The oCRH stimulation test before and after clinical recovery from depression.
A substantial body of data suggests that excessive cortisol secretion in depression may result from a dysregulation at several sites within the hypothalamic-pituitary-adrenocortical (HPA) axis. These alterations in regulatory mechanisms are thought to be the result of a hypothalamic 'overdrive' of corticotropin-releasing hormone (CRH). Previous studies have demonstrated a diminished adrenocorticotropin (ACTH) secretory response, as well as a heightened adrenocortical responsiveness after ovine-CRH administration in depressed patients. In the present investigation, we examined pituitary and adrenocortical responsiveness after an ovine-CRH stimulation test before and during clinical recovery in seven depressed patients. Cumulative ACTH responses increased significantly during clinical recovery (P = 0.014). Paradoxically, maximum and peak cortisol responses increased after recovery, suggesting that heightened adrenocortical responsiveness to ACTH during depression may take longer to 'normalize' than abnormal pituitary responsiveness to ovine-CRH stimulation.
Amsterdam
J D
JD
Department of Psychiatry, School of Medicine, University of Pennsylvania, Philadelphia 19104.
Maislin
G
G
Winokur
A
A
Berwish
N
N
Kling
M
M
Gold
P
P
D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000328:Adult; D000928:Antidepressive Agents / Q000627:therapeutic use*; D003346:Corticotropin-Releasing Hormone; D003866:Depressive Disorder / Q000097:blood / Q000188:drug therapy* / Q000523:psychology; D003907:Dexamethasone; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011569:Psychiatric Status Rating Scales
D000928:Antidepressive Agents; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D006854:Hydrocortisone