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Circulating erythroid progenitors in the anemia of prematurity
Insights
Premature infants with anemia have normal erythroid burst-forming unit (BFU-E) responsiveness to erythropoietin. Inadequate erythropoietin production, not progenitor cell issues, likely causes this anemia, suggesting recombinant erythropoietin as a potential therapy.
Area of Science:
- Hematology
- Neonatology
- Cell Biology
Background:
- Anemia of prematurity is a common condition in premature infants.
- Erythropoiesis, the process of red blood cell production, is crucial for oxygen transport.
- Erythroid burst-forming units (BFU-E) are key progenitor cells in erythropoiesis.
Purpose of the Study:
- To investigate the erythropoiesis in premature infants suffering from anemia.
- To compare the responsiveness of BFU-E to erythropoietin in premature infants, adults, and term infants.
- To identify the underlying cause of anemia of prematurity.
Main Methods:
- Collected blood samples from 11 premature infants before transfusion.
- Compared BFU-E colony growth in premature infant blood with adult and cord blood.
- Assessed BFU-E response to varying concentrations of erythropoietin (0-2000 mU/mL).
- Measured serum erythropoietin concentrations and hematocrit levels.
Main Results:
- BFU-E colony growth increased stepwise with erythropoietin concentration in all groups.
- Premature infant and cord blood showed higher BFU-E colony counts than adult blood at high erythropoietin levels.
- Intrinsic BFU-E responsiveness to erythropoietin was similar across all studied groups.
- Infant serum erythropoietin levels were not significantly different from adult controls.
Conclusions:
- Premature infants possess progenitor cells committed to erythroid differentiation.
- The circulating BFU-E pool in premature infants exhibits normal intrinsic responsiveness to erythropoietin.
- Inadequate erythropoietin production is implicated as the cause of anemia of prematurity.
- Recombinant erythropoietin may serve as a therapeutic alternative to transfusions for symptomatic premature infants.
Abstract:
We studied erythropoiesis in infants with the anemia of prematurity by counting the number of colonies derived from erythroid burst-forming units (BFU-E) in the blood of 11 premature infants before they received transfusions. Colony growth in blood from the infants was compared with growth in blood from adults and umbilical-cord blood from term infants, in the presence of erythropoietin, 0 to 2000 mU per milliliter. Addition of increasing concentrations of erythropoietin resulted in a stepwise increase in the number of colonies derived from BFU-E (P less than 0.0005) of all three groups of subjects. Cultures stimulated with 2000 mU of erythropoietin yielded 28.1 +/- 7.6, 88.0 +/- 19.4, and 121.0 +/- 22.5 bursts (mean +/- SE) per 10(5) cells plated in blood from adults, blood from premature infants, and cord blood, respectively. Although more BFU-E-derived colonies appeared when 200 or 2000 mU were present per milliliter in cultures of the infants' blood and cord blood, the intrinsic responsiveness of BFU-E to erythropoietin was similar in all groups. Although the mean hematocrit was 26 percent, mean serum erythropoietin concentrations (+/- SD) in the infants (20.7 +/- 10.0 mU per milliliter) were not significantly different from those in the adult controls (24.0 +/- 6.5). We conclude that progenitor cells committed to erythroid differentiation are present during the anemia of prematurity, and that the intrinsic responsiveness of the circulating BFU-E pool to erythropoietin is normal. These results implicate inadequate production of erythropoietin as the cause of the anemia of prematurity and suggest that recombinant erythropoietin might provide a therapeutic alternative to transfusion for symptomatic babies with this condition.