The central mechanism of hypothalamic-pituitary-adrenocortical system hyperfunction in depressed patients

Hann Kuang Jiang, Jia Yi Wang, Jiann Chyun Lin

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)


While hypercortisolemia is commonly observed in depression, exactly where in the hypothalamic-pituitary-adrenocortical (H-P-A) axis this dysfunction arises remains undefined. In attempting to distinguish between central or peripheral locus of dysfunction, we studied in 12 patients (10 females, two males) with primary major depression and eight age-matched controls (six females, two males) in their adrenal cortisol response to infused adrenocorticotropic hormone (ACTH) (cosyntropin 0.05μg/kg bodyweight) while endogenous ACTH was suppressed with 1 mg of dexamethasone. Compared with the control group, pre-dexamethasone plasma baseline cortisol level was significantly higher in depressed patients while ACTH level remained normal. Post-dexamethasone responses of both hormones were greatly non-suppressed in the depressed group. Exogenous cosyntropin-elicited rise in plasma cortisol was significantly lower in depressed patients while the ACTH response was not significantly different. These findings suggest that an adrenal cortisol response to ACTH was significantly decreased during depression as compared with normals in Chinese depressed patients. Therefore, the central mechanism of hyperfunctioning H-P-A axis causing hypercortisolemia should be emphasized.

Original languageEnglish
Pages (from-to)227-234
Number of pages8
JournalPsychiatry and Clinical Neurosciences
Issue number2
Publication statusPublished - Apr 2000
Externally publishedYes


  • Hypercortisolemia
  • Hypothalamic-pituitary-adrenocortical function
  • Major depression

ASJC Scopus subject areas

  • Neuroscience(all)
  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health


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