Background: A single course of maternal glucocorticoid treatment is effective in reducing neonatal mortality after preterm birth. However, in animals, maternal glucocorticoid treatment is associated with lifelong hyperglycaemia and hypertension, and impaired nephrogenesis in offspring. Findings from studies in humans on this topic are highly contradictory due to a number of methodologic flaws and renal function after glucocorticoid exposure has never been assessed.
Objectives: To assess in individuals born <32 gestational weeks whether antenatal glucocorticoid treatment for preterm birth is associated with long-term metabolic risks, including renal function, in adulthood.
Design: Birth cohort study.
Setting: Multicenter study.
Patients: 412 Nineteen-year-olds born <32 gestational weeks from the Project On Preterm and Small-for-gestational-age infants (POPS) cohort.
Interventions:Maternal betamethasone 12 mg administered twice with a 24-h interval.
Main outcome measures: Body composition, insulin resistance, the serum lipid profile, blood pressure and estimated renal function
Results: We did not find any long-term adverse effects of antenatal betamethasone, with the exception of an effect on glomerular filtration rate (GFR). In 19-year-old survivors, GFR was lower after betamethasone: -5.2 (95% CI: -8.9 to -1.4) ml/min per 1.73 m2.
Conclusions: The reduction in neonatal mortality associated with a single course of maternal betamethasone is not accompanied by long-term metabolic risks in survivors of preterm birth. The only adverse effect found was lower GFR. Although this difference was not clinically relevant at 19 years, it might predict an increased risk of chronic renal failure in prematurely born individuals who were exposed antenatally to betamethasone.
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