Background. Opioidergic pathways have an inhibitory regulatory
influence on the hypothalamic–pituitary–adrenal axis (HPA)
man. Previous studies have suggested impairment of pituitary–adrenal
activation in chronic fatigue syndrome (CFS). We, therefore, decided to
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
criteria, were compared with
thirteen healthy subjects. Adrenocorticotropin (ACTH) and cortisol (CORT)
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
Conclusions. Naloxone mediated activation of the HPA is attenuated in CFS.
inhibition of the HPA is thus an unlikely explanation for the
HPA dysregulation in this disorder.