No abstract

These findings suggest that the adrenocortical response to stress is attenuated in atopic children. A hyporesponsive hypothalamus-pituitary-adrenal (HPA) axis might explain in part the stress-induced eruptions of AD symptoms.

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.

No abstract