Blunted HPA axis responsiveness to stress in atopic patients is associated with the acuity and severeness of allergic inflammation.
Previously we could demonstrate attenuated responsiveness of the hypothalamus-pituitary-adrenal (HPA) axis to stress in patients with chronic allergic inflammatory disease (i.e., atopic dermatitis, allergic asthma). The present study was designed to investigate HPA axis function in an acute manifestation of allergy. Patients with seasonal allergic rhinitis (SAR; n = 20) and non-atopic controls (n = 20) were exposed to a standardized laboratory stressor ('Trier Social Stress Test'; TSST). Cortisol responses to the TSST and cortisol awakening responses (CAR) were measured in SAR subjects while suffering from acute symptoms of SAR (pollen season), and during a non-active state of their disease (pollen-free season). To assess the acuity and severity of SAR, eosinophil and basophil numbers and SAR symptomatology were determined. Non-allergic control subjects were examined at identical times during the year. To control for possible sequence effects, a cross-over design was used. SAR patients showed significantly increased symptom severity (t = 9.4; p<.001) as well as eosinophil (F(1,31) = 9.8; p<.01) and basophil (F(1,38) = 6.4; p<.05) numbers during the pollen season when compared to a pollen-free period. When exposed to the TSST, significantly attenuated cortisol responses were found in SAR subjects during acute manifestation of the disease (pollen season) when compared to the pollen-free season (F(16,456) = 1.65; p<.05). In SAR patients, there was a significant negative correlation between symptom severity and the cortisol response to the stressor (r = .53; p<.05). No significant between-group or between-condition differences with respect to the CAR could be determined (all p>.05). These findings support previous data of attenuated HPA axis responsiveness to stress in atopic conditions and further, suggest that HPA axis hyporesponsiveness in atopy may be linked to the severity of the allergic inflammatory process.
Buske-Kirschbaum
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Dept of Biopsychology, Technical University of Dresden, Dresden, Germany. buske@biopsych.tu-dresden.de
Ebrecht
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Hellhammer
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D000328:Adult; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006969:Hypersensitivity, Immediate / Q000503:physiopathology*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D007073:Immunoglobulin E / Q000097:blood; D007249:Inflammation / Q000503:physiopathology*; D007958:Leukocyte Count; D007962:Leukocytes / Q000276:immunology; D008297:Male; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D011058:Pollen / Q000276:immunology; D006255:Rhinitis, Allergic, Seasonal / Q000503:physiopathology; D012931:Social Environment; D013315:Stress, Psychological / Q000503:physiopathology*
D007073:Immunoglobulin E; D006854:Hydrocortisone