24-hour pituitary and adrenal hormone profiles in chronic fatigue syndrome.
OBJECTIVE
Disturbances of neuroendocrine function, particularly the hypothalamo-pituitary-adrenal (HPA) axis, have been implicated in the pathophysiology of chronic fatigue syndrome (CFS). However, few studies have attempted to measure blood levels of pituitary or adrenal hormones across a whole 24-hour period in CFS, and those that did so have used infrequent sampling periods. Our aim was to assess 24-hour pituitary and adrenal function using frequent blood sampling.


METHODS
We recruited 15 medication-free patients with CFS without comorbid psychiatric disorder and 10 healthy control subjects. Blood samples were collected over 24 hours and assayed for cortisol, corticotropin (ACTH), growth hormone (GH), and prolactin (PRL) levels on an hourly basis during daytime hours (10 am to 10 pm) and every 15 minutes thereafter (10 pm to 10 am).


RESULTS
Repeated-measures analyses of variance were undertaken using hormone levels averaged over 2-hour blocks to smooth curves by reducing the influence of sample timing relative to secretory burst. For ACTH, there was both a main effect of group, suggesting reduced mean ACTH secretion in patients with CFS over the whole monitoring period, and a group-by-time interaction, suggesting a differential pattern of ACTH release. Post hoc analysis showed reduced ACTH levels in CFS during the 8 am to 10 am period. In contrast, there were no significant abnormalities in the levels of cortisol, GH, and PRL in patients with CFS over the full cycle compared with control subjects. Cosinor analysis found no differences in the cortisol circadian rhythm parameters, but the ACTH rhythm did differ, patients with CFS showing an earlier acrophase.


CONCLUSIONS
Patients with CFS demonstrated subtle alterations in HPA axis activity characterized by reduced ACTH over a full circadian cycle and reduced levels during the usual morning physiological peak ACTH secretion. This provides further evidence of subtle dysregulation of the HPA axis in CFS. Whether this dysregulation is a primary feature of the illness or instead represents a biologic effect secondary to having the illness itself remains unclear.
Di Giorgio
Annabella
A
Department of Neurological and Psychiatric Services, University of Bari, Bari, Italy
Hudson
Marina
M
Jerjes
Walid
W
Cleare
Anthony J
AJ
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D021081:Chronobiology Disorders / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D015673:Fatigue Syndrome, Chronic / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D005260:Female; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010908:Pituitary Hormones, Anterior / Q000097:blood*; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D011388:Prolactin / Q000097:blood
D010908:Pituitary Hormones, Anterior; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D013006:Growth Hormone; D006854:Hydrocortisone