Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome

被引:14
作者
Gaab, J [1 ]
Rohleder, N [1 ]
Heitz, V [1 ]
Schad, T [1 ]
Engert, V [1 ]
Schürmeyer, TH [1 ]
Ehlert, U [1 ]
机构
[1] Univ Trier, Ctr Psychobiol & Psychosomat Res, Trier, Germany
来源
ACTA NEUROPSYCHIATRICA | 2003年 / 15卷 / 04期
关键词
ACTH; chronic fatigue syndrome; cortisol; dexa-methasone; glucocorticoid sensitivity; HPA axis; interleukin-6; psychosocial stress; tumor necrosis factor-alpha;
D O I
10.1034/j.1601-5215.2003.00033.x
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Objective: Alterations of the immune-neuroendocrine interplay have been described in chronic fatigue syndrome (CFS). Employing a recently developed method, the study set out to investigate whether patients with CFS have an altered sensitivity to glucocorticolds (GCs) when under stress. Methods: A total of 21 CFS patients and 20 healthy age- and gender-matched controls underwent a standardized psychosocial stress test (Trier Social Stress Test, TSST). Salivary and plasma cortisol levels were measured repeatedly following exposure to the stressor. GC sensitivity was assessed in vitro by dexamethasone inhibition of lipopolysaccharide-stimulated production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNC-alpha). Results: Cortisol responses following the TSST did not differ significantly between CFS patients and healthy controls. GC sensitivity differed significantly between CFS patients and healthy controls, with CFS patients showing a greater sensitivity towards GCs (TNF-alpha: F-1/39 = 7.32, P = 0.01; IL-6: F-1/39 = 9.73, P = 0.004). Conclusion: Consistent with recent evidence, CFS patients are characterized by an enhanced sensitivity to glucocorticoids. The implications for secondary processes, such as the regulatory influence of glucocorticoids on immune processes, are discussed.
引用
收藏
页码:184 / 191
页数:8
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