Original Article
Major congenital malformations following prenatal exposure to serotonin reuptake inhibitors and benzodiazepines using population-based health data
Article first published online: 21 FEB 2008
DOI: 10.1002/bdrb.20144
© 2008 Wiley-Liss, Inc.
Issue
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Birth Defects Research Part B: Developmental and Reproductive Toxicology
Volume 83, Issue 1, pages 68–76, February 2008
Additional Information
How to Cite
Oberlander, T. F., Warburton, W., Misri, S., Riggs, W., Aghajanian, J. and Hertzman, C. (2008), Major congenital malformations following prenatal exposure to serotonin reuptake inhibitors and benzodiazepines using population-based health data. Birth Defects Research Part B: Developmental and Reproductive Toxicology, 83: 68–76. doi: 10.1002/bdrb.20144
Publication History
- Issue published online: 21 FEB 2008
- Article first published online: 21 FEB 2008
- Manuscript Accepted: 16 DEC 2007
- Manuscript Revised: 19 NOV 2007
- Manuscript Received: 17 OCT 2007
Funded by
- BC Ministry of Children and Family Development
- The Michael Smith Foundation for Health Research
- Abstract
- Article
- References
- Cited By
Keywords:
- serotonin reuptake inhibitors (SRIs);
- benzodiazepines (BZs);
- congenital malformations;
- prenatal exposure
Abstract
BACKGROUND: To determine a population-based incidence of congenital anomalies following prenatal exposure to serotonin reuptake inhibitor (SRI) antidepressants used alone and in combination with a benzodiazepines (BZ). METHODS: Population health data, maternal health, and prenatal prescription records were linked to neonatal records, representing all live births (British Columbia, Canada, N=119,547) during a 39-month period (1998–2001). The incidence and risk differences (RD) for major congenital anomalies (CA) and congenital heart disease (CHD), including ventricular and atrial septal defects (VSD, ASD), from infants of mothers treated with an SRI alone, a benzodiazepine (BZ) alone, or SRI+BZ in combinationcompared to outcomesno exposure. RESULTS: Risk for a CA or CHD did increase following combined SRI+BZ exposure compared with no exposure. However, using a weighted regression model, controlling for maternal illness characteristics, combination therapy risk remained significantly associated only with CHD. The risk for an ASD was higher following SRI monotherapy compared with no exposure, after adjustment for maternal covariates. Dose/day was not associated with increased risk. CONCLUSIONS: Infants exposed to prenatal SRIs in combination with BZs had a higher a incidence of CHD compared to no exposure, even after controlling for maternal illness characteristics. SRI monotherapy was not associated with an increased risk for major CA, but was associated with an increased incidence of ASD. Risk was not associated with first trimester medication dose/day. Birth Defects Research (Part B) 83:68–76, 2008. © 2008 Wiley-Liss, Inc.

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