Altered Reactivity of the Hypothalamus‐Pituitary‐Adrenal Axis in Patients with Atopic Dermatitis: Pathologic Factor or Symptom?^a

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease with the principal symptoms of dry skin, lichnification, eczematous inflammation, and an intense pruritus. Despite general acceptance that AD is a multifactorial skin disorder, dysregulation of immune functions (e.g., hypersecretion of immunoglobulin-E, altered cytokine profiles) is considered to be mainly involved in AD pathogenesis. Considerable evidence points to an immunoregulatory function for the hypothalamus-pituitary-adrenal (HPA) axis, suggesting that appropriate reactivity of the HPA axis is necessary to prevent the immune system from reaching a level that may be damaging for the host. It is further hypothesized that dysfunctional reactivity of the HPA axis may increase the vulnerability of the organism to immune-related disorders such as inflammatory diseases. In the present paper the role of the HPA axis for the development and chronification of allergic inflammation will be summarized and the potential pathological significance of a dysfunctional HPA axis in AD pathogenesis will be discussed.

Psychosomatics and Dermatology: Comparison between Objective Data and Subjective Impressions Given by Patients and Dermatologists

“…We also did not find any differences between the eczema group and the benign tumor group, but there was a difference in age between the groups. Perhaps this can explain this discrepancy to the literature in which some controlled trials are now showing the possibility of psychophysiological factors in the etiology of atopic dermatitis [6]. Furthermore, the literature reveals that psychological treatments associated with dermatological treatment led to significantly better improvement in skin condition than did intensive or standard dermatological treatment [16].…”

11β-Hydroxysteroid dehydrogenase type 1 is an important regulator at the interface of obesity and inflammation

“…Hence, it is not surprising that a deregulation of HPA axis activation contributes to chronic inflammatory disease in several animal disease models [41]. Whether such a deregulation is an aetiological factor in human disease is plausible, but less well established [41][42][43][44].…”

Stress and atopic dermatitis

“…An increased HPA response to heel stick was observed in neonates with increased cord blood IgE or a family history of atopy [ 24 ]. In addition, children 9 to 14 years old with AD who were subjected to public-speaking stress demonstrated a blunted cortisol response compared with age-matched controls [ 25 ]. This early increased stress response is hypothesized to give way to HPA axis hyporesponsiveness, which leads to altered immune responses and infl ammation susceptibility [ 26 ].…”