BLUNTED ADRENOCORTICOTROPIN AND CORTISOL RESPONSES TO CORTICOTROPIN-RELEASING HORMONE STIMULATION IN CHRONIC-FATIGUE-SYNDROME

Hypofunctioning of the pituitary-adrenal axis has been suggested as th e pathophysiological basis for chronic fatigue syndrome (CFS). Blunted adrenocorticotropin (ACTH) responses but normal cortisol responses to exogenous corticotropin-releasing hormone (CRH), the main regulator o f this axis, have been previously demonstrated in CFS patients, some o f whom had a comorbid psychiatric disorder. We wished to re-examine CR H activation of this axis in CFS patients free from concurrent psychia tric illness. A sample of 14 patients with CDC-diagnosed CFS were comp ared with 14 healthy volunteers. ACTH and cortisol responses were meas ured following the administration of 100 mu g ovine CRH. Basal ACTH an d cortisol values did not differ between the two groups. The release o f 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 exo genous CRH stimulation may be due to an abnormality in CRH levels with a resultant alteration in pituitary CRH receptor sensitivity, or it m ay reflect a dysregulation of vasopressin or other factors involved in HPA regulation. A diminished output of neurotrophic ACTH, causing a r educed adrenocortical secretory reserve, inadequately compensated for by adrenoceptor upregulation, may explain the reduced cortisol product ion demonstrated in this study.