(June 28, 2004) -- Bethesda, MD -- Any parent of a newborn with extremely low birth weight (ELBW) faces the possibility that their child will be diagnosed with severe respiratory distress syndrome, which results in ventilator and/or oxygen dependency, and subsequent onset of chronic lung disease. Until recently, early administration of a prolonged course of postnatal dexamethasone was recommended to decrease the pulmonary inflammatory process during the early neonatal period. This approach changed, however, following a Taiwanese study that demonstrated a significant increase in neurodevelopmental dysfunction in neonates treated with dexamethasone.
The Taiwanese conclusions were reached within the context that the window of exposure to dexamethasone in critically ill ELBW infants spans an extensive period of perinatal viability, ranging from 24 to 40 weeks post-conception. It is during this time that the human brain undergoes significant structural and functional transformations, thereby making it particularly vulnerable to external influences.
Clinical studies examining acute dexamethasone effects on physiology and central nervous system function in premature infants have been limited.
Past research into premature infants who received prolonged dexamethasone therapy experience reduced linear growth, decreased weight gain, and smaller head circumferences. During the acute phase of dexamethasone exposure, changes in gross neuromotor function have also been noted. As a result, use of dexamethasone to improve pulmonary function in ventilator-dependent ELBW infants is undergoing significant modification towards more judicious treatment dexamethasone therapy is given less often and shorter courses are now used.
The concern remains that little is known about dexamethasone effects on long-term neurodevelopment. For obvious reasons, human testing is not desired. Researchers have previously developed a rat moPage: 1 2 3 4 Related biology news :1
Contact: Mayer Resnick
American Physiological Society
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