Postnatal Administration of Dexamethasone for Weaning off the Ventilator Affects Thyroid Function

Abstract

Background: Very preterm neonates are at risk of hypothyroxinemia because of prematurity as well as because of neonatal disease. Hypothyroxinemia is associated with impaired developmental outcome. Preterm infants who cannot be weaned from the ventilator can be treated with dexamethasone. Glucocorticoid administration has been found to alter thyroid hormone parameters. Therefore, dexamethasone treatment in these infants might additionally impair their thyroid function, which could have consequences for developmental outcome. Objective: To assess what changes in thyroid function occur in the first hours after initiating dexamethasone treatment in ventilated preterm infants. Methods: Preterm infants, in whom the decision was taken to start dexamethasone treatment, were included. Thyroxine (T₄), 3,5,3′-triiodothyronine (T₃), reverse T₃ (rT₃), thyroid-stimulating hormone (TSH) and cortisol were determined before and 6–9 h after administration of the first dose of a postnatal dexamethasone course. Details of clinical condition were recorded at both time points. Results: Sixteen very preterm infants were included at a median age of 20 days. While clinical condition was stable between start of dexamethasone and 6–9 h thereafter, TSH and T₃ levels decreased significantly. rT₃ levels significantly increased, resulting in a decrease in the T₃/rT₃ ratio. There was no statistically significant effect on the levels of T₄. Conclusion: Postnatal dexamethasone administration negatively affects thyroid functionin the preterm infant with severe chronic lung disease.