Altered Responsiveness of the Hypothalamus-Pituitary-Adrenal Axis and the Sympathetic Adrenomedullary System to Stress in Patients with Atopic Dermatitis

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.

Increased Heart Rate Variability in Allergic and Highly Trait Anxious Individuals

“…On the other hand, close similarities between allergy and anxiety were documented [8,19,20]. Similar findings in allergy and anxiety were also found in HPA axis reaction to stress, where both allergy and high trait anxiety subjects exhibited lowered cortisol responses [5,26]. In light of these results, we hypothesize, that both allergy and high trait anxiety subjects exhibit an autonomic dysregulation, which can demonstrate itself in the form of hyperreaction or hyporeaction similarly to cortisol reactivity.…”

“…Allostatic load can result in various dysregulations of allostatic systems, nervous, endocrine and immune system. Studies of neuroendocrine HPA (hypothalamus-pituitary-adrenal) axis in allergy [1,5] found lowered levels of salivary cortisol in response to psychosocial stress in patients with AD [5] and AR [1,6]. One of possible mechanisms of hypocortisolism is it being a result of chronic activation of HPA axis and, therefore, its inhibition through feedback regulation [7].…”

“…One of possible mechanisms of hypocortisolism is it being a result of chronic activation of HPA axis and, therefore, its inhibition through feedback regulation [7]. Similarly, autonomic nervous system dysregulation was described, however, while some studies showed sympathetic over-activation in allergy [5,8,9], other studies documented parasympathetic predominance [10][11][12][13].…”

Psychological and biological background of the interaction between psoriasis and stress

“…Ezzel szemben a SAM-tengely két végterméke (adrenalin, noradrenalin) egyaránt erős immunaktiváló hatású [45,46,47,48]. Bár a fentiek ismeretében gyakori, krónikus stressz esetén magas kortizolszintet és csökkent immunműkö-dést várnánk, sok stresszkapcsolt betegségben (például rheumatoid arthritis, irritábilis bél szindróma, krónikus fáradtság szindróma, poszttraumás stressz zavar, fi bromyalgia) ennek pont az ellenkezőjét -normális vagy csökkent kortizolszinteket, túlzott immunaktivációt és autodestrukciót -fi gyelték meg [49,50,51,52]. A most bemutatni tervezett kutatási eredmények egy része pikkelysömör esetében is hasonló megfi gyeléseket tett, és a legfrissebb közlemények szinte kivétel nélkül megemlítik a diszfunkcionális HPA-tengely-működést, mint a pikkelysömörben jelentkező gyulladásos folyamat hátteré-ben meghúzódó egyik potenciális patomechanizmust.…”

Basal functioning of the hypothalamic-pituitary-adrenal (HPA) axis and psychological distress in recreational ecstasy polydrug users

“…Hypersecretion of cortisol across the day has been linked to the metabolic syndrome (Rosmond, 2005), immunologic decline (Elenkov, 2004), the development of mood disorders (Gold et al, 1998) and cognitive dysfunction (Lupien et al, 1998). In contrast, diurnal hyposecretion has been associated with increased risk of the development of autoimmune disorders such as rheumatoid arthritis (Masi & Chrousos, 1996), Sjögren's syndrome (Johnson et al, 1998) and dermatitis (Buske-Kirschbaum et al, 2002).…”