ArticlePediatric cardiology2013
Maternal environmental exposure, infant GSTP1 polymorphism, and risk of isolated congenital heart disease.
Article in Pediatric cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Prenatal Dibutyl Phthalate Exposure Dysregulates Fetal-Placental Vascular Function and Placental Vasculature-Specific Lipid Metabolism.bioRxiv : the preprint server for biology · 2026Article
- Parental risk factors associated with congenital heart disease in a Thai population: multivariable analysis.Asian biomedicine : research, reviews and news · 2021Article
- An update on the CHDGKB for the systematic understanding of risk factors associated with non-syndromic congenital heart disease.Computational and structural biotechnology journal · 2021Article
- Environmental and Socioeconomic Factors Influence the Live-Born Incidence of Congenital Heart Disease: A Population-Based Study in California.Journal of the American Heart Association · 2020Article
- An artificial neural network prediction model of congenital heart disease based on risk factors: A hospital-based case-control study.Medicine · 2017Observational
- A Novel TBX1 Loss-of-Function Mutation Associated with Congenital Heart Disease.Pediatric cardiology · 2015Article
- A novel NKX2.6 mutation associated with congenital ventricular septal defect.Pediatric cardiology · 2015Article
- P-selectin gene polymorphism associates with pulmonary hypertension in congenital heart disease.International journal of clinical and experimental pathology · 2015Article
- Maternal medication use, fetal 3435 C>T polymorphism of the ABCB1 gene, and risk of isolated septal defects in a Han Chinese population.Pediatric cardiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The GSTP1 gene, highly expressed early in fetal life, is the most abundant phase 2 xenobiotic metabolism enzyme in a human placenta. Fetal inherited GSTP1 Ile105Val polymorphism may modify the metabolism and excretion of xenobiotics from fetal tissue and increase the risk of congenital heart disease (CHD). This study aimed to analyze the joint effects of GSTP1 genetic polymorphism (Ile105Val) and maternal environmental exposure on CHD risk. Within a case-control design, a total of 190 children with CHD (104 boys age 4 ± 5.6 years) and 190 healthy children (114 newborn boys) were genotyped for the GSTP1 Ile105Val polymorphism. Mothers completed a structured questionnaire on the demographics as well as the preconceptional and lifestyle exposures. A higher frequency of mothers of children with CHD (38 %) reported a positive history of exposure to toxicants (occupational and environmental) than mothers of healthy children (23 %) (p = 0.0013). Logistic regression analysis showed that maternal occupational and environmental exposures increased the risk of CHD (odds ratio, 2.6; 95 % confidence interval, 1.6-4.2; p < 0.0001). No significant differences in Ile105Val genotype frequencies were observed between the children with CHD and the healthy children (p = 0.9). Furthermore, case-control analysis showed no evidence of significant interaction between the maternal exposures and GSTP1 polymorphism. Maternal exposure to toxicants increased the risk of children with CHD. However, fetal GSTP1 Ile105Val polymorphism did not increase the risk of CHD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.