title: Iron-deficient erythropoiesis in blood donors and red blood cell recovery after transfusion: initial studies with a mouse model.
abstract: BACKGROUND
  Most frequent red cell (RBC) donors and many first-time donors are iron deficient, but meet haemoglobin standards. However, the effects of donation-induced iron deficiency on RBC storage quality are unknown. Thus, we used a mouse model to determine if donor iron deficiency reduced post-transfusion RBC recovery.
  
  
  METHODS
  Weanling mice received a control diet or an iron-deficient diet. A third group receiving the iron-deficient diet was also phlebotomised weekly. This provided 3 groups of mice with different iron status: (1) iron replete, (2) mild iron deficiency with iron-deficient erythropoiesis, and (3) iron-deficiency anaemia. At ten weeks of age, blood was collected, leucoreduced, and stored at 4 ºC. After 12 days of storage, 24-hour (h) post-transfusion RBC recovery was quantified in recipients by flow cytometry.
  
  
  RESULTS
  Before blood collection, mean haemoglobin concentrations in the iron-replete, iron-deficient, and iron-deficiency anaemia donor mice were 16.5±0.4, 11.5±0.4, and 7.0±1.4 [g/dL± 1 standard deviation (SD)], respectively (p<0.01 for all comparisons between groups). The 24-h post-transfusion RBC recoveries in recipients receiving transfusions from these three cohorts were 77.1±13.2, 66.5±10.9, and 46.7±15.9 (% ±1 SD), respectively (p<0.05 for all comparisons between groups).
  
  
  CONCLUSIONS
  In summary, donor iron deficiency significantly reduced 24-h post-transfusion RBC recovery in recipient mice. RBCs from mice with mild iron deficiency and iron-deficient erythropoiesis, with haemoglobin levels similar to those used for human autologous blood donation, had intermediate post-transfusion RBC recovery, as compared to iron-replete donors and those with iron-deficiency anaemia. This suggests that, in addition to the effects of iron deficiency on donor health, frequent blood donation, leading to iron-deficient erythropoiesis, may also have adverse effects for transfusion recipients.
authors.affiliation: Department of Pathology and Cell Biology, Columbia University, New York, NY, United States of America.
authors.forename: Sheila
authors.initials: S
authors.lastname: Bandyopadhyay
authors.affiliation: Department of Pediatrics, Columbia University, New York, NY, United States of America.
authors.forename: Gary M
authors.initials: GM
authors.lastname: Brittenham
authors.affiliation: Department of Pathology and Cell Biology, Columbia University, New York, NY, United States of America.
authors.forename: Richard O
authors.initials: RO
authors.lastname: Francis
authors.affiliation: BloodWorksNW and Departments of Laboratory Medicine and Internal Medicine, University of Washington, Seattle, WA, United States of America.
authors.forename: James C
authors.initials: JC
authors.lastname: Zimring
authors.affiliation: Department of Pathology and Cell Biology, Columbia University, New York, NY, United States of America.
authors.forename: Eldad A
authors.initials: EA
authors.lastname: Hod
authors.affiliation: Department of Pathology and Cell Biology, Columbia University, New York, NY, United States of America.
authors.forename: Steven L
authors.initials: SL
authors.lastname: Spitalnik
mesh_terms: D018798:Anemia, Iron-Deficiency / Q000097:blood / Q000209:etiology; D000818:Animals; D001782:Blood Donors; D004912:Erythrocytes / Q000378:metabolism*; D004920:Erythropoiesis; D006801:Humans; D007501:Iron / Q000097:blood; D000090463:Iron Deficiencies; D051379:Mice; D020127:Recovery of Function
chemical_list: D007501:Iron