Pathophysiology of Male Hypogonadism Associated with Endogenous Hyperestrogenism — Evidence for Dual Defects in the Gonadal Axis

Authors

Johannes D. Veldhuis, University of Virginia
James R. Sower, National Institutes of Health
Alan D. Rogol, University of Virginia
Frederick A. Klein, Medical College of Virginia
Norman Miller, University of Virginia
Maria L. Dufau, National Institutes of Health

Document Type

Article

Original Publication Date

1985

Journal/Book/Conference Title

The New England Journal of Medicine

Volume

312

DOI of Original Publication

10.1056/NEJM198505233122107

Comments

Originally Published at http://dx.doi.org/10.1056/NEJM198505233122107

Date of Submission

January 2015

Abstract

FEMINIZING tumors of the adrenal cortex are associated with symptoms that presumably reflect the combined effects of estrogen excess and androgen deficiency — gynecomastia, diminished libido, attenuated potency, and testicular and prostatic atrophy.1 2 3 4 5 Although such tumors are extremely rare, they provide a unique opportunity to appraise the nature of endogenous estrogen action on the gonadal axis in men. In principle, the pathophysiologic effects of estrogen hypersecretion could be expressed at the level of either the Leydig cell or the hypothalamic–pituitary axis (or both), with consequent suppression of androgen production. In the present studies, we investigated the endocrine consequences of reversible endogenous estrogen excess in a patient with a surgically resectable feminizing adrenal cortical tumor.

Rights

From The New England Journal of Medicine, Veldhuis, J. D., Sowers, J. R., Rogol, A. D. et al., Pathophysiology of Male Hypogonadism Associated with Endogenous Hyperestrogenism — Evidence for Dual Defects in the Gonadal Axis, Vol. 312, Page 1371, Copyright © 1985 Massachusetts Medical Society. Reprinted with permission.

Is Part Of

VCU Surgery Publications