PITUITARY AND ADRENAL-HORMONE RESPONSIVENESS TO SYNACTHEN IN MELANCHOLIC SUBJECTS VERSUS SUBJECTS WITH MINOR DEPRESSION

Citation
M. Maes et al., PITUITARY AND ADRENAL-HORMONE RESPONSIVENESS TO SYNACTHEN IN MELANCHOLIC SUBJECTS VERSUS SUBJECTS WITH MINOR DEPRESSION, Biological psychiatry, 33(8-9), 1993, pp. 624-629
Citations number
26
Categorie Soggetti
Psychiatry
Journal title
ISSN journal
00063223
Volume
33
Issue
8-9
Year of publication
1993
Pages
624 - 629
Database
ISI
SICI code
0006-3223(1993)33:8-9<624:PAARTS>2.0.ZU;2-D
Abstract
Increased adrenal cortex responsiveness to adrenocorticotropic hormone (ACTH) has been suggested to contribute to increased cortisol secreti on in dexamethasone nonsuppression and melancholia. To further examine this hypothesis, the following variables were examined in 68 patients with unipolar depression (minor, n = 24; simple major, n = 25; melanc holic, n = 19): basal or post-Synacthen [ACTH(1-24), 250 mug IV] intac t ACTH(1-39), beta-endorphin/beta-lipotropin, cortisol, and androstene dione concentrations, as well as the post;dexamethasone (DST) plasma A CTH(1-39) and cortisol values. Melancholic subjects showed significant ly higher baseline ACTH(1-39), beta-endorphin/beta-lipotropin, and and rostenedione values compared with subjects with minor depression. No s ignificant differences in post-Synacthen cortisol or androstenedione s ecretion between any of the groups or between [ACTH(1-39) or cortisol] DST nonsuppressors and suppressors were found. No significant relatio nships between DST and ACTH test results were observed. Abnormally inc reased post-DST cortisol values in melancholic subjects were highly pr edicted (>68% of the variance) by post-DST intact ACTH levels. ACTH(1- 39) values were significantly lower after Synacthen administration in melancholic subjects than in subjects with minor depression. These res ults are not consistent with the hypothesis that melancholia is charac terized by an increased adrenocortical responsivity to exogenous ACTH compared with minor depression or that DST nonsuppression is due to ad renal hyperresponsiveness.