Fetal and embryonic hemaglobins in erythroblasts of chromosomally normal and abnormal fetuses at 10-40 weeks of gestation

Background and Objectives. During fetal development a change in erythropoie sis from hepatic to medullary site occurs. In chromosomally abnormal fetuse s this change is delayed. Hemoglobin production also undergoes developmenta l switches from embryonic to fetal hemoglobins in the first trimester of pr egnancy. The aim of study was to determine the proportion of embryonic and fetal hemoglobins in fetal erythroblasts of chromosomally normal and abnorm al fetuses at 10-40 weeks of gestation. Design and Methods. Fetal blood was obtained from 93 chromosomally normal a nd 19 abnormal fetuses at 10-40 weeks of gestation. Fetal erythroblasts wer e isolated by triple density gradient centrifugation and magnetic cell sort ing with CD71 antibody. Fluorescent antibodies were used to immunostain for zeta (zeta), epsilon (epsilon) and gamma (gamma) hemoglobin chains. Results. The percentages of the positively stained cells were calculated. I n chromosomally normal fetuses the percentage of erythroblasts expressing t he zeta chain was 25% at 10 weeks but this decreased exponentially with ges tation to less than 1% by 17 weeks. Similarly, the percentage of cells expr essing the epsilon chain decreased from 97% at 10 weeks to less than 1% by 25 weeks. In contrast, expression of the gamma chain increased from about 3 0% at 10 weeks to 90% by 16 weeks and decreased thereafter to 60% at 40 wee ks. In the abnormal fetuses, the percentage of erythroblasts expressing the zeta chain and the epsilon chain decreased to less than 1% by 23 and 28 we eks respectively, while maximum expression of the gamma chain was at about 22 weeks. Interpretation and Conclusions. In the chromosomally abnormal group the pat tern of change in the expression of the various hemoglobin chains during ge station was similar to that in the normal fetuses but was delayed by three to six weeks. These findings suggest that in fetuses with chromosomal abnor malities there is a developmental delay in the switch from embryonic to fet al hemoglobin chains. (C)2000, Ferrata Storti Foundation.