Chronic fatigue syndrome and the endocrine system

Abstract

Studies of the endocrine system, particularly the hypothalamic-pituitary-adrenal axis, in chronic fatigue syndrome are reviewed. Basal plasma cortisol concentrations have been found to be lower than in healthy control subjects in some but not all studies. The adrenocorticotropic hormone (ACTH) release induced by corticotropin-releasing hormone (CRH) is less than in control subjects and this has been interpreted to mean that hypothalamic secretion of CRH in patients with chronic fatigue syndrome is diminished. The response of serum dehydroepiandrosterone (DHEA) to ACTH in chronic fatigue syndrome patients was reduced compared with the response in normal subjects. The relationship of cortisol response to ACTH with respect to the time of sampling, sleep-wake cycles, sleep deprivation, physical inactivity, and comorbid conditions such as depression has not been fully evaluated. Growth hormone responses to insulin-induced hypoglycemia were also less than in normal controls. Hydrocortisone replacement, especially in small doses, 5 to 10 mg/day, was effective in reducing the expression of fatigue in short-term studies. Supplemental fludrocortisone was not beneficial in ameliorating symptoms in the chronic fatigue syndrome.