Preeclampsia: Effect on the fetus and newborn


Autoria(s): Rugolo, Ligia Maria Suppo de Souza; Bentlin, Maria Regina; Trindade, Cleide Enoir Petean
Contribuinte(s)

Universidade Estadual Paulista (UNESP)

Data(s)

27/05/2014

27/05/2014

01/04/2011

Resumo

Preeclampsia (PE) is the most common medical complication in pregnancy and a major cause of maternal and fetal morbidity and mortality. This disease is a great challenge for obstetricians because there are no effective interventions to treat or prevent it, and antenatal care involves a difficult balance between the risks for women to continue pregnancy and the risks for the baby's early birth. Fetal complications in PE are directly related to gestational age and the severity of maternal disease and include increased rates of preterm delivery, intrauterine growth restriction, placental abruption, and perinatal death. The major complications for the newborn are related to prematurity, although the data on the morbidity and outcome for preterm infants of women who have PE are conflicting, and few studies address this issue. The pathogenesis of PE involves abnormal placentation associated with immune and vascular events that result in endothelial dysfunction and clinical manifestations of PE. This disease has been associated with imbalance in angiogenic factors and oxidative stress. Nevertheless, only a limited number of studies have been carried out on fetuses and newborns that suggest that infants born from women who have PE are exposed to increased oxidative stress. Because oxidative stress and free radicals may play roles in several neonatal diseases, a direct effect of maternal disease on neonatal outcome is expected, and further research on such neonates, in the short- and long-term, is urgently needed. © 2011 by the American Academy of Pediatrics.

Identificador

http://dx.doi.org/10.1542/neo.12-4-e198

NeoReviews, v. 12, n. 4, 2011.

1526-9906

http://hdl.handle.net/11449/72352

10.1542/neo.12-4-e198

2-s2.0-79959875420

Idioma(s)

eng

Relação

NeoReviews

Direitos

closedAccess

Tipo

info:eu-repo/semantics/article