Introduction: Preeclampsia (PE) is the primary obstetrical cause in one of the four perinatal deaths. Although the etiology and pathogenesis of preeclampsia is not fully known, a proinflammatory immune state prevails and can disrupt fetal hematopoiesis. Some of the effects on the newborn include neonatal thrombocytopenia, neutropenia, a reduction in T regulatory cells, and an increased cytotoxic natural killer cell profile.
Methods: Electronic databases were searched, and defined criteria were applied to select articles for review. The review covered literature on the effects on neonatal due to maternal preeclampsia, fetal outcomes, and new treatments in research aimed at reducing morbidity and mortality of the disease.
Discussion: The cytotoxic environment present in PE affects the development of fetal cell lineages. Neutropenia is observed in 50% of neonates and is correlated with mortality, although its treatment is not well-established. The enhancement in erythropoietin and the hypoxic setting present in the disease can also lead to thrombocytopenia. Per partum management includes platelet transfusion in order to avoid severe complications such as intraventricular hemorrhage. Regarding other cell lines, a cytotoxic profile is observed to be reflecting the milieu present in the mothers' bloodstream. This disruption alters the immune system response into a proinflammatory profile and can be correlated to neonatal necrotizing enterocolitis. An antiangiogenic environment is also part of the preeclampsia presentation and can be responsible for the enhancement of bronchopulmonary dysplasia observed in this population. Meanwhile, the reduction in angiogenic factors, such as vascular endothelial growth factor (VEGF), can be a protective mechanism for retinopathy of prematurity. Studies of the long-term effects of these observations are lacking, but lower neurodevelopmental scores and a higher cardiovascular risk are noted. New treatments in research propose a prevention of the disease during gestation in order to reduce the effects more efficiently in the fetus. Phosphodiesterase inhibitors, endothelin 1 receptor antagonists and manipulation of heme oxygenase-1 enzyme pathway are possible therapeutic alternatives. This review summarizes the current understanding of how preeclampsia affects neonates. As a conclusion, further studies are needed to build up a guideline to manage those effects. A research agenda is proposed.
Keywords: Immune cells; neonatal; preeclampsia.