Fetal programming and early identification of newborns at high risk of free radical-mediated diseases.

Nowadays metabolic syndrome represents a real outbreak affecting society. Paradoxically, pediatricians must feel involved in fighting this condition because of the latest evidences of developmental origins of adult diseases. Fetal programming occurs when the normal fetal development is disrupted by an abnormal insult applied to a critical point in intrauterine life. Placenta assumes a pivotal role in programming the fetal experience in utero due to the adaptive changes in structure and function. Pregnancy complications such as diabetes, intrauterine growth restriction, pre-eclampsia, and hypoxia are associated with placental dysfunction and programming. Many experimental studies have been conducted to explain the phenotypic consequences of fetal-placental perturbations that predispose to the genesis of metabolic syndrome, obesity, diabetes, hyperinsulinemia, hypertension, and cardiovascular disease in adulthood. In recent years, elucidating the mechanisms involved in such kind of process has become the challenge of scientific research. Oxidative stress may be the general underlying mechanism that links altered placental function to fetal programming. Maternal diabetes, prenatal hypoxic/ischaemic events, inflammatory/infective insults are specific triggers for an acute increase in free radicals generation. Early identification of fetuses and newborns at high risk of oxidative damage may be crucial to decrease infant and adult morbidity.

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.

Effects of lutein on oxidative stress in the term newborn: a pilot study.

BACKGROUND: Oxidative stress (OS) plays a crucial role in pathological conditions during the early neonatal period. The newborns are susceptible to oxidative damage due to high metabolic rate and low levels of antioxidant enzymes. Lutein has been found to have protective functions in adult humans as antioxidant. AIM: To evaluate the effects of lutein on OS in newborns. We tested the hypothesis that lutein would act both by increasing antioxidant capacity and inhibiting OS. METHODS: This was a randomized, double-blind, placebo-controlled, single-center study. 20 healthy term newborns were assigned to receive lutein or placebo (lutein and control group, respectively) at 12 and 36 h after birth. Total hydroperoxides (TH), as marker of OS, and biological antioxidant potential (BAP), as marker of antioxidant power, were detected on cord blood and at 48 h of life in all babies. RESULTS: TH significantly increased from birth to 48 h in the control group (p = 0.02), but not in the lutein group. In the lutein group, BAP significantly increased after 48 h (p = 0.02), showing a strengthening of antioxidant activity due to lutein. At 48 h of life, compared with those in the control group, neonates assigned to receive lutein had significantly lower TH levels (p = 0.04) and higher BAP levels (p = 0.028). CONCLUSIONS: Lutein administration in newborns increases the levels of BAP decreasing TH. The enhancement of antioxidant activity in plasma clearly results in protecting newborn from perinatal OS. These preliminary results, adding a new contribution in antioxidant strategies, strongly require to be confirmed by RCT.