4.7 Article

Persistent Effects of Antenatal Synthetic Glucocorticoids on Endocrine Stress Reactivity From Childhood to Adolescence

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ENDOCRINE SOC
DOI: 10.1210/jc.2018-01566

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  1. German Research Foundation (Deutsche Forschungsgemeinschaft) [AL 1485/5-1, KI 537/36-1, LI 879/15-1]

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Context: Antenatal synthetic glucocorticoid (sGC) therapy has been identified as a potent programming factor of the hypothalamic-pituitary-adrenal (HPA) axis. We previously observed significantly increased cortisol stress responses in 6- to 11-year-old, term-born children exposed to antenatal sGCs compared with controls. These findings call for longitudinal follow-up studies to evaluate long-term effects of antenatal sGCs, given that adolescence is marked by a substantial shift of HPA axis functioning. Objective: This study aimed to longitudinally investigate the stability of antenatal sGC-related effects on cortisol stress reactivity from childhood to adolescence. Design, Setting, and Participant: To evaluate long-term trajectories of antenatal sGCs, we longitudinally followed a subsample (n = 44) of our children's cohort into adolescence (14 to 18 years old) for a second assessment. To this end, 22 adolescents with antenatal sGC exposure and 22 untreated controls underwent a standardized laboratory stressor [Trier Social Stress Test (TSST)]. Results: Besides a general increase in HPA axis reactivity from childhood to adolescence (P < 0.05), participants treated with antenatal sGCs showed significantly higher cortisol levels in response to the TSST compared with controls during both developmental stages (P < 0.05). Furthermore, we observed a moderating effect of sGCs on rank-order stability of cortisol stress reactivity from childhood to adolescence (P < 0.05) with a trend (P = 0.07) for higher rank-order stability in sGC-exposed individuals (r = 0.37) compared with controls (r = -0.20). Conclusion: These findings suggest that antenatal sGCs yield long-term changes of HPA axis reactivity that persist into adolescence and may confer increased vulnerability for developing stress-related disorders.

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