In utero beta 2 adrenergic agonist exposure and adverse neurophysiologic and behavioral outcomes

Received 9 June 2009; received in revised form 18 June 2009; accepted 6 July 2009.

Beta 2 adrenergic receptor overstimulation during critical periods of prenatal development can induce a permanent shift in the balance of sympathetic-to-parasympathetic tone. This is a biologically plausible mechanism whereby beta 2 adrenergic agonists can induce functional and behavioral teratogenesis, which explains their association with increases in autism spectrum disorders, psychiatric disorders, poor cognitive, motor function and school performance, and changes in blood pressure in the offspring. The use of beta 2 adrenergic agonists should be limited to proven indications when alternate drugs are ineffective or unavailable; the risks of untreated disease to the mother and fetus are greater than the risk of the beta 2 adrenergic agonist.

Key words: asthma, autism spectrum disorder, beta 2 adrenergic agonist, preterm labor, ritodrine, terbutaline

a Division of Maternal-Fetal Medicine, Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD

b Department of Neurology and Developmental Medicine, Kennedy Krieger Institute, Johns Hopkins University School of Medicine, Baltimore, MD

c Departments of Neurology, Psychiatry, and Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD

d Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD

e American Home Patient, Brentwood, TN

f LADDERS Clinic of Mass General Hospital and Harvard Medical School, Boston, MA

Reprints not available from the authors.

Authorship and contribution to the article is limited to the 4 authors indicated. There was no outside funding or technical assistance with the production of this article.

PII: S0002-9378(09)00776-5

doi:10.1016/j.ajog.2009.07.010

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