Influence of tamoxifen on sex hormones, gonadotrophins and sex hormone binding globulin in postmenopausal breast cancer patients
Autor: | Per Eystein Lønning, Ernst A. Lien, Dag Clement Johannessen, Theodore Fotsis, Dagfinn Ekse, Herman Adlercreutz |
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Rok vydání: | 1995 |
Předmět: |
medicine.medical_specialty
Estrone medicine.drug_class Endocrinology Diabetes and Metabolism Clinical Biochemistry Breast Neoplasms Biochemistry Excretion Endocrinology Sex hormone-binding globulin Sex Hormone-Binding Globulin Internal medicine medicine Humans Testosterone Gonadal Steroid Hormones Molecular Biology Aged Estradiol biology Estrogens Cell Biology Luteinizing Hormone Middle Aged Antiestrogen Androgen Postmenopause Tamoxifen Estrogen Gonadotropins Pituitary Androgens biology.protein Molecular Medicine Female Follicle Stimulating Hormone Gonadotropin hormones hormone substitutes and hormone antagonists Hormone medicine.drug |
Zdroj: | The Journal of Steroid Biochemistry and Molecular Biology. 52:491-496 |
ISSN: | 0960-0760 |
DOI: | 10.1016/0960-0760(94)00189-s |
Popis: | Estrone sulphate (E1S) may be an important estrogen source in breast cancers, particularly in postmenopausal women. Recent studies have shown that tamoxifen inhibits the uptake and metabolism of E1S to estradiol (E2) in cell cultures. To evaluate a possible influence of tamoxifen on E1S dispositionin vivo, we measured plasma levels of E1S together with unconjugated estrogens (E1 and E2), androgens (T, A, DHEA and DHEAS), SHBG, FSH and LH in 32 postmenopausal breast cancer patients before and during tamoxifen treatment. In a subgroup of 10 patients, we measured 24 h urinary excretion of estrogen metabolites to evaluate the influence of tamoxifen treatment on estrogen metabolism and total estrogen production. Tamoxifen increased plasma levels of E1 S (mean increase of 18.1%, P < 0.05) and the ratio of E1/SE1 (mean increase of 25.7%, P < 0.01) and E1/SE2 (mean increase of 34.7%, P < 0.0005). No significant change in plasma E1 was seen, but plasma E2 was reduced (mean reduction of 12.1%, P < 0.005). The fall in plasma E2 was probably secondary to a fall in plasma T (mean reduction of 11.9%, P < 0.05) due to a reduced ovarian excretion of this androgen. The mechanism may be a reduced gonadotrophin stimulation of the ovary, as plasma FSH and LH fell by mean values of 45.5 and 48.1%, respectively (P < 0.0001 for both). The increase in plasma E1S was accompanied by a reduced ratio of 2OHE1/E1 in urine (mean reduction of 38.2%, P < 0.025) indicating reduced 2-hydroxylation. Possible mechanisms for these alterations are discussed. |
Databáze: | OpenAIRE |
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