A Abramovici1, R E Gandley2, R G Clifton3, K J Leveno4, L Myatt5, R J Wapner6, J M Thorp7, B M Mercer8, A M Peaceman9, P Samuels10, A Sciscione11, M Harper12, G Saade13, Y Sorokin14. 1. Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, AL, USA. 2. Department of Obstetrics and Gynecology, University of Pittsburgh, Pittsburgh, PA, USA. 3. Department of Obstetrics and Gynecology, The George Washington University Biostatistics Center, Washington, DC, USA. 4. Department of Obstetrics and Gynecology, Southwestern Medical Center, University of Texas, Dallas, TX, USA. 5. Department of Obstetrics and Gynecology, University of Cincinnati, Cincinnati, OH, USA. 6. Department of Obstetrics and Gynecology, Columbia University, New York, NY, USA. 7. Department of Obstetrics and Gynecology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 8. Department of Obstetrics and Gynecology, Case Western Reserve University-MetroHealth Medical Center, Cleveland, OH, USA. 9. Department of Obstetrics and Gynecology, Northwestern University, Chicago, IL, USA. 10. Department of Obstetrics and Gynecology, The Ohio State University, Columbus, OH, USA. 11. Department of Obstetrics and Gynecology, Drexel University, Philadelphia, PA, USA. 12. Department of Obstetrics and Gynecology, Wake Forest University Health Sciences, Winston-Salem, NC, USA. 13. Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, TX, USA. 14. Department of Obstetrics and Gynecology, Wayne State University, Detroit, MI, USA.
Abstract
OBJECTIVE: Smoking and pre-eclampsia (PE) are associated with increases in preterm birth, placental abruption and low birthweight. We evaluated the relationship between prenatal vitamin C and E (C/E) supplementation and perinatal outcomes by maternal self-reported smoking status focusing on outcomes known to be impacted by maternal smoking. DESIGN/SETTING/POPULATION: A secondary analysis of a multi-centre trial of vitamin C/E supplementation starting at 9-16 weeks in low-risk nulliparous women with singleton gestations. METHODS: We examined the effect of vitamin C/E by smoking status at randomisation using the Breslow-Day test for interaction. MAIN OUTCOME MEASURES: The trial's primary outcomes were PE and a composite outcome of pregnancy-associated hypertension (PAH) with serious adverse outcomes. Perinatal outcomes included preterm birth and abruption. RESULTS: There were no differences in baseline characteristics within subgroups (smokers versus nonsmokers) by vitamin supplementation status. The effect of prenatal vitamin C/E on the risk of PE (P = 0.66) or PAH composite outcome (P = 0.86) did not differ by smoking status. Vitamin C/E was protective for placental abruption in smokers (relative risk [RR] 0.09; 95% CI 0.00-0.87], but not in nonsmokers (RR 0.92; 95% CI 0.52-1.62) (P = 0.01), and for preterm birth in smokers (RR 0.76; 95% CI 0.58-0.99) but not in nonsmokers (RR 1.03; 95% CI 0.90-1.17) (P = 0.046). CONCLUSION: In this cohort of women, smoking was not associated with a reduction in PE or the composite outcome of PAH. Vitamin C/E supplementation appears to be associated with a reduction in placental abruption and preterm birth among smokers.
OBJECTIVE: Smoking and pre-eclampsia (PE) are associated with increases in preterm birth, placental abruption and low birthweight. We evaluated the relationship between prenatal vitamin C and E (C/E) supplementation and perinatal outcomes by maternal self-reported smoking status focusing on outcomes known to be impacted by maternal smoking. DESIGN/SETTING/POPULATION: A secondary analysis of a multi-centre trial of vitamin C/E supplementation starting at 9-16 weeks in low-risk nulliparous women with singleton gestations. METHODS: We examined the effect of vitamin C/E by smoking status at randomisation using the Breslow-Day test for interaction. MAIN OUTCOME MEASURES: The trial's primary outcomes were PE and a composite outcome of pregnancy-associated hypertension (PAH) with serious adverse outcomes. Perinatal outcomes included preterm birth and abruption. RESULTS: There were no differences in baseline characteristics within subgroups (smokers versus nonsmokers) by vitamin supplementation status. The effect of prenatal vitamin C/E on the risk of PE (P = 0.66) or PAH composite outcome (P = 0.86) did not differ by smoking status. Vitamin C/E was protective for placental abruption in smokers (relative risk [RR] 0.09; 95% CI 0.00-0.87], but not in nonsmokers (RR 0.92; 95% CI 0.52-1.62) (P = 0.01), and for preterm birth in smokers (RR 0.76; 95% CI 0.58-0.99) but not in nonsmokers (RR 1.03; 95% CI 0.90-1.17) (P = 0.046). CONCLUSION: In this cohort of women, smoking was not associated with a reduction in PE or the composite outcome of PAH. Vitamin C/E supplementation appears to be associated with a reduction in placental abruption and preterm birth among smokers.
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