title: Increased responsiveness of the hypothalamus-pituitary-adrenal (HPA) axis to stress in newborns with atopic disposition.
abstract: In previous studies, atopic patients showed attenuated cortisol responses to psychosocial stress which is suggestive of a hyporeactive hypothalamus-pituitary-adrenal (HPA) axis in this patient group. Regarding the anti-inflammatory role of glucocorticoids, reduced responsiveness of the HPA axis under stress may be one potential explanation of stress-induced exacerbation of atopic symptoms. The present study evaluated whether hyporeactivity of the HPA axis is a feature related to the disposition of atopy rather than a consequence of an ongoing chronic allergic inflammatory process. Newborns with an atopic disposition (parental atopy; n=31) and without atopic disposition (no parental atopy; n=20) were recruited. To further assess atopic disposition, total IgE levels were determined in the cord blood of the neonates. Three days after birth, a blood sample was obtained by a heel prick which is part of a standard pediatric examination. Blood sampling by heel prick is well known to be a significant stressor resulting in activation of the HPA axis in newborns. Analysis of salivary cortisol indicated a significant increase of cortisol levels in the newborns after the stressor with a trend towards an elevated cortisol response in babies with a family history of atopy or with elevated levels of cord IgE (> or = 0.5 kU/l). Neonates with a positive parental atopic heritage and elevated cord IgE were found to show significantly elevated cortisol responses to the heel prick stress when compared to newborns without a parental atopic history and normal cord IgE values. Moreover, cord IgE levels were significantly correlated with basal cortisol levels and the cortisol response to the stressor. These findings suggest that atopic disposition in neonates is associated with altered responsiveness of the HPA axis to stress which may increase the vulnerability to develop manifestation of atopy in later life.
authors.affiliation: Center for Psychobiological and Psychosomatic Research, University of Trier, Universitätsring 15, 54286 Trier, Germany. buske@uni-trier.de
authors.forename: Angelika
authors.initials: A
authors.lastname: Buske-Kirschbaum
authors.forename: Sonja
authors.initials: S
authors.lastname: Fischbach
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Rauh
authors.forename: Jürgen
authors.initials: J
authors.lastname: Hanker
authors.forename: Dirk
authors.initials: D
authors.lastname: Hellhammer
mesh_terms: D001800:Blood Specimen Collection / Q000009:adverse effects; D005260:Female; D005312:Fetal Blood / Q000276:immunology; D006801:Humans; D006854:Hydrocortisone / Q000032:analysis / Q000378:metabolism*; D006967:Hypersensitivity / Q000503:physiopathology*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007073:Immunoglobulin E / Q000097:blood; D007231:Infant, Newborn; D008297:Male; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D012016:Reference Values; D012463:Saliva / Q000737:chemistry; D013315:Stress, Psychological / Q000209:etiology / Q000503:physiopathology*
chemical_list: D007073:Immunoglobulin E; D006854:Hydrocortisone