Noera Kieviet1, Silke de Groot2, Gerard Noppe3, Yolanda B de Rijke4, Elisabeth F C van Rossum5, Erica L T van den Akker6, Koert M Dolman7, Adriaan Honig8. 1. Department of Pediatrics, Psychiatry Obstetric Pediatric Center of Expertise, OLVG West Hospital, Jan Tooropstraat 164, 1061AE Amsterdam, the Netherlands. Electronic address: noera.kieviet@gmail.com. 2. Department of Pediatrics, Psychiatry Obstetric Pediatric Center of Expertise, OLVG West Hospital, Jan Tooropstraat 164, 1061AE Amsterdam, the Netherlands. Electronic address: silkedegroot@gmail.com. 3. Department of Internal Medicine, Division of Endocrinology, Erasmus MC, University Medical Center, 's-Gravendijkwal 230, 3015 CE Rotterdam, the Netherlands. Electronic address: g.noppe@erasmusmc.nl. 4. Department of Clinical Chemistry, Erasmus MC, University Medical Center, 's-Gravendijkwal 230, 3015 CE Rotterdam, the Netherlands. Electronic address: y.derijke@erasmusmc.nl. 5. Department of Internal Medicine, Division of Endocrinology, Erasmus MC, University Medical Center, 's-Gravendijkwal 230, 3015 CE Rotterdam, the Netherlands. Electronic address: e.vanrossum@erasmusmc.nl. 6. Department of Pediatrics, Division of Endocrinology, Sophia's Childrens Hospital, Erasmus MC, University Medical Center, 's-Gravendijkwal 230, 3015 CE Rotterdam, the Netherlands. Electronic address: e.l.t.vandenakker@erasmusmc.nl. 7. Department of Pediatrics, Psychiatry Obstetric Pediatric Center of Expertise, OLVG West Hospital, Jan Tooropstraat 164, 1061AE Amsterdam, the Netherlands. Electronic address: k.dolman@olvg.nl. 8. Department of Psychiatry, Psychiatry Obstetric Pediatric Center of Expertise, OLVG West Hospital, Jan Tooropstraat 164, 1061AE Amsterdam, the Netherlands; Department of Psychiatry, VU Medical Center, de Boelenlaan 1118, 1081 HZ Amsterdam, the Netherlands. Electronic address: a.honig@olvg.nl.
Abstract
BACKGROUND: As a marker for poor neonatal adaptation (PNA) is lacking, the diagnostic process is difficult and includes invasive additional testing. AIMS: In order to develop a marker, it is essential to gain insight into the etiology of PNA. We hypothesized that the fetal cortisol level may play a role in this etiology. STUDY DESIGN: Non-randomized, prospective controlled study. OUTCOME MEASURES: We examined hair cortisol levels of infants exposed and not exposed to selective antidepressants (SADs) during pregnancy. These cortisol levels represent the mean cortisol level during the last trimester of pregnancy. Infants exposed to SADs who developed PNA according to the pediatrician (PNA+, n=25), infants exposed to SADs who did not develop PNA (PNA-, n=40) and infants not exposed to SADs (controls, n=105) were compared. RESULTS: In infants with PNA, hair cortisol levels were higher compared to infants without PNA. However this difference was only statistically significant in female infants (girls B0.33, p=0.04, boys B0.05, p=0.82). There was no correlation between nonspecific distress, measured by the Finnegan score and fetal hair cortisol levels (B-0.15, p=0.30). All analyses were adjusted for type of delivery and gestational age. CONCLUSIONS: Our results suggest that the hypothalamic pituitary adrenal (HPA) axis activity may play a sex-specific role in the development of PNA. As PNA is most likely of a multifactorial origin, it would be interesting to examine other factors possibly involved in the etiology of PNA in future studies, such as (epi) genetics.
BACKGROUND: As a marker for poor neonatal adaptation (PNA) is lacking, the diagnostic process is difficult and includes invasive additional testing. AIMS: In order to develop a marker, it is essential to gain insight into the etiology of PNA. We hypothesized that the fetal cortisol level may play a role in this etiology. STUDY DESIGN: Non-randomized, prospective controlled study. OUTCOME MEASURES: We examined hair cortisol levels of infants exposed and not exposed to selective antidepressants (SADs) during pregnancy. These cortisol levels represent the mean cortisol level during the last trimester of pregnancy. Infants exposed to SADs who developed PNA according to the pediatrician (PNA+, n=25), infants exposed to SADs who did not develop PNA (PNA-, n=40) and infants not exposed to SADs (controls, n=105) were compared. RESULTS: In infants with PNA, hair cortisol levels were higher compared to infants without PNA. However this difference was only statistically significant in female infants (girls B0.33, p=0.04, boys B0.05, p=0.82). There was no correlation between nonspecific distress, measured by the Finnegan score and fetal hair cortisol levels (B-0.15, p=0.30). All analyses were adjusted for type of delivery and gestational age. CONCLUSIONS: Our results suggest that the hypothalamic pituitary adrenal (HPA) axis activity may play a sex-specific role in the development of PNA. As PNA is most likely of a multifactorial origin, it would be interesting to examine other factors possibly involved in the etiology of PNA in future studies, such as (epi) genetics.
Authors: Hilal Ince-Askan; Erica L T van den Akker; Yolanda B de Rijke; Elisabeth F C van Rossum; Johanna M W Hazes; Radboud J E M Dolhain Journal: RMD Open Date: 2019-01-30