Suppression of tumorous adrenal hyperfunction by aminoglutethimide
1967; Elsevier BV; Volume: 16; Issue: 4 Linguagem: Inglês
10.1016/0026-0495(67)90048-0
ISSN1532-8600
AutoresRenata P. Smilo, Jerry M. Earll, Peter H. Forsham,
Tópico(s)Adrenal Hormones and Disorders
ResumoSix patients with Cushing's syndrome were treated with aminoglutethimide in doses ranging from 1000 to 1500 mg./day. Two had adrenocortical adenomas, 1 carcinoma and 3 bilateral hyperplasia. The 3 with tumors responded with a marked decrease in cortisol secretion rates, urinary 17-hydroxycorticosteroids (17-OHCS), and 17-ketosteroids (17-KS) after the initial 2 days of treatment and showed no rebound for a further 8 days of therapy. This suppression was achieved with doses less than those recommended for maximal anti-convulsant therapy. In contrast, the 3 cases of bilateral hyperplasia showed incomplete suppression of steroid secretion even at higher dose levels. There were no unfavorable reactions to the drug. Aminoglutethimide is a promising agent for the control of excess steroid secretion in adrenocortical tumors.
Referência(s)