Abstract
Antenatal maternal steroid administration has been widely used to accelerate fetal lung maturation. There is evidence that this therapy may be associated with an increased risk of infection in the neonate. Inhibition of multiple aspects of neutrophil (PMN) function by glucocorticoids has been widely documented in adults and children. Because the host defense system of the neonate is less than fully competent, further compromise of existing PMN function may be of major importance. We performed an in vitro study to determine the effect of betamethasone on the random migration (chemokinesis) and directed migration (chemotaxis) on neonatal PMN. A separated cell micropore filter assay was used to study the effect of betamethasone on PMN's obtained from cord blood of healthy term neonates. The addition of therapeutic concentrations of betamethasone (1.0 μgm/100 ml) resulted in a significant inhibition in PMN chemokinesis and chemotaxis.
Betamethasone inhibition of PMN motility, if present in vivo may lead to a clinically significant susceptability to perinatal bacterial infection.
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Fuenfer, M., Ingardia, C., Raye, J. et al. 1094 THE EFFECT OF BETAMETHASONE ON THE CHEMOTACTIC RESPONSE OF NEONATAL NEUTROPHILS. Pediatr Res 19, 293 (1985). https://doi.org/10.1203/00006450-198504000-01124
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DOI: https://doi.org/10.1203/00006450-198504000-01124