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      Dehydroepiandrosterone Response to the Adrenocorticotropin Test and the Combined Dexamethasone and Corticotropin-Releasing Hormone Test in Patients with Multiple Sclerosis

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          Basic and clinical research suggest that disturbed neuroendocrine function may be involved in the pathogenesis and course of autoimmune diseases including multiple sclerosis (MS). Dehydroepiandrosterone (DHEA) in this connection is of particular interest as it appears to have effects on the immune system. Moreover, DHEA levels are decreased in chronic inflammatory diseases. To further investigate the role of DHEA in MS, we administered the adrenocorticotropin (ACTH) stimulation test and the combined dexamethasone and corticotropin-releasing hormone (DEX-CRH) test to 24 patients with active MS (13 women, 11 men; age 39 ± 2 years, mean ± SEM; Expanded Disability Status Scale, EDSS score 4.4 ± 0.4, mean ± SEM; 12 with acute relapse, 12 with chronic progression) and to 18 healthy controls matched for age and sex (8 women, 10 men; age 37 ± 3 years). There were no statistically significant differences in the plasma cortisol response to ACTH between any groups. In the DEX-CRH test, plasma cortisol concentrations showed higher values before (DEX-pretreated) and after CRH stimulation in the MS patients than in the controls (AUC<sub>cortisol</sub> 738.3 ± 154.5 vs. 295.7 ± 55.8; p < 0.05), this finding was more pronounced in chronic progressive patients. DHEA concentrations were decreased in MS patients (AUC <sub>DHEA</sub> 14.4 ± 1.6 vs. 23 ± 2.4; p < 0.05) and cortisol/DHEA ratios were increased in the patients compared to the controls (p < 0.05). There was a positive correlation between the EDSS score and maximum cortisol/DHEA ratio (r = 0.45; p = 0.031). As with the hypothalamic-pituitary-adrenal axis system, our results suggest a dysfunction in the DHEA secretion in patients with MS.

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          Most cited references 6

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          The combined dexamethasone/CRH test: A refined laboratory test for psychiatric disorders

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            Hormones, peripherally activated prohormones and regulation of the Th1/Th2 balance.

            There is much interest in the factors that control the cytokine profile of T-helper (Th) lymphocytes, and attention has focused on feedback from the cytokines themselves. In general, Th1 cytokines promote Th1 activity and inhibit Th2 activity, and vice versa. Both Th1 and Th2 responses should therefore be stable. However, in vivo, many responses start predominantly as Th1 and then shift to Th2. Why do they do this? As discussed here, an important influence on this shift that has been largely ignored in in vitro work is the endocrine system.
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              Sex steroids, glucocorticoids, stress and autoimmunity


                Author and article information

                S. Karger AG
                December 1999
                24 December 1999
                : 70
                : 6
                : 431-438
                Max Planck Institute of Psychiatry, Munich, Germany
                54505 Neuroendocrinology 1999;70:431–438
                © 1999 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 4, References: 50, Pages: 8
                Corticotropin and Corticotropin-Releasing Hormone


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