Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/33961
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dc.contributor.authorParker A.C.en
dc.contributor.authorWallace E.M.en
dc.contributor.authorWu F.C.W.en
dc.contributor.authorGroome N.P.en
dc.contributor.authorRiley S.C.en
dc.date.accessioned2021-05-14T11:29:55Zen
dc.date.available2021-05-14T11:29:55Zen
dc.date.copyright1997en
dc.date.created19971004en
dc.date.issued2012-10-22en
dc.identifier.citationJournal of Clinical Endocrinology and Metabolism. 82 (9) (pp 3111-3115), 1997. Date of Publication: 1997.en
dc.identifier.issn0021-972Xen
dc.identifier.urihttps://repository.monashhealth.org/monashhealthjspui/handle/1/33961en
dc.description.abstractTo investigate the role of inhibin in the control of follicle- stimulating hormone (FSH) secretion, we have measured levels of immunereactive inhibin (ir-inhibin), inhibin B, Pro-alphaC containing inhibins, FSH, luteinizing hormone (LH), and testosterone in twelve men with hematological malignancies before, during, and after chemotherapy. Inhibin B levels fell significantly by i month from a mean +/- SE baseline level of 273.2 +/- 32.8 pg/mL, reaching a nadir of 52.6 +/- 15.3 pg/mL at 4 months (P < 0.0001). FSH levels increased within the first month from a baseline level of 3.9 +/- 0.6 IU/L, reaching a peak level of 22.4 +/- 3.3 IU/L at 4 months (P < 0.0001). FSH and inhibin B were significantly and inversely correlated (r = 0.69, P < 0.0001). Pro-alphaC containing inhibin levels increased significantly (P < 0.05) at 8 months and were significantly and positively correlated with FSH (r = 0.88, P = 0.002). LH levels increased significantly but to a much lesser extent than FSH, the increase becoming evident only 4 months after treatment commenced (P < 0.03). Levels of ir-inhibin and testosterone remained unchanged throughout the study. These data provide strong support to the hypothesis that inhibin B is the physiologically important form of inhibin in men, negatively regulating FSH secretion at the pituitary. Furthermore, they suggest that FSH stimulates inhibin alpha-subunit secretion by the testis.en
dc.languageEnglishen
dc.languageenen
dc.publisherEndocrine Society (8401 Connecticut Ave. Suite 900, Chevy Chase MD 20815, United States)en
dc.subjecttestosterone releaseen
dc.subjectfollitropin/ec [Endogenous Compound]en
dc.subject*gonadotropin/ec [Endogenous Compound]en
dc.subject*inhibin/ec [Endogenous Compound]en
dc.subjectluteinizing hormone/ec [Endogenous Compound]en
dc.subject*testosterone/ec [Endogenous Compound]en
dc.subjectregulatory mechanismen
dc.subjectadulten
dc.subjectalpha chainen
dc.subjectarticleen
dc.subject*cancer chemotherapyen
dc.subjectclinical articleen
dc.subjectenzyme linked immunosorbent assayen
dc.subjectfollitropin blood levelen
dc.subjectfollitropin releaseen
dc.subjectgonadotropin releaseen
dc.subjecthumanen
dc.subjectluteinizing hormone blood levelen
dc.subjectmaleen
dc.subjectnegative feedbacken
dc.subjectpriority journalen
dc.subject*testis injury/co [Complication]en
dc.subjecttestosterone blood levelen
dc.subjecttestosterone metabolismen
dc.titleEffects of chemotherapy-induced testicular damage on inhibin, gonadotropin, and testosterone secretion: A prospective longitudinal study.en
dc.typeArticleen
dc.identifier.affiliationObstetrics and Gynaecology (Monash Women's)-
dc.identifier.doihttp://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1210/jcem.82.9.4238en
dc.publisher.placeUnited Statesen
dc.identifier.pubmedid9284754 [http://www.ncbi.nlm.nih.gov/pubmed/?term=9284754]en
dc.identifier.source27385684en
dc.identifier.institution(Wallace) Dept. of Obstetrics and Gynaecology, Monash University, Clayton, Vic. 3168, Australia (Groome) Sch. of Biol. and Molecular Sciences, Oxford Brookes University, Oxford, United Kingdom (Riley) Dept. of Obstetrics and Gynaecology, University of Edinburgh, Edinburgh EH3 9EW, United Kingdom (Parker) Department of Haematology, University of Edinburgh, Western General Hospital, Manchester, United Kingdom (Wu) Department of Medicine, University of Manchester, Manchester Royal Infirmary, Manchester, United Kingdom (Wu) Department of Reproductive Medicine, St. Mary's Hospital, Manchester, United Kingdom (Wallace) Dept. of Obstetrics and Gynaecology, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton, Vic. 3168, Australiaen
dc.description.addressE.M. Wallace, Department of Obstetrics/Gynaecology, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton, Vic. 3168, Australiaen
dc.subject.keywordpriority journalen
dc.subject.keywordregulatory mechanismen
dc.subject.keyword*testis injury / *complicationen
dc.subject.keyword*cancer chemotherapyen
dc.subject.keywordtestosterone blood levelen
dc.subject.keywordtestosterone metabolismen
dc.subject.keywordtestosterone releaseen
dc.subject.keywordclinical articleen
dc.subject.keywordalpha chainen
dc.subject.keywordadulten
dc.subject.keywordarticleen
dc.subject.keywordenzyme linked immunosorbent assayen
dc.subject.keywordfollitropin blood levelen
dc.subject.keywordfollitropin releaseen
dc.subject.keywordgonadotropin releaseen
dc.subject.keywordhumanen
dc.subject.keywordluteinizing hormone blood levelen
dc.subject.keywordmaleen
dc.subject.keywordnegative feedbacken
dc.relation.libraryurlLibKey Linken
dc.description.publicationstatusEmbaseen
dc.rights.statementCopyright 2012 Elsevier B.V., All rights reserved.en
dc.identifier.authoremailWallace E.M.; Euan.Wallace@med.monash.edu.auen
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.openairetypeArticle-
crisitem.author.deptObstetrics and Gynaecology (Monash Women's)-
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