The Cushing Syndrome Induced by Medroxyprogesterone Acetate
Authors: Kerry Siminoski
Journal: Annals of Internal Medicine (1989)

Brief Reports1 November 1989The Cushing Syndrome Induced by Medroxyprogesterone AcetateKerry Siminoski, MD, Paul Goss, MD, PhD, Daniel J. Drucker, MDKerry Siminoski, MDSearch for more papers by this author, Paul Goss, MD, PhDSearch for more papers by this author, Daniel J. Drucker, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-111-9-758 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe 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 ReportRenal 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...References1. Carpenter P. Diagnostic evaluation of Cushing's syndrome. Endocrin Metab Clin North Am. 1988;17:445-72. CrossrefMedlineGoogle Scholar2. LundbladRoberts JJ. Regulation of pro-opiomelanocortin gene expression in pituitary. Endocr Rev. 1988;9:135-58. CrossrefMedlineGoogle Scholar3. DruckerPhilippeMojsov DJS. Proglucagon gene expression and posttranslational processing in a hamster islet cell line. Endocrinology. 1988;123:1861-7. CrossrefMedlineGoogle Scholar4. UhlerHerbert ME. Complete amino acid sequence of mouse pro-opiomelanocortin derived from the nucleotide sequence of pro-opiomelanocortin cDNA. J Biol Chem. 1983;258:257-61. CrossrefMedlineGoogle Scholar5. CastegnaroSala EG. Pharmacokinetics and metabolism of medroxyprogesterone acetate. Influence of the route of administration and of its physical state. Steroidologia. 1971;2:13-26. MedlineGoogle Scholar6. PannutiMartoniLenazPianaNanni FAGEP. A possible new approach to the treatment of metastatic breast cancer: massive doses of medroxyprogesterone acetate. Cancer Treat Rep. 1978;62:499-504. MedlineGoogle Scholar7. GanzinaRobustelli Della Cuna FG. Adverse events during high-dose medroxyprogesterone acetate therapy for endocrine tumours. In: Cavalli F, McGuire WL, Pannuti F, Pellegrini A, Robustelli Delia Cuna G, eds. Proceedings of the International Symposium on Medroxyprogesterone Acetate. Amsterdam: Excerpta Medica; 1982:158-76. Google Scholar8. SvecYeakleyHarrison FJR. Progesterone enhances glucocorticoid dissociation from the AtT-20 cell glucocorticoid receptor. Endocrinology. 1980;107:566-72. CrossrefMedlineGoogle Scholar9. MathewsAbramsMorishima JCA. Pituitary-adrenal function in ten patients receiving medroxyprogesterone acetate for true precocious puberty. J Clin Endocrinol Metab. 1970;30:653-8. CrossrefMedlineGoogle Scholar10. DanguyLegrosLeclercqHeuson ANGJ. Effects of medroxyprogesterone acetate on the development of dimethylbenzanthracene-induced mammary tumours: possible modes of action. In: Cavalli F, McGuire WL, Pannuti F, Pellegrini A, Robustelli Della Cuna G, eds. Proceedings of the International Symposium on Medroxyprogesterone Acetate. Amsterdam: Excerpta Medica; 1982:63-79. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: From Toronto General Hospital, Toronto, Ontario, Canada. For current author addresses, see end of text. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCushing DiseaseCushing's diseaseOsteoporosi indotta da farmaciHypothalamic Pituitary Adrenal Function during Critical Illness: Limitations of Current Assessment MethodsMedroxyprogesterone acetate binds the glucocorticoid receptor to stimulate α-ENaC and sgk1 expression in renal collecting duct epitheliaMegestrol attenuates the hormonal response to CCK-4–induced panic attacksDecline in Lung Function in Patients With Lymphangioleiomyomatosis Treated With or Without ProgesteroneOsteoporosis Associated With Megestrol AcetateGlucose Disorders Associated with HIV and its Drug TherapyHypercalcaemia of hypoadrenal crisis mistaken for hypercalcaemia of malignancy in a patient with known bone metastases: a case reportProgestin-induced growth hormone (GH) production in the treatment of dogs with congenital GH deficiencyMedroxyprogesterone Acetate-Induced Secondary Adrenal InsufficiencyEditorial Comment “Child of a Looser God”ENDOCRINOLOGIC COMPLICATIONS OF HIV INFECTIONCushing's Syndrome and Hypothalamic-Pituitary Adrenal Axis Suppression Induced by Medroxyprogesterone AcetateBinding specificity of medroxyprogesterone acetate and proligestone for the progesterone and glucocorticoid receptor in the dogSteroids and ProgestinsLes pièges de l'exploration diagnostique dans le syndrome de CushingDisorders of the Adrenal CortexSyndromes of Corticosteroid ExcessEffect of Megestrol Acetate on the Human Pituitary-Adrenal AxisMedroxyprogesterone induced Cushing's syndromeManagement of hypovolaemic shock.Hepatitis B vaccine associated with erythema nodosum and polyarthritis.Cushing's syndrome induced by medroxyprogesterone.Cushing syndrome and medroxyprogesterone acetate 1 November 1989Volume 111, Issue 9Page: 758-760KeywordsAdenocarcinomaAdrenalectomyAdrenocorticotropic hormoneComplementary DNAEndocrinologyNephrectomy Issue Published: 1 November 1989 PDF downloadLoading ...