کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6236699 1608208 2009 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Glucocorticoid receptor mediated negative feedback in chronic fatigue syndrome using the low dose (0.5 mg) dexamethasone suppression test
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی روانپزشکی و بهداشت روانی
پیش نمایش صفحه اول مقاله
Glucocorticoid receptor mediated negative feedback in chronic fatigue syndrome using the low dose (0.5 mg) dexamethasone suppression test
چکیده انگلیسی

BackgroundChronic fatigue syndrome (CFS) is associated with hypocortisolism, but it is not yet clear the extent to which enhanced negative feedback may underlie this finding.MethodsWe undertook a low-dose dexamethasone (0.5 mg) suppression test in 18 CFS patients and 20 matched, healthy controls. We measured salivary cortisol levels at 0800 h, 1200 h, 1600 h and 2000 h before and after the administration of 0.5 mg of dexamethasone.ResultsBasal cortisol output was raised in this group of CFS patients compared to controls. Overall, the percentage suppression following dexamethasone administration was no different between CFS (mean ± sem: 80.4 ± 4.4%) and controls (76.2 ± 4.9 %). However, the sub-group of patients with CFS and comorbid depression (n = 9) showed a significant hypersuppression of salivary cortisol in response to dexamethasone (89.0 ± 1.9%; p < 0.05 v controls).LimitationsThe sub-group analysis was on small numbers and should be considered preliminary. Dexamethasone probes only glucocorticoid medicated negative feedback but does not probe mineralocorticoid feedback, the other main physiological feedback mechanism.ConclusionWe found partial support for the hypothesis of enhanced negative feedback in CFS but only in patients with comorbid depression and also in the context of a sample of patients with elevated basal cortisol levels, which is an atypical finding in the literature.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Affective Disorders - Volume 112, Issues 1–3, January 2009, Pages 289-294
نویسندگان
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