Association of maternal diseases during pregnancy with the risk of single ventricular septal defects in the offspring – a population-based case-control study

Csáky-Szunyogh, Melinda; Vereczkey, Attila; Kósa, Zsolt; Czeizel, Andr̀ew E.

doi:10.3109/14767058.2012.755170

Cited by 13 publications

(10 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All of the studies were published between 1995 and 2013. These studies included 1 randomized controlled trial 8 , 1 cohort study 9 , and 16 case-control studies 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 . The main characteristics of the included studies are presented in Table 1 .…”

Section: Resultsmentioning

confidence: 99%

Maternal Folic Acid Supplementation and the Risk of Congenital Heart Defects in Offspring: A Meta-Analysis of Epidemiological Observational Studies

Feng

Wang

Chen

et al. 2015

Sci Rep

100

View full text Add to dashboard Cite

Epidemiological studies have reported conflicting results regarding the association between maternal folic acid supplementation and the risk of congenital heart defects (CHDs). However, a meta-analysis of the association between maternal folic acid supplementation and CHDs in offspring has not been conducted. We searched the MEDLINE and EMBASE databases for articles cataloged between their inceptions and October 10, 2014 and identified relevant published studies that assessed the association between maternal folate supplementation and the risk of CHDs. Study-specific relative risk estimates were pooled using random-effects or fixed-effects models. Out of the 1,606 articles found in our initial literature searches, a total of 1 randomized controlled trial, 1 cohort study, and 16 case-control studies were included in our final meta-analysis. The overall results of this meta-analysis provide evidence that maternal folate supplementation is associated with a significantly decreased risk of CHDs (RR = 0.72, 95% CI: 0.63–0.82). Statistically significant heterogeneity was detected (Q = 82.48, P < 0.001, I2 = 79.4%). We conducted stratified and meta-regression analyses to identify the origin of the heterogeneity among the studies, and a Galbraith plot was generated to graphically assess the sources of heterogeneity. This meta-analysis provides a robust estimate of the positive association between maternal folate supplementation and a decreased risk of CHDs.

show abstract

Section: Resultsmentioning

confidence: 99%

Maternal Folic Acid Supplementation and the Risk of Congenital Heart Defects in Offspring: A Meta-Analysis of Epidemiological Observational Studies

Feng

Wang

Chen

et al. 2015

Sci Rep

100

View full text Add to dashboard Cite

show abstract

“…Fetal damage also occurs in the absence of direct influenza virus infection of the fetus [ 50 , 51 ]. Indirect mechanisms of fetal damage include hypoxia secondary to viral pneumonia in the mother, fever, changes in maternal pro-inflammatory tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and anti-inflammatory cytokines such as IL-10 and chemokines (CXCL8, CXCL10) compared to healthy pregnant women [ 9 , 10 , 52 , 53 ]. Finally, maternal infections are suspected to cause epigenetic changes in the DNA of the placenta and fetus perhaps decreasing the expression of key genes necessary for healthy development and competent immune responses [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

“…Data collected regarding the health of pregnant women and their infants during the 2009 influenza pandemic has since confirmed the negative impact of maternal influenza infections on children [ 4 , 5 ]. Specifically, the link between maternal influenza infections with pre-term birth, low birth weight, congenital defects of the heart, cardiovascular disease as adults, and neurologic/behavioral abnormalities such as schizophrenia has been established [ 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 ]. Emerging data suggest that affected infants are also at risk for immune-related diseases, such as asthma or type 1 diabetes; however, the effects of maternal influenza A virus infection on the immune system of infants and children has not been extensively explored [ 7 , 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Maternal Influenza A Virus Infection Restricts Fetal and Placental Growth and Adversely Affects the Fetal Thymic Transcriptome

Campen

Bishop

Abrahams

et al. 2020

Viruses

View full text Add to dashboard Cite

Maternal influenza A viral infections in humans are associated with low birth weight, increased risk of pre-term birth, stillbirth and congenital defects. To examine the effect of maternal influenza virus infection on placental and fetal growth, pregnant C57BL/6 mice were inoculated intranasally with influenza A virus A/CA/07/2009 pandemic H1N1 or phosphate-buffered saline (PBS) at E3.5, E7.5 or E12.5, and the placentae and fetuses collected and weighed at E18.5. Fetal thymuses were pooled from each litter. Placentae were examined histologically, stained by immunohistochemistry (IHC) for CD34 (hematopoietic progenitor cell antigen) and vascular channels quantified. RNA from E7.5 and E12.5 placentae and E7.5 fetal thymuses was subjected to RNA sequencing and pathway analysis. Placental weights were decreased in litters inoculated with influenza at E3.5 and E7.5. Placentae from E7.5 and E12.5 inoculated litters exhibited decreased labyrinth development and the transmembrane protein 150A gene was upregulated in E7.5 placentae. Fetal weights were decreased in litters inoculated at E7.5 and E12.5 compared to controls. RNA sequencing of E7.5 thymuses indicated that 957 genes were downregulated 2-fold including Mal, which is associated with Toll-like receptor signaling and T cell differentiation. There were 28 upregulated genes. It is concluded that maternal influenza A virus infection impairs fetal thymic gene expression as well as restricting placental and fetal growth.

show abstract

“…Similar but milder intrauterine fetal growth restriction was observed in the fetuses with VSD of non-drinking and non-smoking mothers as well. Maternal diseases and related drug treatments are analyzed in another study [20] without any reasonable association with higher risk of intrauterine growth restriction, (iii) The VSD and intrauterine growth restriction as two developmental errors may have a common route, mainly in males and full-term or average weighted babies. Recently the association of some gene polymorphisms with fetal growth and birth weight was shown [39], thus it would be interesting to test the effect of these gene variants in the origin of VSD.…”

Section: Discussionmentioning

confidence: 99%

“…The possible effects of acute and chronic maternal diseases and related drug treatments in the origin of VSD are published in a separate paper [20].…”

Section: Introductionmentioning

confidence: 99%

Ventricular septal defects in function of maternal sociodemographic aspects

Vereczkey¹,

Kósa²,

Csáky-Szunyogh

et al. 2012

Open Medicine

Self Cite

View full text Add to dashboard Cite

AbstractThe objective of our project is to reveal the possible etiological factors of different congenital cardiovascular abnormalities. In this study, we evaluated single ventricular septal defect (VSD) after surgical correction or with lethal outcome. The birth outcomes of these cases in the function of maternal socio-demographic features were evaluated. Data are based on 1,659 VSD cases, 2,534 matched controls and 38,151 all controls without any defects, in addition in the mothers of 19,393 malformed controls with other isolated defects in the population-based large dataset of the Hungarian Case-Control Surveillance of Congenital Abnormalities. VSD had mild female excess with a higher rate of preterm birth and mainly low birth weight indicating intrauterine growth restriction of affected fetuses, particularly in males and full-term or average weighted cases. The mothers of cases with VSD had lower socioeconomic status and higher rate of smoking and particularly drinking habit. The evaluation of medically recorded pregnancy complications showed an association of gestational diabetes with a higher risk of VSD. In conclusion, the association of small localized size of VDS and obvious fetal growth restriction needs further explanation in these cases, while gestational diabetes, lower socioeconomic status and adverse lifestyle of pregnant women may have a role in the origin of VSD.

show abstract

Association of maternal diseases during pregnancy with the risk of single ventricular septal defects in the offspring – a population-based case-control study

Abstract: High-fever-related maternal diseases may have a role in the origin of VSD which is preventable with antifever drug therapy, and the high doses of folic acid in early pregnancy reduced the risk of VSD.

Cited by 13 publications

References 39 publications

Maternal Folic Acid Supplementation and the Risk of Congenital Heart Defects in Offspring: A Meta-Analysis of Epidemiological Observational Studies

Maternal Folic Acid Supplementation and the Risk of Congenital Heart Defects in Offspring: A Meta-Analysis of Epidemiological Observational Studies

Maternal Influenza A Virus Infection Restricts Fetal and Placental Growth and Adversely Affects the Fetal Thymic Transcriptome

Ventricular septal defects in function of maternal sociodemographic aspects

Contact Info

Product

Resources

About