Prenatal Glucocorticoid Exposure and Autism Spectrum Disorder: Current Evidence, Mechanisms, and Clinical Implications

Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterised by social difficulties and repetitive behaviours. Genetic and environmental factors play a key role in its aetiology. Antenatal glucocorticoids, widely used to improve outcomes in preterm infants, have raised questions about potential long-term neurodevelopmental effects. This review aims to summarise the current literature on the association between prenatal glucocorticoid exposure and neurodevelopmental outcomes, including ASD, explore proposed biological mechanisms, and discuss clinical and public health implications. A comprehensive literature search was conducted in PubMed, Web of Science and Google Scholar using relevant keywords, focusing on observational studies, meta-analyses, and clinical studies that addressed neurodevelopmental consequences of prenatal glucocorticoid exposure, with priority given to studies evaluating ASD risk. Glucocorticoids reduce neonatal respiratory complications in preterm infants. Long-term neurodevelopmental outcomes, including ASD, are uncertain: some observational studies suggest increased risk, especially in late-preterm or term infants, while randomised trials show minimal adverse effects. Potential mechanisms include epigenetic changes, HPA axis disruption, and altered hippocampal development. Glucocorticoids are essential for improving the survival of preterm infants. Current evidence does not establish a causal link with ASD, but potential long-term neurodevelopmental effects warrant cautious use, careful patient selection, and continued long-term follow-up. Further well-controlled studies using standardised neurodevelopmental assessments are needed.