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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-5012

Schäffer, L; Müller-Vizentini, D; Burkhardt, T; Rauh, M; Ehlert, U; Beinder, E (2009). Blunted stress response in small for gestational age neonates. Pediatric Research, 62(5):231-235.

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Abstract

There is evidence, that adverse conditions during intrauterine development affect future health of the offspring. Hypothalamus-pituitary-adrenal (HPA) axis dysregulation is assumed to play an important role in the association of small-for-gestational-age (SGA) and the pathogenesis of hypertension and the metabolic syndrome. Stress response patterns in SGA neonates may identify a link with intrauterine induced permanent maladaptation of the HPA axis. Salivary cortisol and cortisone levels were therefore analyzed during resting conditions and in response to a pain induced stress event in SGA (<5 percentile) and appropriate-for-gestational-age (AGA) neonates born >/=34 weeks of gestation. In AGA neonates, salivary cortisol and cortisone levels significantly increased after the stress event (p<0.05). In contrast, SGA infants exhibited a blunted steroid release after stress induction (p=0.76, p=0.65, respectively). No influence of mode of delivery (p=0.93), gender (p=0.21) and gestational age (p=0.57) on stress response patterns was observed in a multiple stepwise regression. SGA neonates show a blunted physiological activation of the HPA axis in response to a stress stimulus. Thus, intrauterine induced alteration of HPA axis regulation appears to persist into the postnatal period and represents a prerequisite for the hypothesis of HPA axis involvement in the fetal origin of adult diseases.

Item Type:Journal Article, refereed, original work
Communities & Collections:06 Faculty of Arts > Institute of Psychology
04 Faculty of Medicine > University Hospital Zurich > Clinic for Obstetrics
DDC:150 Psychology
610 Medicine & health
Language:English
Date:2009
Deposited On:07 Nov 2008 13:21
Last Modified:01 Dec 2012 17:12
Publisher:Lippincott Wiliams & Wilkins
ISSN:0031-3998
Publisher DOI:10.1203/PDR.0b013e318191fb44
PubMed ID:18948839
Citations:Google Scholar™
Scopus®. Citation Count: 11

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