Naloxone-mediated activation of the hypothalamic-pituitary-adrenal axis in Chronic Fatigue Syndrome (CFS)

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.


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.

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