Pathophysiology of hypercortisolism in depression.

Pathophysiology of hypercortisolism in depression. Research Abstract Details 

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Pathophysiology of hypercortisolism in depression. Abstract Text:

B J Carroll,F Cassidy,D Naftolowitz,N E Tatham,W H Wilson,A Iranmanesh,P Y Liu,J D Veldhuis,B J Carroll,F Cassidy,D Naftolowitz,N E Tatham,W H Wilson,A Iranmanesh,P Y Liu,J D Veldhuis,

OBJECTIVE: The mechanisms mediating hypercortisolemia in depression remain controversial. Adopting the biomarker strategy, we studied adrenocorticotropin (ACTH) and cortisol dynamics in hypercortisolemic and non-hypercortisolemic depressed in-patients, and in normal volunteers. METHOD: Deconvolution analysis of 24-h pulsatile secretion, approximate entropy (ApEn) estimation of secretory regularity, cross-ApEn quantitation of forward and reverse ACTH-cortisol synchrony, and cosine regression of 24-h rhythmicity. RESULTS: Hypercortisolemia was strongly associated with melancholic and psychotic depressive subtypes. Hypercortisolemic patients had elevated ACTH and cortisol secretion, mediated chiefly by increased burst masses. Basal ACTH secretion was increased, ACTH half-life was reduced, and mean 24-h ACTH concentration was normal. Cortisol secretion was increased in a highly irregular pattern (high ApEn), with high ACTH --> cortisol cross-ApEn (impaired feedforward coupling). Cortisol-mediated feedback on the secretory pattern of ACTH was normal. Hypercortisolemic depressed patients had normal programming of the central hypothalamo-pituitary-adrenal (HPA) axis pulse generator: ACTH pulse frequency, cortisol pulse frequency, circadian acrophases, and ApEn of ACTH secretion were normal. Responsiveness of the adrenal cortex to endogenous ACTH was normal. Non-hypercortisolemic patients resembled hypercortisolemic patients on ACTH regulatory parameters but had low total cortisol secretion. CONCLUSION: Increased ACTH secretion occurs in depressed in-patients regardless of cortisolemic status, confirming central HPA axis overdrive in severe depression. Depressive hypercortisolemia results from an additional change in the adrenal cortex that causes ACTH-independent, disorderly basal cortisol release, a sign of physiological stress in melancholic/psychotic depression.

Pathophysiology of hypercortisolism in depression. Publishing Authors By Initials

BJ Carroll,F Cassidy,D Naftolowitz,NE Tatham,WH Wilson,A Iranmanesh,PY Liu,JD Veldhuis,BJ Carroll,F Cassidy,D Naftolowitz,NE Tatham,WH Wilson,A Iranmanesh,PY Liu,JD Veldhuis,

For similar endocrine system: endocrine glands: pituitary-adrenal system research abstracts see: endocrine system: endocrine glands: pituitary-adrenal system research

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MEDLINE DATE:

Pathophysiology of hypercortisolism in depression. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Acta psychiatrica Scandinavica. Supplementum

VOLUME:

Page Numbers: 90-103

Journal Abbreviation:

ISSN: 0065-1591

DAY: 3

MONTH: 12

YEAR: 2007

Pathophysiology of hypercortisolism in depression. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 370365

Pathophysiology of hypercortisolism in depression. Keywords Mesh Terms:

KEYWORDS: Pituitary-Adrenal System

MESH TERMS: physiopathology

Chemical & Substance for Abstract: Pathophysiology of hypercortisolism in depression. Information

Substance Name: Adrenocorticotropic Hormone

Registry Number: 9002-60-2

Grant and Affiliation Information for Pathophysiology of hypercortisolism in depression.

AFFILIATION: Pacific Behavioral Research Foundation, Carmel, CA, USA. bcarroll@redshift.com

Country: Denmark

AGENCY: United States NIDDK

GRANT: R01 DK060717

ACRONYM: DK

MEDLINETA: Acta Psychiatr Scand Suppl

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