Fetal and embryonic hemoglobins in erythroblasts from fetal blood and fetal cells enriched from maternal blood in fetal anemia

Background and Objectives. To determine whether there is a delay or reversa l in switch mechanisms from embryonic (epsilon and zeta) to fetal (gamma) h emoglobins accompanying the erythroblastosis of anemic fetuses and whether an increased erythroblast count in fetal blood is associated with an increa se in fetomaternal cell trafficking. Design and Methods. Fetal and maternal blood samples were obtained from 10 cases with rhesus isoimmunization and 2 cases with maternal Parvo-B19 virus at 19-33 weeks' gestation. Blood samples were also taken as controls from 61 fetuses and 86 mothers. Fetal erythroblasts were isolated by triple dens ity gradient centrifugation and magnetic cell sorting with CD71 antibody. F luorescent antibodies were used to immuno-stain for zeta (zeta), epsilon (e psilon) and gamma (gamma) hemoglobin chains. In the maternal samples, fluor escence in situ hybridization (FISH) for X and Y chromosomes was also carde d out to confirm the presence and proportion of the enriched fetal cells fr om maternal blood. Results. In both fetal and maternal blood the percentage of erythroblasts p ositive for gamma -globin chain was significantly higher in the anemic fetu ses compared to the controls (fetal blood, p<0.001, R=0.91; maternal blood, p<0.001, R=0.56), but there was no significant difference in expression of the epsilon and zeta -chains. The percentage of cells with Y-signals was a lso higher in the maternal samples of anemic fetuses compared to normal con trols (p<0.001, R=0.56). Interpretation and Conclusions. These findings suggest that the erythroblas tosis of anemic fetuses is not accompanied by a delay or a reversal in swit ch from embryonic to fetal hemoglobin chains. Severe fetal anemia is associ ated with an increase in fetomaternal cell trafficking. (C) 2001, Ferrata S torti Foundation.