Altered Intrahepatic Hematopoiesis in Neonates from Women with Pregnancy Induced Hypertension/Pre-Eclampsia

Demetrio Tamiolakis,Sylva Nikolaidou,Panagiotis Boglou,Sophia Barbagadaki,Maria Lambropoulou,Panagiotis Tsikouras,Ioannis Venizelos,Evagelia Seliniotaki,Vasiliki Arvanitidou,George Chimonis,Nikolas Papadopoulos,Demetrio Karamanidis,Gerasimos Koutsougeras,Anna Efthymiadou

doi:10.14712/18059694.2018.76

Abstract

To detect whether preeclampsia influences neonatal intrahepatic hematopoiesis, given that an activation of fetal neutrophils and monocytes during the course of this disorder occurs. We examined liver samples from 10 neonates of hypertensive/preeclamptic women at 27 to 28 weeks of gestation delivered by a cessarian section. All neonates were placed in incubators but they all died within 24 hours due to immaturity. The control group comprised 10 fetuses of the same gestational age, after voluntary abortion due to a neural defect. Specific antibodies against CD34, glycophorin C, hemoglobins A and F, myeloperoxidase, CD61, CD68, terminal desoxynucleotidyl transferase and the pax-5/B-cell specific activator protein, were used in each sample. Neonates from hypertensive/preeclamptic women, in comparison with controls, showed: a statistically significant reduction of erythropoiesis by 25% (p=0.015); a statistically significant increase of granulopoiesis (p=0.019); a statistically significant increase in the expression of CD68 positive cells of the monocytic lineage (p=0.017); a statistically significant increase in the expression of CD34 progenitor/stem positive cells (p=0.021). No statistically significant differences were observed in both examined groups, concerning megakaryopoiesis and B lymphopoiesis. Preeclampsia of pregnancy has an impact on neonatal intrahepatic hematopoiesis by increasing granulopoiesis, reducing erythropoiesis and triggering endothelial and stem cell activation. We suggest that these findings reflect a state of persistent inflammation and a loss of red blood cell production possibly contributing to the neonatal morbidity related to this disorder.

Highlights

Preeclampsia, a severe hypertensive disorder in pregnancy, represents one of the major causes of maternal and fetal mortality in developing countries
It is known that activation of fetal neutrophils and monocytes during preeclampsia involves enhanced chemokine activation, which contributes to the fetal morbidity of this disorder [17]. To elucidate whether this activation of fetal neutrophils and monocytes is associated with respective changes at the level of intrahepatic hematopoiesis, we examined by using immunohistochemistry liver samples from neonates from preeclamptic women and correlated our findings with those after voluntary abortion
The sections were examined independently by two observers, and positive cellular staining for each antibody was manifested as fine red cytoplasmic granularity

Summary

Introduction

Preeclampsia, a severe hypertensive disorder in pregnancy, represents one of the major causes of maternal and fetal mortality in developing countries. The etiology of the condition is unknown, but placental disorders are probably involved in the pathophysiologic mechanism [16]. Both the fetus and the placenta are often growth retarded when hypertension occurs before mid-gestation. There are ischemic changes and often-placental infarcts. Onset of preeclampsia in early gestation greatly increases the risk of spontaneous abortion, abruptio placenta, fetal death, spontaneous pre-term labor, and pre-term delivery. In mid-trimester fetuses the principal site of hematopoiesis is the liver, where two functionally different compartments can be observed. Erythropoiesis mainly takes place within the sinusoids of the parenchyma while granulopoiesis is restricted to the mesenchymal tissue of the portal fields

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Discussion

Conclusion