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Herbert Y. Meltzer, MD; Victor S. Fang, PhD
University of Chicago pritzker School of Medicine 950 E 59th St Chicago, IL 60637

Betty Jo Tricou, MD
Illinois State Psychiatric Institute 1601 Taylor St Chicago, IL 60612

Arch Gen Psychiatry. 1982;39(2):236.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—There has been considerable interest in the dexamethasone suppression test (DST) in the study of endogenous depression, or the melancholia variant thereof.¹ Approximately 40% to 60% of patients with depression fail to lower plasma cortisol levels to 5.0 µs/DL 8, 16, or 24 hours after a 1.0-mg dose of dexamethasone.^1-3 This has been taken as evidence of limbic system hyperfunction in them and has led to the suggestion that the DST should be used to validate clinical diagnosis and clarify nosological issues in depression.^1-3

Dexamethasone also normally suppresses levels of plasma prolactin in man and rats.^4,5 Evidence indicates that this effect is mainly at the pituitary level,^6,7 although the possibility that central mechanisms may also participate in the suppression by corticosteroids of prolactin secretions has not been ruled out.⁸ We hypothesized that depressed patients whose systems fail to suppress cortisol after receiving dexamethasone would also not show lower levels of plasma prolactin after receiving dexamethasone . . . [Full Text PDF of this Article]

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