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Endocrine stress responses in TH1-mediated chronic inflammatory skin disease (psoriasis vulgaris)--do they parallel stress-induced endocrine changes in TH2-mediated inflammatory dermatoses (atopic dermatitis)?
Psychoneuroendocrinology. 2006 May; 31(4):439-46.P

Abstract

In previous research we reported attenuated responsiveness of the hypothalamus-pituitary-adrenal (HPA) axis and further, an increased reactivity of the sympathetic adrenomedullary (SAM) system to stress in patients suffering from atopic dermatitis (AD). AD is a chronic inflammatory skin disease mainly triggered by TH(2)-dependent inflammatory processes. The specific goal of the present study was to investigate whether altered HPA axis and SAM system responsiveness to stress can also be found in TH(1)-mediated inflammatory conditions. Patients with psoriasis (PSO; n=23), a TH(1)-mediated inflammatory (autoimmune) skin disease and healthy controls (n=25) were exposed to a standardized laboratory stressor (TSST) which mainly consists of a free speech and a mental arithmetic task in front of an audience. To investigate HPA axis and SAM system responsiveness, cortisol, ACTH, and catecholamines were determined before and after the stress test. In addition, cortisol levels after awakening and cortisol levels during the day (short diurnal profile) were determined. In order to test feedback sensitivity of the HPA axis, a dexamethasone (DEX) suppression test (0.5 mg) was performed. Analysis of cortisol and ACTH levels after the stress test yielded no significant differences between PSO subjects and controls indicating no altered HPA axis function in this patient group. Further, no between-group differences were found in cortisol levels after awakening or during the day (short diurnal profile). Additionally, no difference between PSO and healthy subjects in the feedback sensitivity of the system could be found (DEX test). However, PSO patients showed elevated epinephrine (F(3,102)=4.7; p<0.005) and norepinephrine (F(3,135)=2.7; p<0.05) levels in response to the stress test when compared to the controls. These findings suggest no altered HPA axis responsiveness, but increased reactivity of the SAM system in TH(1)-mediated chronic inflammatory skin disease.

Authors+Show Affiliations

Department of Biopsychology, University of Dresden, D-01026 Dresden, Germany. buske@biopsych.tu-dresden.deNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Controlled Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16359823

Citation

Buske-Kirschbaum, A, et al. "Endocrine Stress Responses in TH1-mediated Chronic Inflammatory Skin Disease (psoriasis Vulgaris)--do They Parallel Stress-induced Endocrine Changes in TH2-mediated Inflammatory Dermatoses (atopic Dermatitis)?" Psychoneuroendocrinology, vol. 31, no. 4, 2006, pp. 439-46.
Buske-Kirschbaum A, Ebrecht M, Kern S, et al. Endocrine stress responses in TH1-mediated chronic inflammatory skin disease (psoriasis vulgaris)--do they parallel stress-induced endocrine changes in TH2-mediated inflammatory dermatoses (atopic dermatitis)? Psychoneuroendocrinology. 2006;31(4):439-46.
Buske-Kirschbaum, A., Ebrecht, M., Kern, S., & Hellhammer, D. H. (2006). Endocrine stress responses in TH1-mediated chronic inflammatory skin disease (psoriasis vulgaris)--do they parallel stress-induced endocrine changes in TH2-mediated inflammatory dermatoses (atopic dermatitis)? Psychoneuroendocrinology, 31(4), 439-46.
Buske-Kirschbaum A, et al. Endocrine Stress Responses in TH1-mediated Chronic Inflammatory Skin Disease (psoriasis Vulgaris)--do They Parallel Stress-induced Endocrine Changes in TH2-mediated Inflammatory Dermatoses (atopic Dermatitis). Psychoneuroendocrinology. 2006;31(4):439-46. PubMed PMID: 16359823.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endocrine stress responses in TH1-mediated chronic inflammatory skin disease (psoriasis vulgaris)--do they parallel stress-induced endocrine changes in TH2-mediated inflammatory dermatoses (atopic dermatitis)? AU - Buske-Kirschbaum,A, AU - Ebrecht,M, AU - Kern,S, AU - Hellhammer,D H, Y1 - 2005/12/13/ PY - 2005/06/15/received PY - 2005/10/17/revised PY - 2005/10/21/accepted PY - 2005/12/20/pubmed PY - 2006/6/2/medline PY - 2005/12/20/entrez SP - 439 EP - 46 JF - Psychoneuroendocrinology JO - Psychoneuroendocrinology VL - 31 IS - 4 N2 - In previous research we reported attenuated responsiveness of the hypothalamus-pituitary-adrenal (HPA) axis and further, an increased reactivity of the sympathetic adrenomedullary (SAM) system to stress in patients suffering from atopic dermatitis (AD). AD is a chronic inflammatory skin disease mainly triggered by TH(2)-dependent inflammatory processes. The specific goal of the present study was to investigate whether altered HPA axis and SAM system responsiveness to stress can also be found in TH(1)-mediated inflammatory conditions. Patients with psoriasis (PSO; n=23), a TH(1)-mediated inflammatory (autoimmune) skin disease and healthy controls (n=25) were exposed to a standardized laboratory stressor (TSST) which mainly consists of a free speech and a mental arithmetic task in front of an audience. To investigate HPA axis and SAM system responsiveness, cortisol, ACTH, and catecholamines were determined before and after the stress test. In addition, cortisol levels after awakening and cortisol levels during the day (short diurnal profile) were determined. In order to test feedback sensitivity of the HPA axis, a dexamethasone (DEX) suppression test (0.5 mg) was performed. Analysis of cortisol and ACTH levels after the stress test yielded no significant differences between PSO subjects and controls indicating no altered HPA axis function in this patient group. Further, no between-group differences were found in cortisol levels after awakening or during the day (short diurnal profile). Additionally, no difference between PSO and healthy subjects in the feedback sensitivity of the system could be found (DEX test). However, PSO patients showed elevated epinephrine (F(3,102)=4.7; p<0.005) and norepinephrine (F(3,135)=2.7; p<0.05) levels in response to the stress test when compared to the controls. These findings suggest no altered HPA axis responsiveness, but increased reactivity of the SAM system in TH(1)-mediated chronic inflammatory skin disease. SN - 0306-4530 UR - https://www.unboundmedicine.com/medline/citation/16359823/Endocrine_stress_responses_in_TH1_mediated_chronic_inflammatory_skin_disease__psoriasis_vulgaris___do_they_parallel_stress_induced_endocrine_changes_in_TH2_mediated_inflammatory_dermatoses__atopic_dermatitis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4530(05)00221-0 DB - PRIME DP - Unbound Medicine ER -