Considerable research over the past 20 years has documented alterations in the hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-adrenal (HPA) axes in patients with affective disorders, especially depression. Although plasma concentrations of thyroid hormones (T3, T4) are generally unaltered in patients with major depression, plasma thyroid stimulating hormone (TSH) responses after intravenous administration of thyrotropin-releasing hormone (TRH) are blunted in approximately 25% and abnormally elevated in approximately 15% of depressed patients. Data are presented supporting the hypothesis that TSH blunting may be secondary to central nervous system (CNS) hypersecretion of TRH, and that the enhanced TSH response may be secondary to subclinical hypothyroidism associated with autoimmune thyroiditis. The HPA axis has received considerable scrutiny in depressed patients and there is universal agreement that 50% to 75% of patients with major depression exhibit hyperactivity of the HPA axis characterized by hypercortisolemia, ACTH hypersecretion, and nonsuppression of plasma cortisol concentrations after administration of the synthetic glucocorticoid dexamethasone. Evidence is presented that hypersecretion of corticotropin-releasing factor (CRF) contributes, at least in part, to HPA axis hyperactivity and perhaps to certain of the signs and symptoms of major depression.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Clinical Psychiatry|
|Issue number||5 SUPPL.|
|State||Published - Jan 1 1989|
ASJC Scopus subject areas
- Psychiatry and Mental health