Prenatal treatment with dexamethasone or betamethasone: neurodevelopmental outcomes of extremely low birth weight infants

Prenatal steroid therapy has historically been associated with reduced risk of respiratory distress syndrome, intraventricular hemorrhage (IVH), and overall neonatal death. More than 10 years ago, the National Institutes of Health and the American College of Obstetricians and Gynecologists recommended the use of prenatal steroid treatment before the imminent delivery of pregnancies at gestational ages of 24 to 34 weeks, in order to induce fetal maturity. At present, dexamethasone and betamethasone are the only 2 steroids that could be used for such purposes. Although no randomized, controlled trial has directly compared the outcomes associated with prenatal treatment with these two molecules, the results of some animal and human studies might suggest that prenatal dexamethasone may be associated with an increased risk of adverse neonatal neurologic outcomes and of neonatal death when compared with prenatal betamethasone. However, little is known regarding any possible differences between the two molecules in terms of long-term neurodevelopmental outcomes.
On these bases, an American group compared the neurodevelopmental outcomes at corrected gestational ages of 18 to 22 months in an historical cohort of extremely low birth weight (ELBW; 401-1000g) infants exposed to prenatal administration of dexamethasone (n=408), betamethasone (n=563) or no steroids (n=153), using registry data from the NICHD Neonatal Research Network. Primary outcomes were Bayley Scales of Infant Development-II Mental Development Index of <70, Bayley Scales of Infant Development-II Psychomotor Development Index of <70, bilateral blindness, hearing impairment, cerebral palsy (CP), and neurodevelopmental impairment. Neurodevelopmental impairment was defined as ≥1 of the aforementioned outcomes while unimpaired status was considered as the absence of blindness, deafness, CP, MDI ≥85 and PDI≥85.
Overall, no statistically significant associations were found between prenatal dexamethasone exposure and any follow-up outcome, compared with no prenatal steroid exposure. Instead 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. Moreover, if compared with betamethasone, dexamethasone was associated with a trend for increased risk of Psychomotor Development Index of <70, an increased risk of hearing impairment, and a decreased likelihood of unimpaired status.
The results of this study may suggest that prenatal betamethasone exposure could increase the likelihood of unimpaired neurodevelopmental status and reduce the incidence of hearing impairment in ELBW infants, compared with infants with prenatal dexamethasone exposure or no prenatal steroid exposure. In conclusion, although these results must be further confirmed in a randomized clinical trial, on the basis of the findings of the current study and other studies, it may be in the best interest of neonates to receive prenatal betamethasone treatment, rather than prenatal dexamethasone treatment, when the option is available.

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