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

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By Scott LV, Medbak S, Dinan TG • www.ProHealth.com • June 9, 1998


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.




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