Nucleated red blood cells are a direct response to mediators of inflammation in newborns with early-onset neonatal sepsis

Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06520-8063, USA.
American journal of obstetrics and gynecology (Impact Factor: 4.7). 04/2008; 198(4):426.e1-9. DOI: 10.1016/j.ajog.2008.01.040
Source: PubMed


The objective of the study was to test the hypothesis that inflammation modulates fetal erythroblastosis and/or the release of nucleated red blood cells (NRBCs) independent of hypoxia or fetal stress. We sought to determine whether fetal inflammation is associated with an elevation in neonatal NRBC count in the setting of inflammation-associated preterm birth.
The relationships between peripheral NRBC count, histological chorioamnionitis, umbilical cord interleukin (IL)-6, erythropoietin (EPO), cortisol, and acid-base status were analyzed in 68 preterm singletons, born to mothers who had an amniocentesis to rule out infection. Proteomic profiling of amniotic fluid identified presence of intraamniotic inflammation according to established parameters. NRBC counts were assessed within 1 hour of birth. Early-onset neonatal sepsis (EONS) was established based on hematological and microbiological indices. IL-6, EPO, and cortisol levels were measured by immunoassays. Fetal acid-base status was determined within 10 minutes of delivery. Parametric or nonparametric statistics were used.
Fetuses with EONS (n = 19) were delivered at earlier gestational ages (mean +/- SD: 27.1 +/- 2.8 weeks, P = .001) and more often by mothers with intraamniotic inflammation (P = .022) and histological chorioamnionitis (P < .001). Neonates with EONS had higher absolute NRBC counts (P = .011). NRBC counts were directly correlated with cord blood IL-6 levels (P < .001) but not with EPO, cortisol or parameters of acid-base status levels regardless of EONS status. These relationships remained following correction for gestational age, diabetes, intrauterine growth restriction, and steroid exposure.
In the setting of inflammation-associated preterm birth and in the absence of hypoxia, elevations in NRBCs in the early neonatal period may be a direct response of exposure to inflammatory mediators in utero.

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    • "No difference in the mean nRBC count based on the stage after birth was found in ROP and PDA, among the perinatal complications. A previous study reported that the nRBC count increased in infants with early sepsis due to inflammatory reaction36). However, no correlation between newborn infants with sepsis and nRBC count was found in this study. "
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    • "Recent publications indicate that the mechanisms driving nRBC production may not be related only to EPO as previously thought and that it is possible that elevation of nRBCs in the fetal circulation may be an epiphenomenon related to other pathological processes such as oxidative stress and inflammation [26]. Inflammation and specifically IL-6 have been found to have a distinct role in nRBC production and release into the peripheral circulation [12] [23] [27]. The link between systemic inflammation and fetal erythropoiesis is intriguing when investigating SDB since systemic inflammation has long been implicated in the pathophysiology of this disorder. "
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