Objective: Atopic dermatitis (AD) is an inflammatory skin disease characterized by a hyperactivity of the humoral immune system with an onset in infancy or early childhood. Although most of the research has focused on the pathophysiological role of the immune system in AD, the impact of endocrine signals in the pathology of AD has received only little attention. However, because the endocrine system may play a regulatory role in immune functioning, it might be of major interest to study endocrine reactivity in AD patients. The present two-part study investigated the relationship between adrenocortical stress response, heart rate response, and psychological parameters in children with AD.
Method and results: In Study 1, a protocol for induction of psychosocial stress in children aged 8 to 14 years was evaluated. Healthy children (N = 16) were exposed to the Trier Social Stress Test for Children (TSST-C) that mainly consists of public speaking and mental arithmetic tasks in front of an audience. Salivary cortisol was measured 35, 15, and 1 minute before as well as 1, 10, 20, and 30 minutes after the stress; heart rate was monitored continuously. Results showed that the protocol induced a highly significant increase in free cortisol response (p < .001) and heart rate (p < .001). In Study 2, the TSST-C was applied to AD children (N = 15) and age- and sex-matched healthy controls (N = 15). All patients were in remission and medication-free for at least 3 weeks. Again, the stress test induced significant increases in cortisol and heart rate. However, the AD children showed a significantly blunted cortisol response to the stressor compared with the control group (p < .05). Heart rate responses were similar in both experimental groups. Neither subjective stress ratings nor personality traits were related to the blunted cortisol response.
Conclusions: 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.