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Corticotropin, Cortisol and β‐endorphin responses to the human corticotropin‐releasing hormone during melancholia and after unilateral electroconvulsive therapy
Author(s) -
Dored G.,
Stefansson S.,
D'Elia G.,
Kågedal B.,
Karlberg E.,
Ekman R.
Publication year - 1990
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.1600-0447.1990.tb03053.x
Subject(s) - hypercortisolemia , medicine , corticotropin releasing hormone , electroconvulsive therapy , endocrinology , psychology , melancholia , stimulation , depression (economics) , hydrocortisone , adrenocorticotropic hormone , hormone , dexamethasone , electroconvulsive shock , economics , macroeconomics
Previous research in neuroendocrinology has evidenced that hyperactivity of the hypothalamic‐pituitary‐adrenal axis (HPA) depends on hypersecretion of corticotropin‐releasing hormone (CRH). The aim of this study was to investigate the activity of HPA before and after recovery in depressed patients treated with electroconvulsive therapy (ECT). An h‐CRH‐stimulation test was performed on 2 occasions with examination of the HPA axis before ECT treatment during episodes of major depressive disorders with melancholia, and during the recovery phase after treatment. The results showed that patients during depression had significantly higher plasma levels of cortisol at 15 and 30 min after h‐CRH‐administration than after recovery. Depressed patients had significantly higher plasma levels of β‐endorphin 30 min after h‐CRH‐stimulation. The results are in agreement with previous studies, which have shown hypercortisolemia during depression. A possible hypersecretion of CRH may explain the effect on cortisol and β‐endorphin. No significant differences were found between cumulative responses of corticotropin, cortisol and β‐endorphin, calculated as the areas under the concentration curves.