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All about: Aminoglutethimide

Big Image Pronouncation: (ah-MEE-no-glue-TETH-ih-mide)
Class: Adrenal steroid inhibitor

Trade Names:
- Tablets 250 mg

Mechanism of Action


Aminoglutethimide inhibits the enzymatic conversion of cholesterol to Δ 5 -pregnenolone, thereby reducing the synthesis of adrenal glucocorticoids, mineralocorticoids, estrogens, and androgens.



Rapidly and completely absorbed. C max is about 5.9 mcg/mL; T max is about 1.5 h.


Minimally bound to proteins.


T ½ is about 12.5 h. 34.54% is excreted in urine as unchanged drug.

Indications and Usage

Suppression of adrenal function in patients with Cushing syndrome.

Unlabeled Uses

Suppression of adrenal function in advanced breast carcinoma or metastatic prostate carcinoma.


Standard considerations.

Dosage and Administration

Cushing Syndrome

PO 250 mg every 6 h. Titrate to adrenal response in increments of 250 mg/day every 1 to 2 wk. Max daily dose is 2,000 mg.

Dosage Adjustment

PO Dosage reduction may be required for a Ccr less than 10 mL/min; specific guidelines are not established.

Discontinue therapy if patient develops severe rash or rash that lasts more than 5 to 8 days. Therapy may be continued at a lower dose after resolution of mild to moderate skin rashes.


Store at room temperature. Protect from light.

Drug Interactions

CNS depressants

Concurrent use with CNS depressants (eg, narcotics, analgesics, alcohol, antiemetics, benzodiazepines, sedatives, tranquilizers) may potentiate CNS effects.

Dexamethasone, digitoxin, medroxyprogesterone, tamoxifen, theophylline, warfarin

Aminoglutethimide increases oxidative metabolism of these drugs. Higher doses of these agents may be required to achieve therapeutic response during concomitant therapy.

Laboratory Test Interactions

None well documented.

Adverse Reactions


Orthostatic or persistent hypotension; tachycardia.


Headache; dizziness; drowsiness; lethargy.


Morbilliform rash; pruritus.


Adrenocortical insufficiency; hypothyroidism; masculinization and hirsutism in females.


Low potential for nausea and vomiting; elevated LFTs; cholestatic jaundice.


Aminoglutethimide crosses the placenta and has caused pseudohermaphroditism in female infants whose mothers took this agent and anticonvulsants during pregnancy.





Adrenal function

Monitor plasma cortisol to assess response to therapy for suppression of adrenal function.

Thyroid function

Thyroid function may decrease during therapy. Monitor at baseline and throughout therapy. Some patients may require thyroid supplements.


Category D .




Safety and efficacy not established.

Cortical hypofunction

May cause adrenal cortical hypofunction, especially under conditions of stress.


Aminoglutethimide may suppress aldosterone production by the adrenal cortex and may cause orthostatic or persistent hypotension. Monitor BP.



Ataxia, somnolence, lethargy, dizziness, fatigue, coma, hyperventilation, respiratory depression, nausea and vomiting, loss of sodium and water, hyponatremia, hypochloremia, hyperkalemia, hypoglycemia, hypovolemic shock caused by dehydration, hypotension.

Patient Information

  • May produce drowsiness or dizziness; use caution while driving or performing other tasks requiring alertness, coordination, or physical dexterity.
  • May cause rash, fainting, weakness, or headache; notify health care provider if pronounced.
  • Nausea and loss of appetite may occur during the first 2 wk of therapy; notify health care provider if these persist or become pronounced.

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