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October 1988

Adrenal Gland in Major Depression: Enlarged Capacity or Enhanced Sensitivity?-Reply

Author Affiliations

University of Wisconsin Medical School Department of Psychiatry 600 Highland Ave Madison, WI 53792
Department of Psychiatry St Francis Medical Center La Crosse, WI 54601
University of Iowa Department of Psychiatry 500 Newton Rd Iowa City, IA 52242
University of Michigan Mental Health Research Institute 205 Washtenaw Pl Ann Arbor, MI 48109

Arch Gen Psychiatry. 1988;45(10):965-966. doi:10.1001/archpsyc.1988.01800340093018

Reply.—  Dr Fang and his collaborators have raised several points regarding the methods and conclusions in our report regarding enhanced adrenocortical secretory responsiveness to exogenous cosyntropin stimulation in patients with major depression. First, they suggest that our use of a supraphysiologic dose of cosyntropin (250 μg by intravenous bolus) overloads adrenocortical secretory capacity and is therefore a better test of glandular secretory capacity than of sensitivity to ACTH stimulation. We could not agree more with their interpretation. We should have interpreted our study as suggesting that patients with major depression have either an increased adrenocortical secretory pool of cortisol or an increased capacity to release cortisol from the secretory pool given maximal ACTH drive to adrenocortical secretion. The recent finding of Amsterdam and associates1 that patients with major depression have increased adrenal volume measured by computed tomography would be consistent with increased adrenocortical secretory capacity. Obviously, adrenocortical

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