Summary: | Background : Preterm birth is marked by stressful environment in intra- as well as extrauterine life. Furthermore, preterms are exposed to repeated painful procedures, loud noise, and restricted contact with parents in the neonatal intensive care unit. This environment can affect hormonal and physiological systems and lead to long-term negative outcomes. Despite this, little is known about how early-life stress affects preterms later on in childhood. The goals of the current study were threefold: (1) comparing cortisol profile, including cortisol awakening response (CAR), between preterm and full-term children; (2) assessing memory, behavior, and emotion of preterms; (3) evaluating if preterms are more responsive to an acute stressor. Methods : Basal cortisol and α-amylase (sAA) profiles, including CAR of 30 preterm children were evaluated. Salivary samples were measured on two consecutive days at four time points: awakening, 30 min post-awakening, 1600h, and 2100h. Furthermore, we assess memory functions by using the wide range assessment of memory and learning and screen behavior/emotion by using strengths and difficulties questionnaire. The results of preterms were compared to an age- and sex-matched control group (n=31). One week after, the participants were exposed to Trier Social Stress Test for Children (TSST-C). Results : Preterms had higher cortisol concentrations at awakening, a flattened CAR, and an exaggerated response to TSST-C compared to full-terms. In addition, cortisol concentrations at awakening were larger in preterm girls than in preterm boys. A trend of sex-specific differences was also observed on TSST-C exposure, with higher cortisol response in preterm girls. Preterms also showed more emotional problems and poorer memory. Conclusions : Our findings illustrate the long-lasting effects of preterm birth on the hypothalamic pituitary adrenal (HPA) axis, internalizing behavior, and memory. The findings are in line with the idea that early-life stress alters the set-point of the HPA axis thereby creating a more vulnerable phenotype.
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