When we studied the merits of aminoglutethimide for the treatment of metastatic breast cancer in postmenopausal women in a phase II clinical trial we were confronted with an incidence of manifest myxedema in 25% and of subclinical hypothyroidism, still compensated by a rise of serum thyrotropin (TSH) in 78% of the patients after 8 weeks (Bruning et al., 1984). This relatively high incidence of diminished thyroid function seemed to be related to a relatively high frequency of elevated pretreatment TSH levels in our study population.In this report we present evidence that post-

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In a phase II clinical trial, 38 postmenopausal women with advanced breast cancer were treated with aminoglutethimide and replacement hydrocortisone. All women had previously received up to 4 modalities of endocrine therapy. Seventeen patients had also been treated with cytostatic drugs. Twenty-five percent of the 29 evaluable patients experienced objective tumor regression, lasting from 11 to more than 18 months. In 29% the disease was stabilized for 3 to more than 15 months. Toxicity was significant, necessitating drug withdrawal in 3 patients. One patient died within 3 weeks of therapy from multiple perforated gastric ulcers. Two patients developed herpes zoster within 4 weeks of treatment. Many side effects were minor and transient. However, treatment resulted in overt primary hypothyroidism in 25% of the evaluable patients and in a strongly increased need of acenocoumarin in all 3 patients on anticoagulant therapy.