Key result
Cyproterone acetate decreased serum cortisol by 40% and oestrogen increased it by 24% in prostate cancer patients, but neither impaired hypothalamic-pituitary-adrenal feedback.
Why the study?
Does cyproterone acetate or oestrogen treatment impair adrenocortical function in prostate carcinoma patients?
Observational
Does cyproterone acetate or oestrogen treatment impair adrenocortical function in prostate carcinoma patients?
Although cyproterone acetate and oestrogen alter serum hormone levels in prostate cancer patients, they do not impair hypothalamic-pituitary-adrenal feedback and do not require specific treatment.
Reassures against routine HPA monitoring or treatment in these patients; leaves open randomized confirmation of preserved feedback.
The antiandrogen cyproterone acetate (CA), as well as oestrogens have been reported to influence pituitary-adrenal function in prostate cancer patients, but the clinical relevance of these findings is unknown. We therefore investigated serum cortisol (F), dehydro-epiandrosterone sulphate (DS), testosterone (T) and prolactin (Prl) levels in patients treated with CA or oestradiol undecylate for at least 6 months. Hypothalamic-pituitary-adrenal function was further assessed by analysis of diurnal hormone variation and by ACTH stimulation and dexamethasone suppression tests. To differentiate between direct CA or oestrogen effects and secondary effects resulting from therapy-induced hypogonadism, we performed similar tests in untreated normogonadal and hypogonadal patients. CA treatment effected a significant decrease in serum F (-40%), DS (-73%) and T (-58%) levels and an increase in serum Prl (+118%). Oestrogen treatment resulted in markedly lowered T levels (-89%), slightly elevated serum F (+24%) and significantly increased serum Prl (+192%). Corresponding changes of F, DS and Prl could not be found in the untreated hypogonadal controls, thus indicating a direct drug-related effect. Neither diurnal rhythmicity of serum F nor adrenal response to ACTH stimulation or sensitivity to dexamethasone suppression significantly changed under CA or oestrogen treatment. We conclude that, although serum F levels may decrease under CA or increase slightly under oestrogen therapy for prostate carcinoma, these findings do not justify specific treatment, since neither clinical side effects nor an impairment of hypothalamic-pituitary-adrenal feedback occurs.
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Schürmeyer et al. (1986) conducted an observational in Prostate carcinoma. Cyproterone acetate or oestradiol undecylate vs. Untreated normogonadal and hypogonadal patients was evaluated on Serum cortisol (F), dehydro-epiandrosterone sulphate (DS), testosterone (T) and prolactin (Prl) levels, and hypothalamic-pituitary-adrenal function. Cyproterone acetate decreased serum cortisol by 40% and oestrogen increased it by 24% in prostate cancer patients, but neither impaired hypothalamic-pituitary-adrenal feedback.
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