Chorioamnionitis and elevated cord blood inflammatory cytokine concentrations are associated with detectable disturbances of systemic and cerebral hemodynamics in premature newborns. Fifty-five infants (25-31 wk gestation) were enrolled. Chorioamnionitis was defined by placental histology. IL-6, IL-1␤, and tumor necrosis factor-␣ were quantified by ELISA. Blood pressure, heart rate, cardiac output, stroke volume, fractional shortening, and middle cerebral artery blood flow velocities were measured at 3 Ϯ 1 h after birth. Chorioamnionitis was evident in 22 placentas and was associated with increased IL-6 (p Ͻ 0.001), IL-1␤ (p ϭ 0.035), and heart rate (p ϭ 0.027); and with decreased mean and diastolic blood pressure (p ϭ 0.026 and p ϭ 0.019, respectively). IL-6 concentration correlated inversely with systolic, mean, and diastolic blood pressures. Right ventricular cardiac output was elevated (p ϭ 0.028) in infants with fetal vessel inflammation. Maternal temperature Ն38.0°C and newborn immature-to-total white blood cell ratio Ն0.4 were associated with significant decreases in left ventricular fractional shortening (p ϭ 0.001 and p ϭ 0.005, respectively). Neither chorioamnionitis nor elevated cytokine concentrations were associated with changes in middle cerebral artery Doppler blood flow velocities. Chorioamnionitis and elevated cord blood IL-6 concentrations are associated with decreased blood pressure in premature newborns. Inflammation of the fetal vessels and nonspecific indicators of infection are associated with disturbances in cardiac function. Infants with chorioamnionitis and elevated cytokine concentrations do not manifest changes in cerebral Doppler indices within the first few postnatal hours. We speculate that cytokine-associated systemic hemodynamic disturbances in premature infants born after chorioamnionitis predispose such infants to perinatal brain injury. Hemodynamic abnormalities among premature infants are recognized to be important factors in the pathogenesis of perinatal brain injury. For example, IVH is more common in very low birth weight infants with hypotension (1) and fluctuating cerebral blood flow velocities (2). PVL may denote white matter ischemia (3) that results from compromised cerebral blood flow during a critical developmental period in which oligodendroglia undergo myelogenesis (4) in the presence of a tenuous vascular supply (5, 6). In fact, animals at a stage of brain development comparable to the Ͻ32-wk human fetus display a distinct and selective reduction of white matter blood flow in response to hypotension (7), confirming the predisposition for periventricular white matter ischemia at this gestational age.The ischemia theory of white matter injury has been challenged (8 -11) by the epidemiologic observation that chorioamnionitis is a strong predictor of subsequent PVL (12, 13) and cerebral palsy in both term (14) and preterm (13) infants. Although the mechanism of white matter injury in the context of infection has not been fully elucidated, evidence suggests that the p...

These data are consistent with a role for sFlt-1 in the maternal manifestations of preeclampsia. In contrast to preeclampsia, sFlt-1 does not appear to contribute substantially to decreased circulating free PlGF in SGA pregnancies in the absence of a maternal syndrome.

PTSD is a common consequence of RTAs. Liaison with accident and emergency departments would enhance the early detection and follow-up of children at risk of developing PTSD.

No abstract

Inadequate trophoblast invasion and spiral artery remodeling leading to poor placental perfusion are believed to underlie the pregnancy pathologies preeclampsia (PE) and intrauterine growth restriction (IUGR). The main objective of this study was to investigate hypoxia-inducible transcription factor-alpha (HIF-alpha) and downstream genes (VEGF receptor-1) Flt-1 and soluble fms-like tyrosine kinase 1 (sFlt-1) proteins in IUGR placentas. Placentas from normal pregnant (NP; n = 18), PE (n = 18), and IUGR (n = 10) patients were investigated. Normotensive patients with IUGR delivered babies at >or= 37 wk of gestation with birth weights of <10% and asymmetrical growth. HIF-1 alpha, -2 alpha, Flt-1, and sFlt-1 protein, and mRNA were assessed by Western and Northern blot analyses, respectively. The results are expressed as ratios of the densitometric values for each pair of pathologic and normal placentas, a ratio of 1.0 indicating no difference. Comparable to our earlier studies, the PE/NP ratios for HIF-1 alpha, -2 alpha, and Flt proteins were significantly increased by 50-100% (all P < 0.01 vs. 1.0). Unexpectedly, the IUGR/NP ratios for HIF-1 alpha and -2 alpha proteins were 1.03 +/- 0.07 and 0.96 +/- 0.16, respectively, and for Flt and sFlt were 1.14 +/- 0.15 and 0.95 +/- 0.12, respectively (all P = not significant vs. 1.0). Northern blot analysis revealed comparable levels of HIF-alpha mRNA in abnormal and normal placentas. In contrast to PE, HIF-alpha proteins and regulated genes are not increased in placentas from normotensive pregnant women delivering small, asymmetrically grown babies >or= 37 wk of gestation. The absence of an increase in HIF-alpha protein is not due to insufficient HIF-alpha mRNA for protein synthesis. Thus, the placentas from women with PE and late IUGR are fundamentally different at the molecular level.

Inadequate trophoblast invasion and spiral artery remodeling leading to poor placental perfusion and hypoxia are believed to underlie preeclampsia (PE) and intrauterine growth restriction (IUGR). Recent studies implicate increased circulating endoglin as a contributor to the pathogenesis of PE. The objective of this study was to determine whether placental and circulating endoglin concentrations are altered in pregnancies complicated by intrauterine growth restricted (IUGR) infants and to address the role of hypoxia on the regulation of placental endoglin. We analyzed 10 placentas each from normal pregnant (NP), PE, and IUGR subjects. Endoglin levels were 2.5-fold higher in preeclamptic placentas compared to NP (15.4+/-2.6 versus 5.7+/-1.0, p<0.01). In contrast, endoglin levels were similar in NP and IUGR placentas (5.7+/-1.0 vs 5.9+/-1.1, p=NS). Placentas from pregnancies with both PE and IUGR exhibited endoglin levels comparable to the PE group and significantly different from normotensive pregnancies with and without IUGR pregnancies (mean 14.9+/-4.0, n=9, p=0.013). Soluble endoglin concentrations in maternal plasma were comparable in NP and IUGR, but higher in women with PE (n=10 per group, p<0.05). Despite a 2-fold increase in hypoxia inducible factor, HIF-1alpha, we did not observe endoglin upregulation in NP, PE, or IUGR placental villous explants exposed to hypoxia (2% oxygen). In contrast to PE, placental or circulating endoglin is not increased in normotensive women delivering small, asymmetrically grown (IUGR) infants at term. The placentas of women with IUGR appear to be fundamentally different from PE women with respect to endoglin, despite the proposed common pathology of deficient trophoblast invasion/spiral artery remodeling and poor placental perfusion.

Aims To assess the effect of brief motivational enhancement intervention postpartum alcohol use. Design Single-blinded, randomized controlled effectiveness trial in which pregnant women were assigned to receive usual care or up to 5 face-to-face brief motivational enhancement sessions lasting 10–30 minutes each and occurring at study enrollment, 4 and 8 weeks after enrollment, 32 weeks of gestation, and 6 weeks postpartum. Setting Large, urban, obstetrics clinic. Participants Women who were ≥18 years old, < 20 weeks of gestation, and consumed alcohol during pregnancy. Of 3438 women screened, 330 eligible women were assigned to usual care (n=165) or intervention (n=165). Due to missing data, we analyzed 125 in the intervention group and 126 in the usual care group. Measurements The proportion of women with any alcohol use and the number of drinks per day, reported via follow-up telephone interviews at 4 and 8 weeks after enrollment, 32 weeks of gestation, and 6 weeks, 6 months, and 12 months postpartum. Findings In random effects models adjusted for confounders, the intervention group was less likely to use any alcohol (odds ratio 0.50; 95% confidence interval [CI], 0.23 – 1.09; P=0.08) and consumed fewer drinks per day (coefficient −0.11; 95% CI −0.23 − 0.01; P=0.07) than the usual care group in the postpartum period but these differences were non-significant. Missing data during the prenatal period prevented us from modeling prenatal alcohol use. Conclusions Brief motivational enhancement intervention delivered in an obstetrical outpatient setting did not conclusively decrease alcohol use during the postpartum period.

No abstract