TY - JOUR
T1 - Glucocorticoid receptor mediated negative feedback in chronic fatigue syndrome using the low dose (0.5 mg) dexamethasone suppression test
AU - Papadopoulos, Andrew
AU - Ebrecht, Marcel
AU - Roberts, Amanda D L
AU - Poon, Lucia
AU - Rohleder, Nicolas
AU - Cleare, Anthony J
PY - 2009/1
Y1 - 2009/1
N2 - Background: Chronic fatigue syndrome (CFS) is associated with hypocortisolism, but it is not yet clear the extent to which enhanced negative feedback may underlie this finding.
Methods: We undertook a low-dose dexamethasone (0.5 mg) suppression test in 19 CFS patients and 20 matched, healthy controls. We measured salivary cortisol levels at 0800 h, 1200 h, 1600 11 and 2000 h before and after the administration of 0.5 mg of dexamethasone.
Results: Basal 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).
Limitations: The sub-group analysis was oil 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.
Conclusion: We 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 ail atypical finding in the literature. (C) 2008 Elsevier B.V. All rights reserved.
AB - Background: Chronic fatigue syndrome (CFS) is associated with hypocortisolism, but it is not yet clear the extent to which enhanced negative feedback may underlie this finding.
Methods: We undertook a low-dose dexamethasone (0.5 mg) suppression test in 19 CFS patients and 20 matched, healthy controls. We measured salivary cortisol levels at 0800 h, 1200 h, 1600 11 and 2000 h before and after the administration of 0.5 mg of dexamethasone.
Results: Basal 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).
Limitations: The sub-group analysis was oil 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.
Conclusion: We 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 ail atypical finding in the literature. (C) 2008 Elsevier B.V. All rights reserved.
U2 - 10.1016/j.jad.2008.05.001
DO - 10.1016/j.jad.2008.05.001
M3 - Article
C2 - 18573538
SN - 1573-2517
VL - 112
SP - 289
EP - 294
JO - Journal of Affective Disorders
JF - Journal of Affective Disorders
IS - 1-3
ER -