Concentration of beta- Endorphin in Plasma of Patients with Stress - Associated Dermatoses / 대한피부과학회지

ABSTRACT

BACKGROUND: Stress has long been known to play a role in many dermatologic disorders and can affect the onset and course of the disorder in some patients. Stress-induced exacerbation or onset of symptoms has been reported in chronic urticaria, alopecia areata, herpes simplex, herpes zoster, and psoriasis vulgaris, and these diseases can be classified as stress-associated dermatoses. Beta beta-endorphin is one of the most important mediators of stress, which is known to be generated upon stimulation of the pituitary-adrenal axis, and its secretion increases during periods of stress. OBJECTIVE: In order to see wheather beta-endorphin might be related to the onset or recurrence of stress-associated dermatoses, we compared the plasma concentration of beta-endorphin in patients with stress-associated dermatoses with those of healthy subjects. METHODS: The concentration of beta-endorphin. In sera was quantified by radioimmunoassay, using the INCSTAB 125I RIA Kit for plasma beta-endorphin, Each patient was asked to indicate if they believed that their skin problem began after an important stressful event in their lives. RESULTS: There was no significant difference in plasma beta-endorphin levels between patients with chronic urticaria, alopecia areata, herpes simplex, and herpes zoster and healthy subjects(p>0.05), whereas in patients with psoriasis vulgaris, plasma level of beta-endorphin was significantly increased (p<0.001). There was no relationship between the stressful events and plasma beta-endorphin concentrations. CONCLUSIONS: The plasma beta-endorphin level is not correlated with the onset or recurrence of stress-associated dermatoses such as chronic urticaria, alopecia areata, herpes simplex, and herpes zoster. The increase in beta-endorphin in psoriasis vulgaris is more likely that this peptide is generated by the lymphocyte infiltrated in the skin and/or by lymphocytes when they recirculate rather than by the activation of the pituitary-adrenal axis by stress.