Prenatal alcohol exposure, CYP17 gene polymorphisms and fetal growth restriction

Eur J Obstet Gynecol Reprod Biol. 2008 May;138(1):49-53. doi: 10.1016/j.ejogrb.2007.08.006. Epub 2007 Sep 17.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Alcoholic Beverages / adverse effects*
  • Birth Weight
  • Case-Control Studies
  • Female
  • Fetal Growth Retardation / chemically induced*
  • Fetal Growth Retardation / genetics*
  • Genetic Predisposition to Disease
  • Humans
  • Infant, Newborn
  • Infant, Small for Gestational Age
  • Pregnancy
  • Prenatal Exposure Delayed Effects* / chemically induced
  • Prenatal Exposure Delayed Effects* / genetics
  • Steroid 17-alpha-Hydroxylase / genetics*

Substances

  • CYP17A1 protein, human
  • Steroid 17-alpha-Hydroxylase