Brief report Glucocorticoid receptor mediated negative feedback in chronic fatigue syndrome using the low dose (0.5 mg) dexamethasone suppression test Andrew Papadopoulos a, b , Marcel Ebrecht c , Amanda D.L. Roberts b, d , Lucia Poon a, b , Nicolas Rohleder e , Anthony J. Cleare a, b, d, ⁎ a King's College London, Institute of Psychiatry, Section of Neurobiology of Mood Disorders, Division of Psychological Medicine, London SE5 8AF, United Kingdom b National Affective Disorders Unit, Bethlem Royal and Maudsley Hospitals, London, United Kingdom c King's College London, Department of Psychology, Guy's, Kings and St Thomas' School of Medicine, London SE1 9RT, United Kingdom d Chronic Fatigue Syndrome Unit, King's College Hospital, London, United Kingdom e Biopsychology Unit, Technical University of Dresden, Dresden, Germany Received 13 December 2007; received in revised form 2 May 2008; accepted 3 May 2008 Available online 24 June 2008 Abstract 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 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. 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 b 0.05 v controls). Limitations: The 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. 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 an atypical finding in the literature. © 2008 Elsevier B.V. All rights reserved. Keywords: Chronic fatigue syndrome; HPA axis; Dexamethasone suppression test; Glucocorticoid receptor; Negative feedback; Neuroendocrinology Journal of Affective Disorders 112 (2009) 289 – 294 www.elsevier.com/locate/jad ⁎ Corresponding author. Department of Psychological Medicine, Box P074, The Institute of Psychiatry, 103 Denmark Hill, London SE5 8AF, United Kingdom. Tel.: +20 7848 5130; fax: +20 7848 0783. E-mail address: a.cleare@iop.kcl.ac.uk (A.J. Cleare). 0165-0327/$ - see front matter © 2008 Elsevier B.V. All rights reserved. doi:10.1016/j.jad.2008.05.001