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Title: Effect of Testosterone Treatment on Bone Microarchitecture and Bone Mineral Density in Men: A 2-Year RCT.
Austin Authors: Ng Tang Fui, Mark ;Hoermann, Rudolf;Bracken, Karen;Handelsman, David J;Inder, Warrick J;Stuckey, Bronwyn G A;Yeap, Bu B;Ghasem-Zadeh, Ali ;Robledo, Kristy P;Jesudason, David;Zajac, Jeffrey D ;Wittert, Gary A;Grossmann, Mathis 
Affiliation: Medical School, University of Western Australia and Department of Endocrinology and Diabetes, Freemantle & Fiona Stanley Hospital, Perth, Western Australia, 6150, Australia
Medicine (University of Melbourne)
ANZAC Research Institute, University of Sydney and Department of Andrology, Concord Hospital, Sydney New South Wales, 2139, Australia
Princess Alexandra Hospital and the University of Queensland, Queensland, 4102, Australia
Keogh Institute for Medical Research, Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital and University of Western Australia, Western Australia, 6009, Australia
NHMRC Clinical Trials Centre, University of Sydney, New South Wales, 2050, Australia
Freemasons Foundation Centre for Men's Health, University of Adelaide, Adelaide, South Australia, Australia, and The Queen Elizabeth Hospital, South Australia, 5000, Australia
Issue Date: 13-Jul-2021
Publication information: The Journal of Clinical Endocrinology and Metabolism 2021; 106(8): e3143-e3158
Abstract: Testosterone 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.
DOI: 10.1210/clinem/dgab149
ORCID: 0000-0002-4200-7476
Journal: The Journal of Clinical Endocrinology and Metabolism
PubMed URL: 33693907
Type: Journal Article
Subjects: T4DM
Appears in Collections:Journal articles

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