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
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.
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.