The Duffy antigen is found on red blood cells, and the null form [Fy(a-b-)] is caused by homozygosity at a single nucleotide polymorphism (SNP) rs2814778 in the promoter region of the Duffy antigen receptor for chemokines (DARC). This phenotype likely provided selective advantage against Plasmodium vivax and is commonly observed among those of African and Middle Eastern descent. The Duffy antigen also impacts neutrophil localization, and the null form results in lower circulating neutrophils in the periphery. In fact, healthy Duffy null patients are expected to have an absolute neutrophil count (ANC) approximately 2000/μL lower than Duffy non-null patients, and almost a quarter of Duffy null patients will have baseline ANC<1500/μL. This is a normal variant with no known negative health consequences or infectious sequalae. Thus, unnecessary interventions to increase ANC to >1500 cells/μL or delays in standards of care due to this lower baseline ANC are not appropriate.

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Duffy Null-Associated Neutrophil Count

  • Lauren E. Merz,
  • Nancy Berliner

摘要

The Duffy antigen is found on red blood cells, and the null form [Fy(a-b-)] is caused by homozygosity at a single nucleotide polymorphism (SNP) rs2814778 in the promoter region of the Duffy antigen receptor for chemokines (DARC). This phenotype likely provided selective advantage against Plasmodium vivax and is commonly observed among those of African and Middle Eastern descent. The Duffy antigen also impacts neutrophil localization, and the null form results in lower circulating neutrophils in the periphery. In fact, healthy Duffy null patients are expected to have an absolute neutrophil count (ANC) approximately 2000/μL lower than Duffy non-null patients, and almost a quarter of Duffy null patients will have baseline ANC<1500/μL. This is a normal variant with no known negative health consequences or infectious sequalae. Thus, unnecessary interventions to increase ANC to >1500 cells/μL or delays in standards of care due to this lower baseline ANC are not appropriate.