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Poster #64 - NICU-related stress exposure, telomere length erosion and HPA axis stress reactivity in very preterm infants

Fri, March 22, 7:45 to 9:15am, Baltimore Convention Center, Floor: Level 1, Exhibit Hall B

Integrative Statement

Background. Even in absence of severe morbidities, very preterm (VPT) infants (gestational age < 32 weeks) present a neurobehavioral immaturity at birth and they require long-lasting hospitalization in the Neonatal Intensive Care Unit (NICU). During the NICU stay, VPT infants are exposed to life-saving interventions which include invasive and painful skin-breaking procedures (i.e., NICU-related stress). This early exposure to NICU-related stress has been previously associated with dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis in response to stressful conditions even later during infancy and childhood. Telomeres are repeat-sequence at the end of chromosomes, which shorten with age and are highly susceptible to early adversities: the exposure to early stressful conditions is associated with shorter telomere length (TL). Unfortunately, previous research did not assess longitudinally the association between NICU-related stress and TL in VPT infants. Moreover, the involvement of TL shortening on HPA axis dysregulation is understudied in VPT infants. Aims. In the present study, we assessed the association between (1) NICU-related stress and birth-to-discharge TL shortening in VPT infants and (2) TL shortening and HPA axis regulation at 3 months (corrected for prematurity). Methods. Leukocyte TL was assessed from cord blood at birth in 46 VPT infants and in a group of 31 full-term (FT) control infants, as well as at NICU discharge in VPTs only. NICU-related stress was measured as the number of skin-breaking procedures occurring throughout the NICU stay. HPA axis reactivity was assessed in the two groups at 3-month-age (corrected for prematurity) in response to socio-emotional stress elicited through the maternal Still-Face procedure. To assess HPA axis reactivity, salivary cortisol was obtained before (baseline) and after (+10, +20, and +30 minutes) the Still-Face procedure. Salivary cortisol was available for 23 VPT and 30 FT infants. HPA axis reactivity was measured as the highest post-stress salivary cortisol sample for each infant. Results. A significant difference emerged for TL between VPT infants and FT counterparts at birth, t(75)=2.22, p<.05. TL decreased from birth to discharge in VPT infants, although the change was not significant, t(75)=1.78, p<.10. The amount of NICU-related stress emerged as the primary predictor of TL erosion in VPT infants, even controlling for neonatal and clinical confounders, R2=.27, B=-.11, p<.05. At 3 months, VPT infants showed a blunted HPA axis reactivity to the Still-Face procedure, compared to FT infants, t(51)=-2.22, p<.05. The birth-to-discharge TL shortening in VPT infants associated with reduced HPA axis reactivity at 3 months, R2=.55, B=-.76, p<.01. Discussion. The present study confirms previous evidence of longer telomeres in VPT infants at birth compared to FT controls, presumably due to greater lower gestational age. Moreover, NICU-related stress emerged as a key regulator of TL erosion from birth to discharge in VPT infants. This biomarker of early adversity in VPT infants appears to contribute to blunted HPA axis reactivity at 3 months. Future research is warranted to further explore TL erosion in VPT infants and the factors associated with individual differences in NICU-related stress susceptibility at the epigenetic level.

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