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Pathophysiology of Spironolactone-Induced Gynecomastia

LESLIE I. ROSE, M.D., F.A.C.P.; RICHARD H. UNDERWOOD, Ph.D.; STEPHEN R. NEWMARK, M.D., F.A.C.P.; ELDAD S. KISCH, M.D.; and GORDON H. WILLIAMS, M.D., F.A.C.P.
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Grant support: in part by a grant from the John A. Hartford Foundation and a contract from Medcom Inc. The clinical studies were done at the Clinical Research Center supported by Grant #RR0088 from the Research Resources Division, National Institutes of Health.

▸Requests for reprints should be addressed to Gordon H. Williams, M.D.; Endocrinology-Hypertension Unit, Department of Medicine, Peter Bent Brigham Hospital; Boston, MA 02115.


Boston, Massachusetts


Ann Intern Med. 1977;87(4):398-403. doi:10.7326/0003-4819-87-4-398
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Peripheral blood levels of testosterone, estradiol, luteinizing hormone, and follicle-stimulating hormone and the metabolic clearance rates of testosterone and estradiol, as well as the peripheral conversion of testosterone into estradiol, were measured in 16 patients with hypertension. Six of these patients were treated with spironolactone and developed gynecomastia. The other 10 patients served as control subjects. The blood testosterone level in the spironolactone-treated group (2.7 ± 0.5 ng/ml) was significantly less (P < 0.02) than in the control group (4.4 ± 0.4 ng/ml). On the other hand, blood estradiol levels in the spironolactone group (30 ± 4 pg/ml) were significantly greater (P < 0.01) than in the control group (13 ± 2 pg/ml). These changes were primarily due to significant increases in the metabolic clearance rate of testosterone (P < 0.02) and in the rate of peripheral conversion of testosterone into estradiol (P < 0.001) in the spironolactone-treated group. Thus, spironolactone does alter the peripheral metabolism of testosterone resulting in changes in the ratio of testosterone to estradiol, which could contribute to the production of gynecomastia.

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