Abstract

Although prenatal steroid therapy has been linked with lower rates of respiratory distress syndrome, intraventricular hemorrhage, and overall neonatal mortality, both animal and human studies have raised concern that prenatal dexamethasone therapy, compared to betamethasone, may carry an increased risk of adverse neonatal neurological outcomes. This historical cohort study related prenatal steroid treatment to neurodevelopmental outcomes at corrected ages of 18 to 22 months in 1124 extremely low-birth-weight (ELBW, 401–1000 g) infants. There was a history of exposure to dexamethasone in 408 instances and to betamethasone in 563, while 153 infants had not been exposed to any prenatal steroid. Neurodevelopmental impairment was considered to be present with one or more of these outcomes: A Bayley Scales of Infant Development-II Mental Development Index less than 70, a Bayley Scales Psychomotor Development Index less than 70, bilateral blindness, bilateral hearing aid use, and cerebral palsy (CP). Compared to no prenatal steroid exposure, no statistically significant associations were found between prenatal dexamethasone exposure and any adverse outcome. Prenatal exposure to betamethasone exposure was, however, associated with a reduced risk of hearing impairment, less neurodevelopmental impairment, and an increased likelihood of unimpaired status when compared with no prenatal steroid exposure. Compared with betamethasone exposure, prenatal dexamethasone correlated with a trend toward an increased risk of impaired psychomotor development, an elevated risk of hearing impairment, and a lower likelihood of unimpaired status. There were no significant group differences in the risk of CP or of moderate to severe CP. This study, the largest of its type to be reported, suggests that—pending a randomized clinical trial—it may be best to use betamethasone rather than dexamethasone for prenatal steroid therapy whenever possible.

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