Endocrine and immune responses to stress in chronic inflammatory skin disorders

Atopy is a genetically and environmentally determined condition predisposing to different forms such as atopic dermatitis (AD) or allergic asthma (AA). Both AD and AA are considered to be multifactorial diseases; however, distinct immunologic abnormalities have been described that play a crucial role. There is growing evidence that immunoglobulin-E hypersecretion and activation of the predominantly T-helper-2 (TH2)-like T cell subset trigger allergic inflammatory processes and cause the disease to become chronic. In the present paper, data suggesting reduced hypothalamic-pituitary-ad renal (HPA) axis responsiveness in patients with AD and AA are summarized, and the potential etiologic significance of a hyporeactive HPA axis is discussed. We propose that because of defective HPA axis, immunoregulation under stressful conditions is ineffective in patients with atopic conditions, leading to aberrant immune responses and subsequent exacerbation of the disease. Further research into the role of the HPA axis in atopy may elucidate the cause of stress-induced exacerbation of atopic symptoms and may be of clinical relevance.