OBJECTIVE: We compared the development of adverse neurodevelopmental outcomes at corrected ages of 18 to 22 months for extremely low birth weight infants exposed prenatally to dexamethasone, betamethasone, or no steroid. METHODS:Study infants were extremely low birth weight (401-1000 g) infants who were in the care of National Institute of Child Health and Human Development Neonatal Research Network centers between January 1, 2002, and April 30, 2003; they were assessed neurodevelopmentally at corrected ages of 18 to 22 months. Outcomes were defined as Bayley Scales of Infant Development-II Mental Development Index of < 70, Bayley Scales of Infant Development-II Psychomotor Development Index of < 70, bilateral blindness, bilateral hearing aid use, cerebral palsy, and neurodevelopmental impairment. Neurodevelopmental impairment was defined as > or = 1 of the aforementioned outcomes. RESULTS: A total of 1124 infants met entry criteria. There were no statistically significant associations between prenatal dexamethasone exposure and any follow-up outcome, compared with no prenatal steroid exposure. Prenatal betamethasone exposure was associated with reduced risks of hearing impairment and neurodevelopmental impairment and with increased likelihood of unimpaired status, compared with no prenatal steroid exposure. Compared with betamethasone, dexamethasone was associated with a trend for increased risk of Psychomotor Development Index of < 70, increased risk of hearing impairment, and decreased likelihood of unimpaired status. CONCLUSIONS:Prenatal betamethasone exposure was associated with increased likelihood of unimpaired neurodevelopmental status and reduced risk of hearing impairment at corrected ages of 18 to 22 months among extremely low birth weight infants, compared with prenatal dexamethasone exposure or no prenatal steroid exposure. Pending a randomized, clinical trial, it may be in the best interests of infants to receive betamethasone, rather than dexamethasone, when possible.
RCT Entities:
OBJECTIVE: We compared the development of adverse neurodevelopmental outcomes at corrected ages of 18 to 22 months for extremely low birth weight infants exposed prenatally to dexamethasone, betamethasone, or no steroid. METHODS: Study infants were extremely low birth weight (401-1000 g) infants who were in the care of National Institute of Child Health and Human Development Neonatal Research Network centers between January 1, 2002, and April 30, 2003; they were assessed neurodevelopmentally at corrected ages of 18 to 22 months. Outcomes were defined as Bayley Scales of Infant Development-II Mental Development Index of < 70, Bayley Scales of Infant Development-II Psychomotor Development Index of < 70, bilateral blindness, bilateral hearing aid use, cerebral palsy, and neurodevelopmental impairment. Neurodevelopmental impairment was defined as > or = 1 of the aforementioned outcomes. RESULTS: A total of 1124 infants met entry criteria. There were no statistically significant associations between prenatal dexamethasone exposure and any follow-up outcome, compared with no prenatal steroid exposure. Prenatal betamethasone exposure was associated with reduced risks of hearing impairment and neurodevelopmental impairment and with increased likelihood of unimpaired status, compared with no prenatal steroid exposure. Compared with betamethasone, dexamethasone was associated with a trend for increased risk of Psychomotor Development Index of < 70, increased risk of hearing impairment, and decreased likelihood of unimpaired status. CONCLUSIONS: Prenatal betamethasone exposure was associated with increased likelihood of unimpaired neurodevelopmental status and reduced risk of hearing impairment at corrected ages of 18 to 22 months among extremely low birth weight infants, compared with prenatal dexamethasone exposure or no prenatal steroid exposure. Pending a randomized, clinical trial, it may be in the best interests of infants to receive betamethasone, rather than dexamethasone, when possible.
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