Aminoglutethimide as treatment of postmenopausal women with advanced breast carcinoma.
Hormone-dependent breast carcinomas respond to deprivation of biologically active estrogens with objectively quantifiable tumor regression. Aminoglutethimide, a known inhibitor of steroid synthesis, is also a potent blocker of the aromatase enzyme and, thus, of estrogen production. We developed an effective regimen to inhibit estrogen production in postmenopausal women using aminoglutethimide and replacement glucocorticoid. One hundred forty-seven women initially received aminoglutethimide and replacement glucocorticoid as treatment of metastatic breast carcinoma. One hundred twenty-nine women are currently evaluable for assessment of clinical and hormonal responses. Thirty-seven percent of unselected women and 49% of estrogen receptor-positive patients experienced objective tumor regression. Responses occurred predominantly in soft tissue (47%) and bone (35%) and lasted 30 +/- 9.1 months for complete and 14 +/- 1.5 months for partial regressions. Plasma and urinary estrogen levels fell equally in responder versus nonresponder groups whereas androgen levels declined less in patients with progressive disease.
D000616:Aminoglutethimide / Q000009:adverse effects / Q000627:therapeutic use*; D000728:Androgens / Q000097:blood / Q000652:urine; D001943:Breast Neoplasms / Q000188:drug therapy*; D004967:Estrogens / Q000097:blood / Q000652:urine; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D008593:Menopause; D008875:Middle Aged; D009362:Neoplasm Metastasis; D010907:Pituitary Hormones / Q000097:blood
D000728:Androgens; D004967:Estrogens; D005938:Glucocorticoids; D010907:Pituitary Hormones; D000616:Aminoglutethimide