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Endocrine responses to growth hormone‐releasing hormone, thyrotropin‐releasing hormone and corticotropin‐releasing hormone in depression
Author(s) -
Lesch K.P.,
Müller U.,
Rupprecht R.,
Kruse K.,
Schulte H. M.
Publication year - 1989
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1111/j.1600-0447.1989.tb10308.x
Subject(s) - medicine , endocrinology , thyrotropin releasing hormone , hormone , growth hormone–releasing hormone , somatotropic cell , corticotropin releasing hormone , adrenocorticotropic hormone , hypothalamic–pituitary–thyroid axis , psychology , pituitary gland , growth hormone , triiodothyronine
– To explore and to compare hypothalamic‐pituitary‐somatotropic (HPS), hypothalamic‐pituitary‐thyroid (HPT) and hypothalamic‐pituitary‐adreno‐cortical (HPA) axis function in depression, 30 subjects (15 patients with a major depressive episode and individually matched controls) received 50μg growth hormone‐releasing hormone‐44 amide at 9:00, 200 μg thyrotropin‐releasing hormone (TRH) at 9:00 and 100 μg human corticotropin‐releasing hormone (CRH) at 18:00 on consecutive days as an i.v. bolus dose. Compared with controls, depressed patients showed blunted growth hormone (GH) responses to GHRH, decreased TRH‐induced thyrotropin (TSH) release and reduced corticotropin (ACTH) but normal cortisol secretion following CRH. ACTH secretion following CRH and TRH‐induced TSH release were positively correlated across depressed patients and controls but no significant correlations between GH responses to GHRH and TRH‐induced TSH release or ACTH and cortisol secretion following CRH administration were demonstrated. Our findings suggest that altered HPT and HPA axis function associated with depression are triggered by factors that are at least partly different from those that cause HPS system dysfunction. We conclude that the pathophysiological process resulting in aberrant neuroendocrine secretory dynamics associated with depression may primarily occur at a suprapituitary site, and that HPS, HPT and HPA axis dysfunction may be precipitated by complex central and peripheral regulatory mechanisms involving largely independent factors.