Prenatal alcohol exposure, CYP17 gene polymorphisms and fetal growth restriction

Abstract

Objective To determine the association of maternal CYP17 gene polymorphisms and prenatal alcohol consumption with intrauterine growth restriction (IUGR). Study design A case-control study in singleton livebirths was conducted at the Liverpool Women's Hospital between 2004 and 2005. Cases ( n = 90) were mothers with an IUGR baby and controls ( n = 180) those with a normal birthweight infant. Maternal genomic DNA was extracted from buccal smears and PCR (RFLP) was used for genotyping. Results Amongst cases, the prevalence of the maternal CYP17 homozygous wild type “A1A1”, heterozygous “A1A2” and homozygous “A2A2” variants was 36.7%, 47.7% and 15.6%, which did not differ significantly from their prevalence amongst controls ( p = 0.6). The proportion with prenatal alcohol exposure was significantly higher in cases than controls (45.6% versus 30.6%, p = 0.01). Mean birthweight was significantly lower in mothers with the CYP17 A1A1 genotype compared to those with variant genotypes (A1A2/A2A2) in both the alcohol-exposed ( p = 0.03) and non-exposed groups ( p = 0.01). In all women regardless of genotype, IUGR risk increased in mothers exposed to alcohol during pregnancy (OR, 2.9, 95% CI; 1.8–4.2, p = 0.01). There was a significant interaction between the CYP17 A1A1 genotype and prenatal alcohol consumption for fetal growth restriction (adjusted OR, 1.4, 95% CI; 1.1–1.9, p = 0.04). Conclusion The association between prenatal alcohol exposure and intrauterine fetal growth restriction was modulated by the maternal CYP17 A1A1 genotype.