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Victor S. Fang, PhD; Hann-Kuang Jiang, MD; Robert P. Rose, MD, PhD; Daniel J. Luchins, MD
Departments of Medicine and Psychiatry The University of Chicago 5841 S Maryland Ave Chicago, IL 60637 Illinois State Psychiatric Institute 1601 W Taylor St Chicago, IL 60612

Arch Gen Psychiatry. 1988;45(10):964-965.

	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.—

In the March 1987 issue of the ARCHIVES, Jaeckle et al¹ reported their findings confirming that the adrenal sensitivity to exogenous corticotropin (ACTH) was enhanced in patients with major depressive disorder. Based on their findings, they further suggested that this adrenal abnormality might be related pathophysiologically to the resistance of cortisol secretion to dexamethasone suppression. We want to contest both their confirmation and suggestion, as the article contains several questionable statements.

A major problem was the use of an intravenous bolus of a supraphysiological dose of ACTH ^1-24 (cosyntropin) to test the adrenal sensitivity. In our previous studies,² the dose of cosyntropin to mimic a maximum physiologically stimulated ACTH level, such as that seen during insulin hypoglycemia in normal subjects, was on the order of 0.02 to 0.05 µg/kg. A dose of 250 µg of cosyntropin is 60 to 70 times that in an . . . [Full Text PDF of this Article]

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