{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T04:54:00Z","timestamp":1793249640027,"version":"4.5.0"},"reference-count":41,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2024,6,14]],"date-time":"2024-06-14T00:00:00Z","timestamp":1718323200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["obgyn.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Obstet Gynecol Scand"],"published-print":{"date-parts":[[2024,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Introduction<\/jats:title><jats:p>Prenatal exposure to supraphysiological glucocorticoid (GC) levels may lead to long\u2010lasting developmental changes in numerous biological systems. Our prior study identified an association between prenatal GC prophylaxis and reduced cognitive performance, electrocortical changes, and altered autonomic nervous system (ANS) activity in children aged 8\u20139\u2009years. This follow\u2010up study aimed to examine whether these findings persisted into adolescence.<\/jats:p><\/jats:sec><jats:sec><jats:title>Material and Methods<\/jats:title><jats:p>Prospective observational follow\u2010up study involving twenty\u2010one 14\u2010 to 15\u2010year\u2010old adolescents born to mothers who received betamethasone for induction of fetal lung maturation in threatened preterm birth, but who were born with a normal weight appropriate for their gestational age (median 37<jats:sup>+4<\/jats:sup> gestational weeks). Thirty\u2010five children not exposed to betamethasone served as the reference group (median 37<jats:sup>+6<\/jats:sup> gestational weeks). The primary endpoint was cognitive performance, measured by intelligence quotient (IQ). Key secondary endpoints included symptoms of attention\u2010deficit\/hyperactivity disorder (ADHD) and metabolic markers. Additionally, we determined electrocortical (electroencephalogram), hypothalamus\u2013pituitary\u2013adrenal axis (HPAA), and ANS activity in response to a standardized stress paradigm.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>No statistically significant group difference was observed in global IQ (adjusted mean: betamethasone 103.9 vs references 105.9, mean difference \u22122.0, 95% confidence interval [CI]: \u22127.12 to 3.12, <jats:italic>p<\/jats:italic>\u2009=\u20090.44). Similarly, ADHD symptoms, metabolic markers, the overall and stress\u2010induced activity of the HPAA and the ANS did not differ significantly between groups. However, the betamethasone group exhibited reduced electrocortical activity in the frontal brain region (spectral edge frequency\u2013adjusted means: 16.0\u2009Hz vs 17.8\u2009Hz, mean difference \u22121.83\u2009Hz, 95% CI: \u22123.21 to \u22120.45, <jats:italic>p<\/jats:italic>\u2009=\u20090.01).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>In 14\u2010 to 15\u2010year\u2010old adolescents, prenatal GC exposure was not associated with differences in IQ scores or ANS activity compared to unexposed controls. However, decelerated electrocortical activity in the frontal region potentially reflects disturbances in the maturation of cortical and\/or subcortical brain structures. The clinical significance of these changes remains unknown. Given the small sample size, selective participation\/loss of follow\u2010up and potential residual confounding, these findings should be interpreted cautiously. Further research is required to replicate these results in larger cohorts before drawing firm clinical conclusions.<\/jats:p><\/jats:sec>","DOI":"10.1111\/aogs.14885","type":"journal-article","created":{"date-parts":[[2024,6,15]],"date-time":"2024-06-15T04:38:53Z","timestamp":1718426333000},"page":"1530-1540","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Association between prenatal glucocorticoid exposure and adolescent neurodevelopment: An observational follow\u2010up study"],"prefix":"10.1111","volume":"103","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3603-9711","authenticated-orcid":false,"given":"Florian","family":"Rakers","sequence":"first","affiliation":[{"name":"Hans Berger Department of Neurology Jena University Hospital  Jena Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ekkehard","family":"Schleussner","sequence":"additional","affiliation":[{"name":"Department of 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