title: Hypochromic red blood cells in low-risk myelodysplastic syndromes: effects of treatment with hemopoietic growth factors.
abstract: OBJECTIVE
  The anemia of low-risk myelodysplastic syndromes (MDS), refractory anemia (RA) and RA with ringed sideroblasts (RARS), may respond to treatment with hematopoietic growth factors (GF)); erythropoietin (Epo) +/- granulocyte colony-stimulating factor (G-CSF). The present study was designed to assess whether functional iron deficiency may develop in MDS patients receiving these treatments.
  
  
  METHODS
  Erythrocyte scattergrams from 34 patients with RA and RARS (untreated, transfused, or GF-treated with partial or complete erythroid response) were analyzed with Bayer-Advia equipment.
  
  
  RESULTS
  In untreated RARS, the proportion of hypochromic erythrocytes (Hypo-e, median 6.2%, range 1.1-8%) and hypochromic reticulocytes (Hypo-r, median 45%, range 22-48%), as well as mean corpuscular volume (MCV, median 101 fL) were significantly elevated compared to corresponding values in controls. These values increased further after GF-treatment (median 11%, 57%, and 105 fL, respectively), in spite of improved hemoglobin values and adequate body iron stores. The values observed in untreated RA patients largely fell within the normal range, and there was no significant influence of GF treatment. Notably, the hemoglobin content of reticulocytes (MCHr) did not differ between MDS and controls, and was not influenced by GF treatment.
  
  
  CONCLUSIONS
  The red cell population in RARS shows morphological abnormalities in terms of varying but overall increased size, and reduced hemoglobin concentration. The proportion of abnormal cells increases after successful pro-erythroid GF treatment, indicating that GF promote erythroblast survival, and maturation into erythrocytes. Hence, the finding of hypochromic red cells should not routinely be interpreted as a marker for Epo-induced functional iron deficiency in MDS.
authors.affiliation: Department of Medicine, Division of Hematology, Karolinska Institutet at Huddinge University Hospital, Stockholm, Sweden.
authors.forename: Therese
authors.initials: T
authors.lastname: Ljung
authors.forename: Rune
authors.initials: R
authors.lastname: Bäck
authors.forename: Eva
authors.initials: E
authors.lastname: Hellström-Lindberg
mesh_terms: D000753:Anemia, Refractory / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000628:therapy; D000756:Anemia, Sideroblastic / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D001772:Blood Cell Count; D004359:Drug Therapy, Combination; D004909:Erythrocyte Indices; D017707:Erythrocyte Transfusion; D004912:Erythrocytes / Q000737:chemistry; D004921:Erythropoietin / Q000008:administration & dosage / Q000627:therapeutic use*; D005293:Ferritins / Q000097:blood; D016179:Granulocyte Colony-Stimulating Factor / Q000008:administration & dosage / Q000627:therapeutic use*; D006454:Hemoglobins / Q000032:analysis; D006801:Humans; D007501:Iron / Q000097:blood*; D000090463:Iron Deficiencies; D008764:Methylmalonic Acid / Q000097:blood; D012156:Reticulocytes / Q000737:chemistry / Q000648:ultrastructure; D012306:Risk; D014168:Transferrin / Q000032:analysis
chemical_list: D006454:Hemoglobins; D014168:Transferrin; D004921:Erythropoietin; D016179:Granulocyte Colony-Stimulating Factor; D008764:Methylmalonic Acid; D005293:Ferritins; D007501:Iron