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  • Title: Steroid sex hormones and prolactin in postmenopausal women with generalized mammary carcinoma during prolonged dexamethasone treatment.
    Author: Borkowski A, L'hermite M, Dor P, Longeval E, Rozencweig M, Muquardt C, Van Cauter E.
    Journal: J Endocrinol; 1977 May; 73(2):235-46. PubMed ID: 140915.
    Abstract:
    The endocrine response to prolonged dexamethasone treatment was investigated in six postmenopausal women with generalized mammary carcinoma. Plasma cortisol levels decreased rapidly and became undetectable whereas significant concentrations of plasma dehydroepiandrosterone and androstenedione persisted throughout the study, even in two ovariectomized patients, indicating a certain degree of autonomy or a greater resistance of adrenal 'androgens' to the inhibition of ACTH secretion. Except in the ovariectomized patients, plasma testosterone did not fall significantly whereas the plasma oestrogens tended progressively towards undetectable concentrations. A similar response was found in six normal postmenopausal women although the disappearance of their oestrogens was relatively rapid. This indicates that much of the testosterone present after the menopause could still be produced by the ovaries whereas the ovarian production of oestrogens becomes negligible. The delayed disappearance of oestrogens in the patients with mammary carcinoma indicates that the persisting adrenal 'androgens' remained efficient precursors of oestrogen synthesis within the peripheral tissues and presumably within the mammary tumour itself. Plasma dihydrotestosterone behaved like the plasma oestrogens. Despite the fall in plasma oestrogens, plasma gonadotrophins did not increase further but plasma prolactin rose progressively. The persistance of steroid sex hormones and the rise of plasma prolactin might explain the poor response to dexamethasone treatment in mammary carcinoma. A prolonged suppression of the adrenal cortex was produced by giving dexamethasone to 6 postmenopausal women with generalized mammary carcinoma. Plasma cortisol levels decreased rapidly while plasma dehydroepiandrosterone and androstenedione persisted. Plasma testosterone did not fall, except in ovariectomized patients. Plasma estrogens gradually decreased. This slow disappearance of estrogen indicated that persisting adrenal androgens continued to be precursors of estrogen synthesis in peripheral tissues, and possibly within the tumor tissue also. Plasma dihydrotestosterone estimations were similar to those of plasma estrogens. Plasma gonadotropins remained the same. Prolactin increased gradually. Since the growth of mammary carcinoma in postmenopausal women may be partially under endocrine control and the hormones involved are the sex hormones, and possibly prolactin, the persistence of sex hormones and rise of plasma prolactin may be why dexamethasone produces only a minimal response.
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