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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/20771
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dc.contributor.authorLonning, P. E.en
dc.contributor.authorJohannessen, D. C.en
dc.contributor.authorLien, E. A.en
dc.contributor.authorEkse, D.en
dc.contributor.authorFotsis, T.en
dc.contributor.authorAdlercreutz, H.en
dc.date.accessioned2015-11-24T19:09:58Z-
dc.date.available2015-11-24T19:09:58Z-
dc.identifier.issn0960-0760-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/20771-
dc.rightsDefault Licence-
dc.subjectAgeden
dc.subjectAndrogens/blooden
dc.subjectBreast Neoplasms/drug therapy/*metabolismen
dc.subjectEstradiol/blooden
dc.subjectEstrogens/urineen
dc.subjectEstrone/analogs & derivatives/blooden
dc.subjectFemaleen
dc.subjectFollicle Stimulating Hormone/blooden
dc.subjectGonadal Steroid Hormones/*blooden
dc.subjectGonadotropins, Pituitary/*blooden
dc.subjectHumansen
dc.subjectLuteinizing Hormone/blooden
dc.subjectMiddle Ageden
dc.subject*Postmenopauseen
dc.subjectSex Hormone-Binding Globulin/*metabolismen
dc.subjectTamoxifen/*pharmacology/therapeutic useen
dc.subjectTestosterone/blooden
dc.titleInfluence of tamoxifen on sex hormones, gonadotrophins and sex hormone binding globulin in postmenopausal breast cancer patientsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/7748814-
heal.identifier.secondaryhttp://ac.els-cdn.com/096007609400189S/1-s2.0-096007609400189S-main.pdf?_tid=d1add81fcc0d645976fece8c3697ade3&acdnat=1332752927_8e05bfb715b6862b55cfc0b8db08d6b2-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate1995-
heal.abstractEstrone 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 disposition in 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 E1S (mean increase of 18.1%, P < 0.05) and the ratio of E1S/E1 (mean increase of 25.7%, P < 0.01) and E1S/E2 (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 mechanisms 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.en
heal.journalNameJ Steroid Biochem Mol Biolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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