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Time matters - acute stress response and glucocorticoid sensitivity in early multiple sclerosis.
Brain Behav Immun 2014; 41:82-9BB

Abstract

OBJECTIVE

Psychosocial stress has frequently been associated with disease activity and acute exacerbations in multiple sclerosis (MS). Despite this well established finding, strikingly little is known about the acute hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal-medullary (SAM) stress response in MS.

METHODS

Twenty-six early relapsing-remitting MS (RRMS) patients and seventeen age- and sex-matched healthy control subjects (CS) took part in the Trier Social Stress Test (TSST), a well validated psycho-social laboratory stress protocol. Repeated blood samples were analyzed for stress-related cortisol and catecholamine levels as well as for glucocorticoid sensitivity (GCS) of target immune cells. Chronic and acute stress appraisals were assessed by self-report measures.

RESULTS

RRMS patients and CS did not differ in stress-related cortisol/catecholamine levels, GCS or stress appraisal in response to the TSST. However, cortisol release as well as GCS was strongly correlated with time since diagnosis but not with neurological disability. Patients with shorter disease duration (2-12 months) expressed a significantly higher cortisol stress response while MS patients with longer disease duration (14-36 months) showed a significantly diminished HPA response as well as lower post-stress GCS.

DISCUSSION

There is evidence for a time-dependent variability in the HPA stress system with an increased cortisol stress response in the first year after diagnosis along with a more blunted HPA stress response and a diminished GCS in subsequent disease stages. Data underscore the highly dynamic nature of HPA axis regulation in the MS disease process, which could possibly relate to compensatory mechanisms within a cytokine-HPA axis feedback circuit model.

Authors+Show Affiliations

Department of Neurology, Technische Universität Dresden, Medizinische Fakultät Carl Gustav Carus, Germany. Electronic address: Simone.Kern@uniklinikum-dresden.de.Department of Psychology & Volen National Center for Complex Systems, Brandeis University, Waltham, MA, USA.Institute of Clinical Chemistry and Laboratory Medicine & Department of Medicine III, Technische Universität Dresden, Medizinische Fakultät Carl Gustav Carus, Germany.Department of Psychiatry & Psychotherapy, Technische Universität Dresden, Medizinische Fakultät Carl Gustav Carus, Germany.Department of Neurology, Technische Universität Dresden, Medizinische Fakultät Carl Gustav Carus, Germany.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24880115

Citation

Kern, Simone, et al. "Time Matters - Acute Stress Response and Glucocorticoid Sensitivity in Early Multiple Sclerosis." Brain, Behavior, and Immunity, vol. 41, 2014, pp. 82-9.
Kern S, Rohleder N, Eisenhofer G, et al. Time matters - acute stress response and glucocorticoid sensitivity in early multiple sclerosis. Brain Behav Immun. 2014;41:82-9.
Kern, S., Rohleder, N., Eisenhofer, G., Lange, J., & Ziemssen, T. (2014). Time matters - acute stress response and glucocorticoid sensitivity in early multiple sclerosis. Brain, Behavior, and Immunity, 41, pp. 82-9. doi:10.1016/j.bbi.2014.04.006.
Kern S, et al. Time Matters - Acute Stress Response and Glucocorticoid Sensitivity in Early Multiple Sclerosis. Brain Behav Immun. 2014;41:82-9. PubMed PMID: 24880115.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Time matters - acute stress response and glucocorticoid sensitivity in early multiple sclerosis. AU - Kern,Simone, AU - Rohleder,Nicolas, AU - Eisenhofer,Graeme, AU - Lange,Jan, AU - Ziemssen,Tjalf, Y1 - 2014/05/29/ PY - 2013/12/30/received PY - 2014/04/03/revised PY - 2014/04/13/accepted PY - 2014/6/1/entrez PY - 2014/6/1/pubmed PY - 2015/6/10/medline KW - Cortisol KW - Glucocorticoid sensitivity KW - Multiple sclerosis KW - Stress KW - TSST SP - 82 EP - 9 JF - Brain, behavior, and immunity JO - Brain Behav. Immun. VL - 41 N2 - OBJECTIVE: Psychosocial stress has frequently been associated with disease activity and acute exacerbations in multiple sclerosis (MS). Despite this well established finding, strikingly little is known about the acute hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal-medullary (SAM) stress response in MS. METHODS: Twenty-six early relapsing-remitting MS (RRMS) patients and seventeen age- and sex-matched healthy control subjects (CS) took part in the Trier Social Stress Test (TSST), a well validated psycho-social laboratory stress protocol. Repeated blood samples were analyzed for stress-related cortisol and catecholamine levels as well as for glucocorticoid sensitivity (GCS) of target immune cells. Chronic and acute stress appraisals were assessed by self-report measures. RESULTS: RRMS patients and CS did not differ in stress-related cortisol/catecholamine levels, GCS or stress appraisal in response to the TSST. However, cortisol release as well as GCS was strongly correlated with time since diagnosis but not with neurological disability. Patients with shorter disease duration (2-12 months) expressed a significantly higher cortisol stress response while MS patients with longer disease duration (14-36 months) showed a significantly diminished HPA response as well as lower post-stress GCS. DISCUSSION: There is evidence for a time-dependent variability in the HPA stress system with an increased cortisol stress response in the first year after diagnosis along with a more blunted HPA stress response and a diminished GCS in subsequent disease stages. Data underscore the highly dynamic nature of HPA axis regulation in the MS disease process, which could possibly relate to compensatory mechanisms within a cytokine-HPA axis feedback circuit model. SN - 1090-2139 UR - https://www.unboundmedicine.com/medline/citation/24880115/Time_matters___acute_stress_response_and_glucocorticoid_sensitivity_in_early_multiple_sclerosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0889-1591(14)00119-6 DB - PRIME DP - Unbound Medicine ER -