may still occur due to RBC variants that are not detected on routine screening and transfusions at institutions where extended RBC typing is not done. Extended RBC typing should be the standard of care for patients with SCD. Prospective genotyping may reduce allosensitization to rare variants not detected on routine screening.
Original language | English (US) |
---|---|
Pages (from-to) | 1487-1491 |
Number of pages | 5 |
Journal | Pediatric Blood and Cancer |
Volume | 60 |
Issue number | 9 |
DOIs | |
State | Published - Sep 1 2013 |
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Keywords
- Alloimmunization
- Extended red cell typing
- Red cell transfusion
- Sickle cell anemia
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health
- Hematology
- Oncology
Cite this
}
Alloimmunization in sickle cell anemia in the era of extended red cell typing. / O'Suoji, Chibuzo; Liem, Robert I; Mack, Astrid Kyle; Kingsberry, Paris; Ramsey, Glenn Eugene; Thompson, Alexis A.
In: Pediatric Blood and Cancer, Vol. 60, No. 9, 01.09.2013, p. 1487-1491.Research output: Contribution to journal › Article
TY - JOUR
T1 - Alloimmunization in sickle cell anemia in the era of extended red cell typing
AU - O'Suoji, Chibuzo
AU - Liem, Robert I
AU - Mack, Astrid Kyle
AU - Kingsberry, Paris
AU - Ramsey, Glenn Eugene
AU - Thompson, Alexis A
PY - 2013/9/1
Y1 - 2013/9/1
N2 - Background: Red blood cell (RBC) transfusion remains an essential part of the management of patients with sickle cell disease (SCD). Alloimmunization is a major complication of transfusions. Extended RBC typing is advocated as a means to reduce alloimmunization in SCD. Our goal was to assess alloimmunization among individuals with SCD at our center since implementing extended RBC typing. Materials and Methods: We reviewed electronic medical records of all patients with SCD (N=641) in our comprehensive SCD Program to determine transfusion histories. Cross-referencing with our blood bank database, we extracted data such as antibodies identified, detection date and genotyping in specific cases. Transfusion sources were determined for those with C, E, and Kell antibodies. Results: Of 180 patients transfused from 2002 to 2011, 26 developed at least one new antibody. The majority of alloimmunized patients (14/26) received episodic transfusions only. The most common antibodies formed were against C and E antigens. Of the 16 patients who developed C, E, Kell antibodies, nine had one or more documented transfusions at an outside hospital. Five patients had Rh variants undetectable on routine phenotyping including two novel e alleles related to ceAR and ceS(733G). Conclusion: Despite extended RBC typing, alloimmunization may still occur due to RBC variants that are not detected on routine screening and transfusions at institutions where extended RBC typing is not done. Extended RBC typing should be the standard of care for patients with SCD. Prospective genotyping may reduce allosensitization to rare variants not detected on routine screening.
AB - Background: Red blood cell (RBC) transfusion remains an essential part of the management of patients with sickle cell disease (SCD). Alloimmunization is a major complication of transfusions. Extended RBC typing is advocated as a means to reduce alloimmunization in SCD. Our goal was to assess alloimmunization among individuals with SCD at our center since implementing extended RBC typing. Materials and Methods: We reviewed electronic medical records of all patients with SCD (N=641) in our comprehensive SCD Program to determine transfusion histories. Cross-referencing with our blood bank database, we extracted data such as antibodies identified, detection date and genotyping in specific cases. Transfusion sources were determined for those with C, E, and Kell antibodies. Results: Of 180 patients transfused from 2002 to 2011, 26 developed at least one new antibody. The majority of alloimmunized patients (14/26) received episodic transfusions only. The most common antibodies formed were against C and E antigens. Of the 16 patients who developed C, E, Kell antibodies, nine had one or more documented transfusions at an outside hospital. Five patients had Rh variants undetectable on routine phenotyping including two novel e alleles related to ceAR and ceS(733G). Conclusion: Despite extended RBC typing, alloimmunization may still occur due to RBC variants that are not detected on routine screening and transfusions at institutions where extended RBC typing is not done. Extended RBC typing should be the standard of care for patients with SCD. Prospective genotyping may reduce allosensitization to rare variants not detected on routine screening.
KW - Alloimmunization
KW - Extended red cell typing
KW - Red cell transfusion
KW - Sickle cell anemia
UR - http://www.scopus.com/inward/record.url?scp=84880394768&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84880394768&partnerID=8YFLogxK
U2 - 10.1002/pbc.24530
DO - 10.1002/pbc.24530
M3 - Article
C2 - 23508932
AN - SCOPUS:84880394768
VL - 60
SP - 1487
EP - 1491
JO - Pediatric Blood and Cancer
JF - Pediatric Blood and Cancer
SN - 1545-5009
IS - 9
ER -