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The Cushing Syndrome Induced by Medroxyprogesterone Acetate

Kerry Siminoski, MD; Paul Goss, MD, PhD; and Daniel J. Drucker, MD
[+] Article, Author, and Disclosure Information

Grant Support: Supported in part by grants from the Medical Research Council of Canada and the National Cancer Institute of Canada.

Requests for Reprints: Daniel Drucker, MD, Toronto General Hospital, 200 Elizabeth Street, CCRW3-838, Toronto, Ontario, Canada M5G 2C4.

Current Author Addresses: Dr. Siminoski: Division of Endocrinology and Metabolism, Clinical Sciences Building, University of Alberta, Edmonton, Alberta, Canada T6G 2G3.

Drs. Goss and Drucker: Toronto General Hospital, 200 Elizabeth Street, CCRW3-838, Toronto, Ontario, Canada M5G 2C4.

Ann Intern Med. 1989;111(9):758-760. doi:10.7326/0003-4819-111-9-758
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This excerpt has been provided in the absence of an abstract.

The Cushing syndrome is a constellation of abnormalities resulting from chronic excess glucocorticoid activity (1). We report a case of the Cushing syndrome caused not by adrenocorticotrophic hormone (ACTH) or a glucocorticoid, but by high doses of a progestational agent, 6-alpha methyl-17-alpha acetoxyprogesterone (medroxyprogesterone acetate). In-vitro testing using a pituitary cell line provided additional evidence for the intrinsic glucocorticoid properties of medroxyprogesterone acetate.

Case Report: Renal adenocarcinoma was diagnosed in a 28-year-old woman. After a left radical nephrectomy and adrenalectomy, monthly administration of vinblastine was begun (8 to 10 mg/mo) along with daily medroxyprogesterone acetate (400 mg/d). After 7 years


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