ORCID Profile
0000-0003-4675-7722
Current Organisations
University of California, San Diego
,
California State University Fullerton
,
San Diego State University and the University of California San Diego
,
San Diego State University
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Publisher: Wiley
Date: 26-03-2013
Abstract: There is conflicting literature on the effect of maternal asthma on congenital malformations and neonatal outcomes. This review and meta-analysis sought to determine if maternal asthma is associated with an increased risk of adverse neonatal outcomes. We searched electronic databases for: (asthma or wheeze) and (pregnan* or perinat* or obstet*). Cohort studies published between 1975 and March 2012 reporting at least one perinatal outcome of interest (congenital malformations, neonatal complications, perinatal mortality). In all, 21 studies met inclusion criteria in pregnant women with and without asthma. Further analysis was conducted on 16 studies where asthmatic women were stratified by exacerbation history, corticosteroid use, bronchodilator use or asthma severity. Maternal asthma was associated with a significantly increased risk of congenital malformations (relative risk [RR] 1.11, 95% confidence interval [95% CI] 1.02-1.21, I(2) = 59.5%), cleft lip with or without cleft palate (RR 1.30, 95% CI 1.01-1.68, I(2) = 65.6%), neonatal death (RR 1.49, 95% CI 1.11-2.00, I(2) = 0%), and neonatal hospitalisation (RR 1.50, 95% CI 1.03-2.20, I(2) = 64.5%). There was no significant effect of asthma on major malformations (RR 1.31, 95% CI 0.57-3.02, I(2) = 70.9%) or stillbirth (RR 1.06, 95% CI 0.9-1.25, I(2) = 35%). Exacerbations and use of bronchodilators and inhaled corticosteroids were not associated with congenital malformation risk. Despite limitations related to the observational nature of the primary studies, this review demonstrates a small increased risk of neonatal complications among pregnant women with asthma. Further investigations into mechanisms and potential preventive interventions to improve infant outcomes are required.
Publisher: Springer Science and Business Media LLC
Date: 2013
Publisher: European Respiratory Society (ERS)
Date: 16-08-2012
DOI: 10.1183/09031936.00195111
Abstract: This systematic review and meta-analysis sought to investigate whether asthma exacerbations, oral corticosteroid use or asthma severity are associated with prematurity and intrauterine growth restriction. Cohort studies published between 1975 and March 11, 2012 were considered for inclusion. 138 publications were identified for possible inclusion, and nine papers met the inclusion criteria, by reporting perinatal outcomes of interest (low birth weight, <2500 g), pre-term birth (<37 weeks gestation unless otherwise stated) and small for gestational age (<10th percentile for gestational age and sex) in groups of asthmatic patients stratified by history of exacerbations, oral corticosteroid use or asthma severity. Maternal asthma exacerbations and oral corticosteroid use had a significant effect on outcomes, including low birth weight (RR 3.02, 95% CI 1.87-4.89 and RR 1.41, 95% CI 1.04-1.93, respectively) and pre-term delivery (RR 1.54, 95% CI 0.89-2.69 and RR 1.51, 95% CI 1.15-1.98, respectively). Moderate-to-severe asthma during pregnancy was associated with an increased risk of small for gestational age (RR 1.24, 95% CI 1.15-1.35) and low birth weight (RR 1.15, 95% CI 1.05-1.26) infants. These data suggest that asthma exacerbations, oral corticosteroid use or asthma severity defined as moderate-to-severe may be associated with pre-term delivery, low birth weight, and small for gestational age infants. Further studies on the effect of maternal asthma control on perinatal outcomes are warranted.
Publisher: Life Science Alliance, LLC
Date: 04-03-2019
Abstract: Prenatal alcohol exposure (PAE), like other pregnancy complications, can result in placental insufficiency and fetal growth restriction, although the linking causal mechanisms are unclear. We previously identified 11 gestationally elevated maternal circulating miRNAs ( HEa miRNAs) that predicted infant growth deficits following PAE. Here, we investigated whether these HEa miRNAs contribute to the pathology of PAE, by inhibiting trophoblast epithelial–mesenchymal transition (EMT), a pathway critical for placental development. We now report for the first time that PAE inhibits expression of placental pro-EMT pathway members in both rodents and primates, and that HEa miRNAs collectively, but not in idually, mediate placental EMT inhibition. HEa miRNAs collectively, but not in idually, also inhibited cell proliferation and the EMT pathway in cultured trophoblasts, while inducing cell stress, and following trophoblast syncytialization, aberrant endocrine maturation. Moreover, a single intravascular administration of the pooled murine-expressed HEa miRNAs, to pregnant mice, decreased placental and fetal growth and inhibited the expression of pro-EMT transcripts in the placenta. Our data suggest that HEa miRNAs collectively interfere with placental development, contributing to the pathology of PAE, and perhaps also, to other causes of fetal growth restriction.
Publisher: Informa UK Limited
Date: 22-10-2013
DOI: 10.3109/14767058.2013.847080
Abstract: To investigate if maternal asthma is associated with an increased risk of maternal and placental complications in pregnancy. Electronic databases were searched for the following terms: (asthma or wheeze) and (pregnan* or perinat* or obstet*). Cohort studies published between January 1975 and March 2012 were considered for inclusion. Forty publications met the inclusion criteria, reporting at least one maternal or placental complication in pregnant women with and without asthma. Relative risk (RR) with 95% confidence intervals (CIs) was calculated. Maternal asthma was associated with a significantly increased risk of cesarean section (RR = 1.31, 95%CI = [1.22-1.39]), gestational diabetes (RR = 1.39, 95%CI = [1.17-1.66]), hemorrhage (antepartum: RR = 1.25, 95%CI = [1.10-1.42] postpartum: RR = 1.29, 95%CI = [1.18-1.41]), placenta previa (RR = 1.23, 95%CI = [1.07-1.40]), placental abruption (RR = 1.29, 95%CI = [1.14-1.47]) and premature rupture of membranes (RR = 1.21, 95%CI = 1.07-1.37). Moderate to severe asthma significantly increased the risk of cesarean section (RR = 1.19, 95%CI = [1.09-1.31]) and gestational diabetes (RR = 1.19, 95%CI = [1.06-1.33]) compared to mild asthma. Bronchodilator use was associated with a significantly lowered risk of gestational diabetes (RR = 0.64, 95%CI = [0.57-0.72]). Pregnant women with asthma are at increased risk of maternal and placental complications, and women with moderate/severe asthma may be at particular risk. Further studies are required to elucidate whether adequate control of asthma during pregnancy reduces these risks.
Publisher: Cold Spring Harbor Laboratory
Date: 06-09-2018
DOI: 10.1101/409854
Abstract: Prenatal Alcohol exposure (PAE), like other pregnancy complications, can result in placental insufficiency and fetal growth restriction, though the linking causal mechanisms are unclear. We previously identified 11 gestationally-elevated maternal circulating miRNAs that predicted infant growth deficits following PAE. Here, we investigated whether these HEa miRNAs contribute to the pathology of PAE, by inhibiting trophoblast epithelial-mesenchymal transition (EMT), a pathway critical for placental development. We now report for the first time, that PAE inhibits expression of placental pro-EMT pathway members in both rodents and primates, and that HEa miRNAs collectively, but not in idually, mediate placental EMT inhibition. HEa miRNAs collectively, but not in idually, also inhibited cell proliferation and the EMT pathway in cultured trophoblasts, while inducing cell stress, and following trophoblast syncytialization, aberrant endocrine maturation. Moreover, a single intra-vascular administration of the pooled murine-expressed HEa miRNAs, to pregnant mice, decreased placental and fetal growth and inhibited expression of pro-EMT transcripts in placenta. Our data suggests that HEa miRNAs collectively interfere with placental development, contributing to the pathology of PAE, and perhaps also, to other causes of fetal growth restriction. Maternal gestational circulating microRNAs, predictive of adverse infant outcomes including growth deficits, following prenatal alcohol exposure, contribute to placental pathology by impairing the EMT pathway in trophoblasts.
Location: United States of America
Location: United States of America
Location: United States of America
No related grants have been discovered for Christina D Chambers.