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      Impact of Antenatal Steroids on Intraventricular Hemorrhage in Very Low Birth Weight Infants

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          Abstract

          Objective

          To determine the association between antenatal steroids administration and intraventricular hemorrhage rates.

          Methods

          We used cross-sectional data from the California Perinatal Quality Care Collaborative during 2007-2013 for infants ≤ 32 weeks gestational age. Using multivariable logistic regression, we evaluated the effect of antenatal steroids on intraventricular hemorrhage, stratified by gestational age.

          Results

          In 25,979 very low birth weight infants, antenatal steroid use was associated with a reduction in incidence of any grade of intraventricular hemorrhage (odds ratio = 0.51, 95% confidence interval: 0.45, 0.58) and a reduction in incidence of severe intraventricular hemorrhage (odds ratio = 0.62, 95% confidence interval: 0.57, 0.67). This association was seen across gestational ages ranging from 22 to 29 weeks.

          Conclusions

          While current guidelines recommend coverage for preterm birth at 24 to 34 weeks gestation, our results suggest that treatment with antenatal steroids may be beneficial even before 24 weeks of gestational age.

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          Most cited references14

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          Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth.

          Respiratory distress syndrome (RDS) is a serious complication of preterm birth and the primary cause of early neonatal mortality and disability. To assess the effects on fetal and neonatal morbidity and mortality, on maternal mortality and morbidity, and on the child in later life of administering corticosteroids to the mother before anticipated preterm birth. We searched the Cochrane Pregnancy and Childbirth Group Trials Register (30 October 2005). Randomised controlled comparisons of antenatal corticosteroid administration (betamethasone, dexamethasone, or hydrocortisone) with placebo or with no treatment given to women with a singleton or multiple pregnancy, expected to deliver preterm as a result of either spontaneous preterm labour, preterm prelabour rupture of the membranes or elective preterm delivery. Two review authors assessed trial quality and extracted data independently. Twenty-one studies (3885 women and 4269 infants) are included. Treatment with antenatal corticosteroids does not increase risk to the mother of death, chorioamnionitis or puerperal sepsis. Treatment with antenatal corticosteroids is associated with an overall reduction in neonatal death (relative risk (RR) 0.69, 95% confidence interval (CI) 0.58 to 0.81, 18 studies, 3956 infants), RDS (RR 0.66, 95% CI 0.59 to 0.73, 21 studies, 4038 infants), cerebroventricular haemorrhage (RR 0.54, 95% CI 0.43 to 0.69, 13 studies, 2872 infants), necrotising enterocolitis (RR 0.46, 95% CI 0.29 to 0.74, eight studies, 1675 infants), respiratory support, intensive care admissions (RR 0.80, 95% CI 0.65 to 0.99, two studies, 277 infants) and systemic infections in the first 48 hours of life (RR 0.56, 95% CI 0.38 to 0.85, five studies, 1319 infants). Antenatal corticosteroid use is effective in women with premature rupture of membranes and pregnancy related hypertension syndromes. The evidence from this new review supports the continued use of a single course of antenatal corticosteroids to accelerate fetal lung maturation in women at risk of preterm birth. A single course of antenatal corticosteroids should be considered routine for preterm delivery with few exceptions. Further information is required concerning optimal dose to delivery interval, optimal corticosteroid to use, effects in multiple pregnancies, and to confirm the long-term effects into adulthood.
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            A controlled trial of antepartum glucocorticoid treatment for prevention of the respiratory distress syndrome in premature infants.

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              Intraventricular hemorrhage in premature infants: mechanism of disease.

              Intraventricular hemorrhage (IVH) is a major complication of prematurity. IVH typically initiates in the germinal matrix, which is a richly vascularized collection of neuronal-glial precursor cells in the developing brain. The etiology of IVH is multifactorial and is primarily attributed to the intrinsic fragility of the germinal matrix vasculature and the disturbance in the cerebral blood flow (CBF). Although this review broadly describes the pathogenesis of IVH, the main focus is on the recent development in molecular mechanisms that elucidates the fragility of the germinal matrix vasculature. The microvasculature of the germinal matrix is frail because of an abundance of angiogenic blood vessels that exhibit paucity of pericytes, immaturity of basal lamina, and deficiency of glial fibrillary acidic protein (GFAP) in the ensheathing astrocytes endfeet. High VEGF and angiopoietin-2 levels activate a rapid angiogenesis in the germinal matrix. The elevation of these growth factors may be ascribed to a relative hypoxia of the germinal matrix perhaps resulting from high metabolic activity and oxygen consumption of the neural progenitor cells. Hence, the rapid stabilization of the angiogenic vessels and the restoration of normal CBF on the first day of life are potential strategies to prevent IVH in premature infants.
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                Author and article information

                Journal
                8501884
                5061
                J Perinatol
                J Perinatol
                Journal of perinatology : official journal of the California Perinatal Association
                0743-8346
                1476-5543
                8 January 2016
                24 March 2016
                May 2016
                24 September 2016
                : 36
                : 5
                : 352-356
                Affiliations
                [1 ]University of California, Berkeley School of Public Health
                [2 ]Division of Neonatal and Developmental Medicine, Department of Pediatrics, Stanford University, Stanford, CA
                [3 ]California Perinatal Quality Care Collaborative, Palo Alto, CA
                Author notes
                Corresponding Author: Henry C. Lee, MD, MS, Department of Pediatrics, Division of Neonatal and Developmental Medicine, 750 Welch Rd, Suite 315, Stanford, CA 94305, Office: (650) 723-5711 Fax: (650) 723-8351 hclee@ 123456stanford.edu
                Article
                NIHMS749636
                10.1038/jp.2016.38
                4844862
                27010109
                622c3af5-df1f-433d-b41b-44dfb36b9dfc

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                Pediatrics
                Pediatrics

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