Altered erythropoiesis in newborns with congenital heart disease
Stephanie Y Tseng1, Zhiqian Gao1, Theodosia A Kalfa2,3
1The Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Insights
Term newborns with congenital heart disease (CHD) show altered red blood cell production, indicating ineffective erythropoiesis. Despite signs of stress, their hemoglobin levels are lower, suggesting an incomplete response to in-utero issues.
Area of Science:
- Neonatal Medicine
- Pediatric Cardiology
- Hematology
Background:
- Fetal hypoxia is linked to fetal growth restriction in congenital heart disease (CHD).
- This condition can trigger stress erythropoiesis (red blood cell production) in utero.
- Assessing erythropoiesis and growth in newborns with CHD is crucial.
Purpose of the Study:
- To evaluate erythropoiesis in newborns with congenital heart disease.
- To determine the association between erythropoiesis and fetal growth in these infants.
Main Methods:
- Retrospective review of fetuses with prenatally diagnosed CHD (2013-2018).
- Exclusion of multiple gestations, genetic abnormalities, and other complications.
- Comparison of complete blood count tests at birth with normative values and correlation with anthropometrics and Doppler measures.
Main Results:
- 160 newborns with CHD were analyzed; 130 were born at term.
- Term infants (≥37 weeks) had lower hemoglobin and hematocrit, with elevated nucleated red blood cells (nRBCs).
- No significant differences in erythropoiesis markers were found between CHD subgroups or correlated with growth parameters.
Conclusions:
- Term infants with CHD exhibit altered erythrocyte indices, suggesting ineffective erythropoiesis in late gestation.
- Decreased hemoglobin levels in term newborns with CHD indicate an incomplete compensatory response to in-utero disturbances.
- Altered red blood cell indices were not associated with fetal growth outcomes in this cohort.
Background:
Fetal hypoxia has been implicated in fetal growth restriction in congenital heart disease (CHD) and leads to stress erythropoiesis in utero. The objective is to assess erythropoiesis and its association with growth in newborns with CHD.
Methods:
Fetuses with prenatally diagnosed CHD from 2013 to 2018 were retrospectively reviewed. Pregnancies with multiple gestation, genetic abnormalities, major extra-cardiac anomalies, and placental abruption were excluded. Complete blood count tests at birth were compared to published normative values. Spearman correlation assessed associations of red blood cell (RBC) indices with birth anthropometrics and prenatal Doppler measures.
Results:
A total of 160 newborns were included. Median gestational age was 38.3 (37.3, 39.0) weeks. Infants ≥37 weeks gestation had lower hemoglobin (Hgb), hematocrit, and elevated nucleated RBC (nRBC), mean corpuscular volume, and mean corpuscular hemoglobin compared to reference. No differences in RBC indices were observed in infants <34 and 34-37 weeks gestation. There was no difference in Hgb and nRBC between CHD subgroups. Neither Hgb nor nRBC were associated with birth anthropometrics or Doppler patterns.
Conclusions:
Term infants with CHD demonstrated multiple alterations in erythrocyte indices suggesting ineffective stress erythropoiesis in late gestation resulting in lower Hgb at birth. Altered erythropoiesis was not correlated to growth or Doppler patterns.
Impact:
Newborns with congenital heart disease (CHD) born at term gestation demonstrated altered erythropoiesis. Term newborns with CHD have decreased hemoglobin levels despite having red blood cell indices consistent with stress erythropoiesis, suggesting an incomplete compensatory response to in utero physiologic disturbances associated with CHD. The etiology is unknown; however, it may be influenced by multiple risk factors during pregnancy in the maternal-fetal dyad. Alterations in red blood cell indices were not associated with outcomes of fetal growth.
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