aminoglutethimide


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aminoglutethimide

 [ah-me″no-gloo-teth´ĭ-mīd]
an antihormone that inhibits conversion of cholesterol to pregnenolone, thus reducing adrenocortical steroid synthesis; administered orally in treatment of cushing's syndrome. It also inhibits conversion of androstenedione to estrone in peripheral tissues and is sometimes used as a componnt of hormonal therapy for advanced breast carcinoma.

aminoglutethimide

/ami·no·glu·teth·i·mide/ (-gloo-teth´ĕ-mīd) an inhibitor of cholesterol metabolism, thereby reducing adrenocortical steroid synthesis; used in the treatment of Cushing's syndrome. It also inhibits estrogen production from androgens in peripheral tissue.

aminoglutethimide

Oncology A nonsteroidal aromatase inhibitor which inhibits estrogen production and suppresses estrogen-dependent tumor growth. See Estrogen-receptor.

aminoglutethimide (əmē´nōglōōteth´əmīd),

n brand name: Cytadren;
drug class: antineoplastic, adrenal steroid inhibitor;
action: acts by inhibiting the enzymatic conversion of cholesterol to pregnenolone, thereby blocking synthesis of all adrenal steroids;
uses: suppression of adrenal function in Cushing's syndrome, metastatic breast cancer, and adrenal cancer.

aminoglutethimide

a compound that inhibits the adrenal cortex and peripheral aromatase, thereby blocking production of adrenal steroids. Used in the treatment of hyperadrenocorticism.
References in periodicals archive ?
Three patients in the group treated with formestane, two patients in the aminoglutethimide group, one patient in the exemestane group, and three patients in the megestrol acetate group had tHcy above the value defined as the upper health-related limit for postmenopausal women in our laboratory (18 [micro]mol/L; see Patients and Methods).
Treatment with aminoglutethimide was associated with a significant change in plasma tHcy (Fig.
The selectivity of the increase in plasma tHcy during aminoglutethimide treatment was further documented by an increase in the tHcy/tCys ratio with no increase in tCys.
Thus, data for patients treated with aminoglutethimide were re-analyzed after exclusion of the five patients who had received tamoxifen as their last treatment modality before aminoglutethimide.
To evaluate whether the increase in plasma tHcy caused by treatment with aminoglutethimide could be the result of reduced cobalamin or folate, which are cofactors in Hcy metabolism, we determined serum cobalamin and folate and RBC folate before and during aminoglutethimide therapy.
Previous findings suggested that an increased risk of cardiovascular diseases (14) associated with aminoglutethimide adjuvant treatment may be partly the result of an increase in plasma cholesterol and triglycerides (26).
The possibility that alterations in tHcy during treatment with aminoglutethimide could be secondary to alterations in blood lipids may be considered.
We found that treatment with aminoglutethimide caused a significant and substantial increase in plasma tHcy and the ratio of tHcy to tCys.
It is difficult from our data to identify the mechanism by which aminoglutethimide increases plasma tHcy.
In summary, our data show that aminoglutethimide treatment increases plasma tHcy in breast cancer patients.
Aminoglutethimide as treatment of postmenopausal women with advanced breast carcinoma.
Adjuvant aminoglutethimide for postmenopausal patients with primary breast cancer: analysis at 8 years.