Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/27821
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dc.contributor.authorNg Tang Fui, Mark-
dc.contributor.authorHoermann, Rudolf-
dc.contributor.authorBracken, Karen-
dc.contributor.authorHandelsman, David J-
dc.contributor.authorInder, Warrick J-
dc.contributor.authorStuckey, Bronwyn G A-
dc.contributor.authorYeap, Bu B-
dc.contributor.authorGhasem-Zadeh, Ali-
dc.contributor.authorRobledo, Kristy P-
dc.contributor.authorJesudason, David-
dc.contributor.authorZajac, Jeffrey D-
dc.contributor.authorWittert, Gary A-
dc.contributor.authorGrossmann, Mathis-
dc.date.accessioned2021-10-25T22:34:11Z-
dc.date.available2021-10-25T22:34:11Z-
dc.date.issued2021-07-13-
dc.identifier.citationThe Journal of Clinical Endocrinology and Metabolism 2021; 106(8): e3143-e3158en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/27821-
dc.description.abstractTestosterone treatment increases bone mineral density (BMD) in hypogonadal men. Effects on bone microarchitecture, a determinant of fracture risk, are unknown. We aimed to determine the effect of testosterone treatment on bone microarchitecture using high resolution-peripheral quantitative computed tomography (HR-pQCT). Men ≥ 50 years of age were recruited from 6 Australian centers and were randomized to receive injectable testosterone undecanoate or placebo over 2 years on the background of a community-based lifestyle program. The primary endpoint was cortical volumetric BMD (vBMD) at the distal tibia, measured using HR-pQCT in 177 men (1 center). Secondary endpoints included other HR-pQCT parameters and bone remodeling markers. Areal BMD (aBMD) was measured by dual-energy x-ray absorptiometry (DXA) in 601 men (5 centers). Using a linear mixed model for repeated measures, the mean adjusted differences (95% CI) at 12 and 24 months between groups are reported as treatment effect. Over 24 months, testosterone treatment, versus placebo, increased tibial cortical vBMD, 9.33 mg hydroxyapatite (HA)/cm3) (3.96, 14.71), P < 0.001 or 3.1% (1.2, 5.0); radial cortical vBMD, 8.96 mg HA/cm3 (3.30, 14.62), P = 0.005 or 2.9% (1.0, 4.9); total tibial vBMD, 4.16 mg HA/cm3 (2.14, 6.19), P < 0.001 or 1.3% (0.6, 1.9); and total radial vBMD, 4.42 mg HA/cm3 (1.67, 7.16), P = 0.002 or 1.8% (0.4, 2.0). Testosterone also significantly increased cortical area and thickness at both sites. Effects on trabecular architecture were minor. Testosterone reduced bone remodeling markers CTX, -48.1 ng/L [-81.1, -15.1], P < 0.001 and P1NP, -6.8 μg/L[-10.9, -2.7], P < 0.001. Testosterone significantly increased aBMD at the lumbar spine, 0.04 g/cm2 (0.03, 0.05), P < 0.001 and the total hip, 0.01 g/cm2 (0.01, 0.02), P < 0.001. In men ≥ 50 years of age, testosterone treatment for 2 years increased volumetric bone density, predominantly via effects on cortical bone. Implications for fracture risk reduction require further study.en
dc.language.isoeng
dc.subjectT4DMen
dc.subjectboneen
dc.subjectmicroarchitectureen
dc.subjecttestosteroneen
dc.titleEffect of Testosterone Treatment on Bone Microarchitecture and Bone Mineral Density in Men: A 2-Year RCT.en
dc.typeJournal Articleen
dc.identifier.journaltitleThe Journal of Clinical Endocrinology and Metabolismen
dc.identifier.affiliationMedical School, University of Western Australia and Department of Endocrinology and Diabetes, Freemantle & Fiona Stanley Hospital, Perth, Western Australia, 6150, Australiaen
dc.identifier.affiliationMedicine (University of Melbourne)en
dc.identifier.affiliationEndocrinologyen
dc.identifier.affiliationANZAC Research Institute, University of Sydney and Department of Andrology, Concord Hospital, Sydney New South Wales, 2139, Australiaen
dc.identifier.affiliationPrincess Alexandra Hospital and the University of Queensland, Queensland, 4102, Australiaen
dc.identifier.affiliationKeogh Institute for Medical Research, Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital and University of Western Australia, Western Australia, 6009, Australiaen
dc.identifier.affiliationNHMRC Clinical Trials Centre, University of Sydney, New South Wales, 2050, Australiaen
dc.identifier.affiliationFreemasons Foundation Centre for Men's Health, University of Adelaide, Adelaide, South Australia, Australia, and The Queen Elizabeth Hospital, South Australia, 5000, Australiaen
dc.identifier.doi10.1210/clinem/dgab149en
dc.type.contentTexten
dc.identifier.orcid0000-0002-4200-7476en
dc.identifier.orcid0000-0001-6818-6065en
dc.identifier.orcid0000-0001-8261-3457en
dc.identifier.pubmedid33693907
local.name.researcherGhasem-Zadeh, Ali
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptEndocrinology-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptEndocrinology-
crisitem.author.deptEndocrinology-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptEndocrinology-
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