Tag: naloxone

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

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.

 

Source: Scott LV, Burnett F, Medbak S, Dinan TG. Naloxone-mediated activation of the hypothalamic-pituitary-adrenal axis in chronic fatigue syndrome. Psychol Med. 1998 Mar;28(2):285-93. http://www.ncbi.nlm.nih.gov/pubmed/9572086

 

Naloxone-reversible monocyte dysfunction in patients with chronic fatigue syndrome

Abstract:

We studied monocyte function in 35 consecutive patients with chronic fatigue syndrome (CFS) and 25 healthy controls. Eighty-five per cent of the patients showed monocyte dysfunction characterized by marked reduction in the number of monocytes displaying immunoreactive cytoskeletal vimentin filaments, a low phagocytosis index, and a reduced expression of HLA-DR antigens. These values increased dramatically after incubation of the patients’ monocytes with the opioid antagonist naloxone.

Other immunological abnormalities also noted in the patients were low lymphocyte blastogenesis and diminished numbers of monocytes displaying receptors for Fc of IgG (FcR) and C3b (CR1). These findings suggest that an increased opioid activity acting through a classical receptor mechanism is active on monocytes from a high proportion of patients with CFS and that this represents a novel example of immunomodulation by opioid peptides in human disease.

We suggest that endogenous opioids are involved in the pathogenesis of the chronic fatigue syndrome.

 

Source: Prieto J, Subirá ML, Castilla A, Serrano M. Naloxone-reversible monocyte dysfunction in patients with chronic fatigue syndrome. Scand J Immunol. 1989 Jul;30(1):13-20. http://www.ncbi.nlm.nih.gov/pubmed/2526966