Blunted adrenocorticotropin & cortisol responses to corticotropin-releasing hormone stimulation in Chronic Fatigue Syndrome (CFS)

Hypofunctioning of the pituitary-adrenal axis has been

suggested as the pathophysiological basis for chronic fatigue

syndrome (CFS). Blunted adrenocorticotropin (ACTH) responses

but normal cortisol responses to exogenous

corticotropin-releasing hormone (CRH), the main regulator of

this axis, have been previously demonstrated in CFS patients,

some of whom had a comorbid psychiatric disorder. We wished to

re-examine CRH activation of this axis in CFS patients free

from concurrent psychiatric illness. A sample of 14 patients

with CDC-diagnosed CFS were compared with 14 healthy

volunteers. ACTH and cortisol responses were measured

following the administration of 100 microg ovine CRH. Basal

ACTH and cortisol values did not differ between the two

groups. The release of ACTH was significantly attenuated in

the CFS group (P < 0.005), as was the release of cortisol (P <
0.05). The blunted response of ACTH to exogenous CRH

stimulation may be due to an abnormality in CRH levels with a

resultant alteration in pituitary CRH receptor sensitivity, or

it may reflect a dysregulation of vasopressin or other factors

involved in HPA regulation. A diminished output of

neurotrophic ACTH, causing a reduced adrenocortical secretory

reserve, inadequately compensated for by adrenoceptor

upregulation, may explain the reduced cortisol production

demonstrated in this study.

1 Star2 Stars3 Stars4 Stars5 Stars (25 votes, average: 3.08 out of 5)

1 Star2 Stars3 Stars4 Stars5 Stars (25 votes, average: 3.08 out of 5)

Leave a Reply