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. 2016 Sep;138(3):e20160731.
doi: 10.1542/peds.2016-0731.

Late Pregnancy β Blocker Exposure and Risks of Neonatal Hypoglycemia and Bradycardia

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Late Pregnancy β Blocker Exposure and Risks of Neonatal Hypoglycemia and Bradycardia

Brian T Bateman et al. Pediatrics. 2016 Sep.

Abstract

Background and objectives: β blockers are widely used in the treatment of hypertensive disorders during pregnancy. These medications cross the placenta and may cause physiologic changes in neonates exposed in utero. We sought to define the risks of neonatal hypoglycemia and bradycardia associated with maternal exposure to β blockers at the time of delivery in a large, nationwide cohort of Medicaid beneficiaries.

Methods: We used a cohort of 2 292 116 completed pregnancies linked to liveborn infants of Medicaid-enrolled women from 2003 to 2007. We examined the risks of neonatal hypoglycemia and neonatal bradycardia associated with maternal exposure to β blockers at the time of delivery. Propensity score matching was used to control for potential confounders including maternal demographics, obstetric and medical conditions, and exposure to other medications.

Results: There were 10 585 (0.5%) pregnancies exposed to β blockers at the time of delivery. The risk of neonatal hypoglycemia was 4.3% in the β blocker-exposed neonates versus 1.2% in the unexposed; the risk of neonatal bradycardia was 1.6% in the exposed versus 0.5% in the unexposed. After controlling for confounders, risk remained elevated for both neonatal hypoglycemia and bradycardia among exposed pregnancies versus unexposed (adjusted odds ratio, 1.68, 95% confidence interval, 1.50-1.89 and adjusted odds ratio, 1.29, 95% confidence interval, 1.07-1.55, respectively).

Conclusion: Our findings suggest that neonates born to mothers exposed to β blockers in late pregnancy, including labetalol, are at elevated risk for neonatal hypoglycemia and bradycardia.

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Conflict of interest statement

POTENTIAL CONFLICT OF INTEREST: Dr Hernandez-Diaz has consulted for AstraZeneca and UCB for unrelated projects, and served as investigator on grants to the Brigham & Women’s Hospital from Lilly and Pfizer. The Pharmacoepidemiology Program at the Harvard School of Public Health is supported by Pfizer, Takeda, Bayer, and Asisa. Drs Huybrechts and Bateman are investigators on grants to the Brigham & Women’s Hospital from Lilly and Pfizer, and Dr Bateman is an investigator on grants from Baxalta, unrelated to the topic of this manuscript. The other authors have indicated they have no potential conflicts of interest to disclose.

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