Growth hormone (GH) and prolactin responses after GH-releasing hormone in major depressive disorder: Relationship to somatomedin C levels and dexamethasone suppressibility of cortisol

1988 ◽  
Vol 13 (3) ◽  
pp. 255-263 ◽  
Author(s):  
K Lesch
Keyword(s):  
Growth Hormone ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Major Depressive ◽  
Somatomedin C ◽  
Releasing Hormone

Abnormal responsiveness of growth hormone to human corticotropin-releasing hormone in major depressive disorder

1988 ◽  
Vol 14 (3) ◽  
pp. 245-250 ◽  
Author(s):  
Klaus-Peter Lesch ◽  
Gerd Laux ◽  
Heinrich M. Schulte ◽  
Hans Pfüller ◽  
Helmut Beckmann
Keyword(s):  
Growth Hormone ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Corticotropin Releasing Hormone ◽  
Major Depressive ◽  
Releasing Hormone

The Effect of Desipramine upon Central Adrenergic Function in Depressed Patients

1982 ◽  
Vol 141 (4) ◽  
pp. 372-376 ◽  
Author(s):  
Ilana B. Glass ◽  
Stuart A. Checkley ◽  
Eric Shur ◽  
Sheila Dawling
Keyword(s):  
Growth Hormone ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Diagnostic Criteria ◽  
Statistical Significance ◽  
Adaptive Change ◽  
The Other ◽  
Major Depressive ◽  
Uptake Of Noradrenaline ◽  
Drug Free

SummaryEleven drug free patients meeting Research Diagnostic Criteria for Major Depressive Disorder have been treated with desipramine and given a clonidine infusion after 0, 1 and 3 weeks of treatment. The sedative and hypotensive effects of clonidine were significantly inhibited after three weeks of treatment with desipramine: a similar interaction was seen after one week of treatment although this just failed to reach statistical significance. The growth hormone (GH) response to clonidine was initially impaired, but increased significantly after one week of treatment. A significant reduction in the GH response occurred during the second and third weeks of treatment with desipramine. This last finding is interpreted as evidence of adaptive change of α2 adrenoceptors: the other changes can be explained by the known ability of desipramine to block the re-uptake of noradrenaline.

scholarly journals Growth Hormone Secretion in Children and Adolescents at High Risk for Major Depressive Disorder

2000 ◽  
Vol 57 (9) ◽  
pp. 867 ◽  
Author(s):  
Boris Birmaher ◽  
Ronald E. Dahl ◽  
Douglas E. Williamson ◽  
James M. Perel ◽  
David A. Brent ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Major Depressive Disorder ◽  
High Risk ◽  
Depressive Disorder ◽  
Children And Adolescents ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Major Depressive

Endocrine and behavioural responses to methylphenidate in depression

1986 ◽  
Vol 16 (3) ◽  
pp. 531-540 ◽  
Author(s):  
Peter R. Joyce ◽  
Richard A. Donald ◽  
M. Gary Nicholls ◽  
John H. Livesey ◽  
Robyn M. Abbott
Keyword(s):  
Growth Hormone ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Dexamethasone Suppression Test ◽  
Cortisol Response ◽  
Major Depressive ◽  
Behavioural Responses ◽  
Baseline Cortisol ◽  
Suppression Test ◽  
Dexamethasone Suppression

SynopsisTwenty patients with a major depressive disorder and 20 control subjects were subjected to a 1 mg dexamethasone suppression test (DST) and a challenge with intravenous (IV) methylphenidate (MP)(0·3 mg/kg). None of the controls, but 9 depressives, were DST non-suppressors. Among the depressives there were correlations between DST-cortisol and baseline (4 p.m.) levels of cortisol, growth hormone, prolactin and adrenaline. Compared with the controls the depressives had a decreased cortisol response and an enhanced adrenaline response to the MP challenge. The decreased cortisol response was not related to either DST-cortisol or baseline cortisol, but was correlated with the mood response to MP.

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