Buske-Kirschbaum A, Geiben A, Höllig H, Morschhäuser E, Hellhammer DHAltered responsiveness of the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic adrenomedullary system (SAMS) to stress in patients with atopic dermatitis. J Clin Endocr Metab 87:4245-4251

Center for Psychobiological and Psychosomatic Research, University of Trier, 54286 Trier, Germany.
Journal of Clinical Endocrinology &amp Metabolism (Impact Factor: 6.21). 10/2002; 87(9):4245-51. DOI: 10.1210/jc.2001-010872
Source: PubMed

ABSTRACT A growing number of animal data strongly suggest that a hyporeactive hypothalamus-pituitary adrenal (HPA) axis may be pathologically significant by increasing the susceptibility to chronic inflammation. Following this line of evidence, the specific goal of the present study was to investigate the HPA axis in patients with atopic dermatitis (AD), a chronic allergic inflammatory disease. In addition, the sympathetic adrenomedullary (SAM) system as a second potent immunoregulatory and anti-inflammatory stress-response system has been examined. AD patients (n = 36) and nonatopic control subjects (n = 37) were exposed to a standardized laboratory stressor consisting of a free speech and mental arithmetic task in front of an audience. Cortisol, ACTH, and catecholamine concentrations were assessed before and after the stressor. To investigate feedback sensitivity of the HPA axis, a low dose (0.5 mg) dexamethasone suppression test was also performed. AD patients showed significantly attenuated cortisol and ACTH responses to the stressor, whereas catecholamine levels were significantly elevated in atopic patients. No difference between the experimental groups was found in basal cortisol and ACTH concentrations, whereas basal catecholamine levels were significantly elevated. Analysis of cortisol levels after dexamethasone treatment suggested an intact feedback sensitivity in AD sufferers at the pituitary level. The present findings suggest that patients with AD demonstrate a blunted HPA axis responsiveness with a concurrent overreactivity of the SAM system to psychosocial stress. Considering the important immunoregulatory role of the HPA axis and the SAM system, especially under stressful conditions, an aberrant responsiveness of these neuroendocrine systems may increase the susceptibility to (allergic) inflammation and may be one psychobiological mechanism of stress-related aggravation of the disease.

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Available from: Dirk Hellhammer, Sep 25, 2015
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    • "Therefore, it seems plausible that once a stimulus has been evaluated as threatening, having a low cortisol response can constitute a maladaptive response because it can reduce our chances of success. In support of this, a reduced HPA-axis response to stress has been observed in several stress-related pathologies such as atopic dermatitis, asthma (Buske-Kirschbaum et al., 2002, 2003) and, interestingly, also in depression, which in turn is accompanied by declarative and working memory deficits and a decrease in hippocampal and prefrontal cortex volumes (Burke et al., 2005; Savitz and Drevets, 2009). "
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