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Complex Transfusion Management in a Sickle Cell Patient With Anti-Fy3 Alloimmunization: A Case Report.
Cureus
May 2024
Laboratory for Clinical Biology, Ziekenhuis Netwerk Antwerpen (ZNA), Antwerp, BEL.
Fy3 is a high-prevalence red blood cell antigen of the Duffy (Fy) blood group system. Anti-Fy3 antibodies are rare and solely arise in individuals with a Duffy null phenotype (Fy(a-b-)), which is a phenotype that mainly occurs in people of African descent. Clinically, anti-Fy3 antibodies can cause both acute and delayed hemolytic transfusion reactions in adults as well as hemolytic disease in fetuses and newborns.
View Article and Find Full Text PDFSevere delayed hemolytic transfusion reaction due to anti-Fy3 in a patient with sickle cell disease undergoing red cell exchange prior to hematopoietic progenitor cell collection for gene therapy.
Haematologica
January 2021
New York Blood Center, Sickle Cell Program, Albert Einstein College of Medicine, Bronx, NY.
Duffy blood group phenotype-genotype correlations using high-resolution melting analysis PCR and microarray reveal complex cases including a new null FY*A allele: the role for sequencing in genotyping algorithms.
Vox Sang
October 2015
Research and Development, Australian Red Cross Blood Service, Kelvin Grove, QLD, Australia.
Background And Objectives: Duffy blood group phenotypes can be predicted by genotyping for single nucleotide polymorphisms (SNPs) responsible for the Fy(a) /Fy(b) polymorphism, for weak Fy(b) antigen, and for the red cell null Fy(a-b-) phenotype. This study correlates Duffy phenotype predictions with serotyping to assess the most reliable procedure for typing.
Materials And Methods: Samples, n = 155 (135 donors and 20 patients), were genotyped by high-resolution melt PCR and by microarray.
Measurement of macrophage marker in hyperhaemolytic transfusion reaction: a case report.
Transfus Med
April 2012
Department of Red Cell Immunology (RCI), NHS-Blood and Transplant, Tooting Centre, London, UK.
Background: Hyperhaemolytic transfusion reaction (HHTR) has been well described in patients with sickle cell disease (SCD). It is characterised by a decrease in haemoglobin concentration to levels below those before transfusion and a fall in the absolute reticulocyte count. As red blood cells (RBC) alloantibodies are typically not detected in post-transfusion samples in acute forms of HHTR, we have previously proposed that both the transfused and autologous RBCs cells (HbSS/reticulocytes) are destroyed by activated macrophages.
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