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

Oncology A nonsteroidal aromatase inhibitor which inhibits estrogen production and suppresses estrogen-dependent tumor growth. See Estrogen-receptor.
References in periodicals archive ?
Aminoglutethimide in treatment of metastatic breast carcinoma.
Medical agents for treating Cushing's syndrome Adrenal steroidogenesis Drugs modulating ACTH release inhibitors from the pituitary Metyrapone Dopamine agonists Ketoconazole Somatostatin analogues Mitotane Cyproheptadine Aminoglutethimide Ritanserine Trilostane Sodium valproate Etomidate PPAR agonists
A possible role of"steroidogenic factor" in the corticoidogenic response to ACTH; effect of ACTH, cycloheximide and aminoglutethimide on the content of cholesterol in the outer and inner mitochondrial membrane of rat adrenal cortex.
The first generation drug, aminoglutethimide, has been used for two decades (1), and currently several new, more potent and specific drugs have been developed (2).
Only one small study has compared the long-term effects of aminoglutethimide to placebo treatment in the adjuvant setting (14).
In the present study, we explored possible effects of aminoglutethimide treatment on plasma tHcy in patients suffering from advanced breast cancer.
Patients treated with aminoglutethimide. Thirty patients were treated with aminoglutethimide 250 mg four times per day together with cortisone acetate 50 mg twice per day for the first 2 weeks, followed by aminoglutethimide 250 mg four times per day with cortisone acetate 25 mg twice per day.
Pretreatment values for plasma tHcy in the group treated with aminoglutethimide are shown in Fig.
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.