Buske-Kirschbaum Angelika, Fischbach Sonja, Rauh Wolfgang, Hanker Jürgen, Hellhammer Dirk
Center for Psychobiological and Psychosomatic Research, University of Trier, Universitätsring 15, 54286 Trier, Germany.
Psychoneuroendocrinology. 2004 Jul;29(6):705-11. doi: 10.1016/S0306-4530(03)00100-8.
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.
在以往的研究中,特应性患者对心理社会应激的皮质醇反应减弱,这表明该患者群体下丘脑 - 垂体 - 肾上腺(HPA)轴反应低下。考虑到糖皮质激素的抗炎作用,应激状态下HPA轴反应性降低可能是应激诱发特应性症状加重的一个潜在原因。本研究评估了HPA轴反应低下是与特应性易感性相关的特征,还是持续性慢性变应性炎症过程的结果。招募了有特应性易感性(父母有特应性;n = 31)和无特应性易感性(父母无特应性;n = 20)的新生儿。为进一步评估特应性易感性,测定了新生儿脐血中的总IgE水平。出生后三天,通过足跟采血获取血样,这是标准儿科检查的一部分。众所周知,足跟采血是一个显著的应激源,会导致新生儿HPA轴激活。唾液皮质醇分析表明,应激源刺激后新生儿皮质醇水平显著升高,有特应性家族史或脐血IgE水平升高(>或 = 0.5 kU/l)的婴儿皮质醇反应有升高趋势。与无父母特应性病史且脐血IgE值正常的新生儿相比,父母有特应性遗传且脐血IgE升高的新生儿对足跟采血应激的皮质醇反应显著升高。此外,脐血IgE水平与基础皮质醇水平及对应激源的皮质醇反应显著相关。这些发现表明,新生儿的特应性易感性与HPA轴对应激的反应性改变有关,这可能会增加其在以后生活中出现特应性表现的易感性。