Prenatal alcohol exposure induced congenital heart diseases: From bench to bedside

2020 ◽  
Author(s):  
Zhiyan Chen ◽  
Sheng Li ◽  
Linghong Guo ◽  
Xu Peng ◽  
Yin Liu
PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0130681 ◽  
Author(s):  
Jiaomei Yang ◽  
Huizhen Qiu ◽  
Pengfei Qu ◽  
Ruo Zhang ◽  
Lingxia Zeng ◽  
...  

2019 ◽  
Vol 27 (4) ◽  
pp. 410-421 ◽  
Author(s):  
Senmao Zhang ◽  
Lesan Wang ◽  
Tubao Yang ◽  
Lizhang Chen ◽  
Lijuan Zhao ◽  
...  

Objective The aim of this study was to provide updated evidence to assess the association between parental alcohol consumption and the risk of total congenital heart diseases (CHDs) and specific CHD phenotypes in offspring, and explore the possible dose–response pattern. Methods PubMed, Embase and Chinese databases were searched with an end-date parameter of July 24, 2019 to identify studies meeting pre-stated inclusion criteria. A random-effects model was used to calculate the overall combined risk estimates. A meta-analysis of the dose–response relationship was performed. Subgroup analysis, sensitivity analysis, and Galbraith plot were conducted to explore potential heterogeneity moderators. Results A total of 55 studies involving 41,747 CHD cases and 297,587 controls were identified. Overall, both maternal (odds ratio (OR) = 1.16; 95% confidence interval (CI): 1.05–1.27) and paternal (OR = 1.44; 95% CI: 1.19–1.74) alcohol exposures were significantly associated with risk of total CHDs in offspring. Additionally, a nonlinear dose–response relationship between parental alcohol exposure and risk of total CHDs was observed. With an increase in parental alcohol consumption, the risk of total CHDs in offspring also gradually increases. For specific CHD phenotypes, a statistically significant association was found between maternal alcohol consumption and risk of tetralogy of fallot (OR = 1.20; 95% CI: 1.08–1.33). Relevant heterogeneity moderators have been identified by subgroup analysis, and sensitivity analysis yielded consistent results. Conclusions Although the role of potential bias and evidence of heterogeneity should be carefully evaluated, our review indicates that parental alcohol exposures are significantly associated with the risk of CHDs in offspring, which highlights the necessity of improving health awareness to prevent alcohol exposure during preconception and conception periods.


2012 ◽  
Vol 13 (2) ◽  
pp. 32-42 ◽  
Author(s):  
Yvette D. Hyter

Abstract Complex trauma resulting from chronic maltreatment and prenatal alcohol exposure can significantly affect child development and academic outcomes. Children with histories of maltreatment and those with prenatal alcohol exposure exhibit remarkably similar central nervous system impairments. In this article, I will review the effects of each on the brain and discuss clinical implications for these populations of children.


2000 ◽  
Vol 42 (8) ◽  
pp. 508-514 ◽  
Author(s):  
Béatrice Larroque ◽  
Monique Kaminski ◽  
Phillipe Dehaene ◽  
Damien Subtil ◽  
Denis Querleu

Author(s):  
Manuela Pfinder ◽  
Stefan Liebig ◽  
Reinhold Feldmann

Data on the relation between moderate prenatal alcohol exposure (PAE) and behavioral disorders are inconsistent, and this raises new questions. We examined (1) the association between moderate PAE and problem behaviors and (2) whether these associations differed by levels of socioeconomic status (SES), fetal smoke exposure, or exposure to environmental tobacco smoke (ETS). Data were taken from the German Health Interview and Examination Survey for Children and Adolescents (KiGGS) study. Parents evaluated children’s behaviors using the Strengths and Difficulties Questionnaire (SDQ). Results showed a slight, but insignificant, increase of problem behaviors in children with moderate PAE. In 3- to 6-year-olds, PAE had a stronger effect on hyperactivity/inattention in combination with fetal smoke exposure (odds ratio = 2.82), than did PAE alone. Effects were not stronger in low-SES children, but they were stronger in children with ETS. We conclude that moderate PAE might have adverse effects on neurodevelopment, with stronger effects in disadvantaged populations. To confirm our preliminary findings, further research should be conducted.


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