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.
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.
Authors: Samuella G Bonou; Patrick Levallois; Yves Giguère; Manuel Rodriguez; Alexandre Bureau Journal: Reprod Toxicol Date: 2017-07-31 Impact factor: 3.143
Authors: Digna R Velez Edwards; Roberto Romero; Juan Pedro Kusanovic; Sonia S Hassan; Shali Mazaki-Tovi; Edi Vaisbuch; Chong Jai Kim; Offer Erez; Tinnakorn Chaiworapongsa; Brad D Pearce; Jacquelaine Bartlett; Lara A Friel; Benjamin A Salisbury; Madan Kumar Anant; Gerald F Vovis; Min Seob Lee; Ricardo Gomez; Ernesto Behnke; Enrique Oyarzun; Gerard Tromp; Ramkumar Menon; Scott M Williams Journal: J Matern Fetal Neonatal Med Date: 2010-07-09