Asymptomatic CMV infection at birth following maternal primary infection despite valacyclovir treatment and a subsequent negative amniocentesis. Case report.

Valacyclovir is currently the only pharmacological intervention demonstrated to reduce the risk of vertical CMV congenital infection within a randomized clinical trial in case of primary infection during pregnancy. So far, no data are available on the prognosis of children with congenital CMV infection diagnosed at birth after a negative amniocentesis whose mother were treated with valacyclovir during pregnancy, therefore it is essential to carry out a rigorous neurocognitive follow-up in these children in order to investigate the potential clinical consequence.

Placental histological examination and the relationship with oxidative stress in preterm infants.

BACKGROUND: Prenatal conditions of enhanced oxidative stress (OS) linked to inflammation or hypoxia have been associated with impaired fetal growth and preterm delivery. Little is known regarding biomarkers of OS in the cord blood of preterm infants and placental histological patterns. OBJECTIVES: To test the hypothesis that placental lesions indicating chorioamnionitis (CA) or vascular underperfusion (VU) are associated with increased OS in the offspring. METHODS: 120 neonates born below 29+6 weeks of gestational age (GA) were enrolled. Histological characteristics of placentas from their mothers were classified as normal (CTRL group), histological CA (HCA) and vascular underperfusion (VU). Serum concentrations of isoprostanes (IsoPs), non-protein bound iron (NPBI) and advanced oxidative protein products (AOPP), were determined in cord blood. RESULTS: IsoPs, NPBI and AOPP were significantly increased in HCA group compared to CTRL group. The multivariable regression model, adjusted for GA, maternal age, parity, maternal diabetes, maternal obesity and presence/absence of fetal growth restriction (FGR), showed a significant association between the presence of HCA and increased OS biomarkers levels in cord blood (IsoPs: p = 0.006; NPBI: p = 0.014; AOPP: p = 0.007). Placental VU lesions were significantly associated with higher umbilical IsoPs, NPBI and AOPP levels (IsoPs: p = 0.008; NPBI: p = 0.002; AOPP: p = 0.040). In the cases of placental VU lesions associations were also found between high AOPP levels and low GA (p = 0.002) and the presence of fetal growth restriction (p = 0.014). CONCLUSIONS: Placental lesions indicating inflammation or impaired perfusion are associated with higher cord blood levels of OS biomarkers explaining the fetal susceptibility to oxidative injury and the need of antioxidant protection.

Perinatal outcome and placental histological characteristics: a single-center study.

OBJECTIVE: Placental pathology assists in characterizing the antenatal environment and may provide information about the baby's subsequent development. We aim to assess whether histological patterns of placenta are associated with an increased risk of perinatal diseases and to evaluate how different patterns of placental dysfunction can affect the neurodevelopmental outcome. METHODS: We analyzed the histopathological characteristics of 105 singleton placentas from infants born between 23 and 31 weeks of gestation and we assessed pair-wise correlations with perinatal diseases. Estimated relative risks were calculated from odds ratios. RESULTS: Histological chorioamnionitis (CA group) was detected on 51 of 100 placentas tested. Lesions of uteroplacental circulation (abruption, infarction or thrombosis, perivillous fibrin deposition, syncytial knots; vasculopathy group) were detected on 29. 25 normal placentas served as controls. The incidence of bronchopulmonary dysplasia (BPD) and patent ductus arteriosus (PDA) was higher in CA than in control group. The risk of developing retinopathy of prematurity (ROP), intraventricular hemorrhage (IVH) and PDA was higher in CA than in vasculopathy group. CONCLUSIONS: At low gestational age CA, rather than placental lesions of vasculopathy, negatively impacts perinatal outcome. Clinical significance of histologic vasculopathy remains questionable. Other pathophysiological mechanisms than those associated with placental changes may occur following dysfunction of uteroplacental circulation.