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Previous Volume 356:2675-2683 June 28, 2007 Number 26 Next

	Full Text PDF PDA Full Text PowerPoint Slide Set Supplementary Material Editorial by Greene, M. F. Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited E-mail When Letters Appear

ABSTRACT

Background The risk of birth defects after antenatal exposure to selective serotonin-reuptake inhibitors (SSRIs) remains controversial.

Methods We assessed associations between first-trimester maternal use of SSRIs and the risk of birth defects among 9849 infants with and 5860 infants without birth defects participating in the Slone Epidemiology Center Birth Defects Study.

Results In analyses of defects previously associated with SSRI use (involving 42 comparisons), overall use of SSRIs was not associated with significantly increased risks of craniosynostosis (115 subjects, 2 exposed to SSRIs; odds ratio, 0.8; 95% confidence interval [CI], 0.2 to 3.5), omphalocele (127 subjects, 3 exposed; odds ratio, 1.4; 95% CI, 0.4 to 4.5), or heart defects overall (3724 subjects, 100 exposed; odds ratio, 1.2; 95% CI, 0.9 to 1.6). Analyses of the associations between individual SSRIs and specific defects showed significant associations between the use of sertraline and omphalocele (odds ratio, 5.7; 95% CI, 1.6 to 20.7; 3 exposed subjects) and septal defects (odds ratio, 2.0; 95% CI, 1.2 to 4.0; 13 exposed subjects) and between the use of paroxetine and right ventricular outflow tract obstruction defects (odds ratio, 3.3; 95% CI, 1.3 to 8.8; 6 exposed subjects). The risks were not appreciably or significantly increased for other defects or other SSRIs or non-SSRI antidepressants. Exploratory analyses involving 66 comparisons showed possible associations of paroxetine and sertraline with other specific defects.

Conclusions Our findings do not show that there are significantly increased risks of craniosynostosis, omphalocele, or heart defects associated with SSRI use overall. They suggest that individual SSRIs may confer increased risks for some specific defects, but it should be recognized that the specific defects implicated are rare and the absolute risks are small.

Source Information

From the Slone Epidemiology Center at Boston University (C.L., M.M.W., S.H.-D., A.A.M.), the Genetics Unit, Massachusetts General Hospital for Children (A.E.L.), and the Department of Epidemiology, Harvard School of Public Health (S.H.-D.) — all in Boston.

Address reprint requests to Dr. Louik at the Slone Epidemiology Center, 1010 Commonwealth Ave., Boston, MA 02215, or at clouik{at}slone.bu.edu.

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