TY - JOUR
T1 - Medical adrenalectomy using aminoglutethimide and dexamethasone in advanced breast cancer
AU - Lipton, Allan
AU - Santen, Richard J.
N1 - Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1974/2
Y1 - 1974/2
N2 - Twelve women with advanced breast carcinoma were given aminoglutethimide (up to 2 gm q.d. p.o.), in addition to dexamethasone (1.0–3.0 mg daily) and Florinef (0.1 mg b.i.w.) in order to produce a medical adrenalectomy. Adequacy of adrenal blockade was assessed by measuring A.M. plasma and 24‐hour urinary free cortisol by specific competitive protein binding techniques. Seven of 9 patients who had received an adequate trial had constant suppression of adrenal cortical function for at least a period of 8 weeks. Escape from blockade, when observed, was attributed to the rapid metabolism of dexamethasone induced by aminoglutethimide, demonstrated by determining the half‐life of 3H‐dexamethasone before and during treatment. Three patients with soft tissue involvement demonstrated a 1‐A response (12+, 5+ 6 months). Three patients with bone involvement showed a 0‐A response (7, 5, and 4 months). Lethargy and allergy to aminoglutethimide prevented an adequate trial in two patients. A third patient who was adequately suppressed for 7 weeks died before the 8‐week trial period. Minor side effects attributable to aminoglutethimide (nystagmus, ataxia, lethargy, skin rash) were seen frequently but abated with reduction in dosage. No Cushingoid side effects related to dexamethasone administration were noted.
AB - Twelve women with advanced breast carcinoma were given aminoglutethimide (up to 2 gm q.d. p.o.), in addition to dexamethasone (1.0–3.0 mg daily) and Florinef (0.1 mg b.i.w.) in order to produce a medical adrenalectomy. Adequacy of adrenal blockade was assessed by measuring A.M. plasma and 24‐hour urinary free cortisol by specific competitive protein binding techniques. Seven of 9 patients who had received an adequate trial had constant suppression of adrenal cortical function for at least a period of 8 weeks. Escape from blockade, when observed, was attributed to the rapid metabolism of dexamethasone induced by aminoglutethimide, demonstrated by determining the half‐life of 3H‐dexamethasone before and during treatment. Three patients with soft tissue involvement demonstrated a 1‐A response (12+, 5+ 6 months). Three patients with bone involvement showed a 0‐A response (7, 5, and 4 months). Lethargy and allergy to aminoglutethimide prevented an adequate trial in two patients. A third patient who was adequately suppressed for 7 weeks died before the 8‐week trial period. Minor side effects attributable to aminoglutethimide (nystagmus, ataxia, lethargy, skin rash) were seen frequently but abated with reduction in dosage. No Cushingoid side effects related to dexamethasone administration were noted.
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U2 - 10.1002/1097-0142(197402)33:2<503::AID-CNCR2820330227>3.0.CO;2-L
DO - 10.1002/1097-0142(197402)33:2<503::AID-CNCR2820330227>3.0.CO;2-L
M3 - Article
C2 - 4812767
AN - SCOPUS:0016211635
SN - 0008-543X
VL - 33
SP - 503
EP - 512
JO - Cancer
JF - Cancer
IS - 2
ER -