Autologous Infant and Allogeneic Adult Red Cells Demonstrate Similar Concurrent Post-Transfusion Survival in Very Low Birth Weight Neonates

Abstract

Objective Based on the hypothesis that neonatal autologous red blood cell (RBC) survival (RCS) is substantially shorter than adult RBC, we concurrently tracked the survival of transfused biotin-labeled autologous neonatal and allogeneic adult RBC into ventilated, very low birth weight (VLBW) infants. Study design RBC aliquots from the first clinically ordered, allogeneic adult RBC transfusion and from autologous infant blood were labeled at separate biotin densities (BioRBC) and transfused. Survival of these BioRBCs populations were concurrently followed over weeks by flow cytometric enumeration using leftover blood. Relative tracking of infant autologous and adult allogeneic BioRBC was analyzed by linear mixed modeling of batched weekly data. When possible, Kidd antigen (Jka and Jkb) mismatches between infant and donor RBCs were also used to track these two populations. Results Contrary to our hypothesis, concurrent tracking curves of RCS of neonatal and adult BioRBC in 15 study infants did not differ until week 7, after which neonatal RBC survival became shortened to 59% to 79% of adult enumeration values for uncertain reasons. Analysis of mismatched Kidd antigen RBC showed similar results, thus confirming that BioRBC tracking is not perturbed by biotin RBC labeling. Conclusions This study illustrates the utility of multi-density BioRBC labeling for concurrent measurement of RCS of multiple RBC populations in vivo. The similar RCS results observed for neonatal and adult BioRBCs transfused into VLBW infants provides strong evidence that the circulatory environment of the newborn infant—not intrinsic infant-adult RBC differences—is the primary determinant of erythrocyte survival. Trial registration Clinicaltrials.gov: NCT 00731588.

In premature infants there is no decrease in 24‐hour posttransfusion allogeneic red blood cell recovery after 42 days of storage

“…Neonatal subjects included a convenience sample of 46 anemic infants with an estimated gestational age at birth of not more than 31 weeks who were being ventilated for respiratory distress and anticipated to survive. All neonates were anemic and receiving clinically indicated allogeneic adult donor RBC transfusions as reported previously . Infants with major congenital anomalies were excluded.…”

“…The different circulatory environments have been demonstrated in studies reporting markedly different long‐term RBC survival in newborns and in adults. Specifically, adult RBCs survive approximately half as long in the circulation of infants as in adults . The opposite has also been demonstrated: fetal RBCs from infants delivering at term survive approximately twice as long when in the adult circulation as they do in newborn infants …”

“…Further, we hypothesize that PTR 24 in neonates will not decrease with increasing duration of RBC storage. To test these hypotheses, we retrospectively compared PTR 24 data from three previously reported neonatal studies with PTR 24 data from four PTR 24 adult studies …”

“…4,5 No prior RBC kinetic studies have performed direct statistical comparisons of PTR 24 in infants and adults. This study offers this comparison by utilizing PTR 24 data from three previously reported neonatal RBC kinetic studies 2,6,7 and from four adult RBC studies. [8][9][10][11] Doing so is desirable for comparing PTR 24 results in two such markedly different subject populations with their different RBC circulatory environments.…”

Research Opportunities to Improve Neonatal Red Blood Cell Transfusion

“…Biotin labelling of populations of red cells (BioRBCs) has been used to determine RBC lifespan and time-dependent changes in RBC populations [54]. Because BioRBCs can track several different cell populations at the same time, they have also been used to simultaneously determine the survival characteristics of both autologous neonatal and allogeneic adult donor RBCs in very low birth weight infants, with resulting observations substantially at odds with current assumptions about autologous and allogeneic RCS in neonates [55, 56]. …”