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Naloxone-mediated activation of the hypothalamic–pituitary–adrenal axis in chronic fatigue syndrome

Published online by Cambridge University Press:  01 March 1998

L. V. SCOTT ,
F. BURNETT ,
S. MEDBAK  and
T. G. DINAN
L. V. SCOTT
Affiliation:
From the Departments of Psychological Medicine and Chemical Endocrinology, St Bartholomew's and the Royal London School of Medicine, London
F. BURNETT
Affiliation:
From the Departments of Psychological Medicine and Chemical Endocrinology, St Bartholomew's and the Royal London School of Medicine, London
S. MEDBAK
Affiliation:
From the Departments of Psychological Medicine and Chemical Endocrinology, St Bartholomew's and the Royal London School of Medicine, London
T. G. DINAN
Affiliation:
From the Departments of Psychological Medicine and Chemical Endocrinology, St Bartholomew's and the Royal London School of Medicine, London
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Abstract

Background. Opioidergic pathways have an inhibitory regulatory influence on the hypothalamic–pituitary–adrenal axis (HPA) in man. Previous studies have suggested impairment of pituitary–adrenal activation in chronic fatigue syndrome (CFS). We, therefore, decided to investigate the extent of opioid inhibition of HPA activity in CFS as a possible explanation for the reputed HPA hypofunctioning in patients with CFS.

Method. Thirteen patients with CFS, diagnosed according to CDC criteria, were compared with thirteen healthy subjects. Adrenocorticotropin (ACTH) and cortisol (CORT) responses were measured following the administration of the opiate antagonist naloxone.

Results. Baseline ACTH and cortisol levels did not differ between the two groups. The release of ACTH (but not cortisol) was significantly blunted in the CFS subjects compared with controls.

Conclusions. Naloxone mediated activation of the HPA is attenuated in CFS. Excessive opioid inhibition of the HPA is thus an unlikely explanation for the HPA dysregulation in this disorder.

Type
Research Article
Information
Psychological Medicine , Volume 28 , Issue 2 , March 1998 , pp. 285 - 293
Copyright
© 1998 Cambridge University Press

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