Testosterone treatment for two years increases volumetric bone mineral density (vBMD) in Australian men with pre- or early type 2 diabetes.

The T4Bone sub-study of the T4DM study – previously reported here in the limbic – comprised 136 men 50-74 years within impaired glucose tolerance or newly diagnosed type 2 diabetes, waist adiposity and fasting serum testosterone levels ≤14 nmol/L.

The men were randomised to receive intramuscular injections of testosterone undecanoate 1000mg or placebo every three months for two years. All men received a Weight Watcher’s lifestyle program.

Bone microarchitecture was assessed by high resolution-peripheral quantitative CT (HR-pQCT) at one study centre and areal BMD by DXA at five centres.

The study found testosterone treatment significantly increased the vBMD at both the tibia and the radius.

“The increased vBMD was predominantly in cortical bone at both sites with highly significant treatment effect sizes ranging from 2.9% to 3.1%,” the study said.

The effect sizes were similar in magnitude to those seen with antiresorptive drug treatments.

“By contrast, effects on trabecular bone parameters were not significant in the treatment group over placebo with the exception of an isolated increase of tibial trabecular vBMD and in bone volume/tissue volume ratio observed at week 66, but not at study end.”

Testosterone treatment was associated with an increased risk of a raised haematocrit ≥0.54% compared to placebo (20% v 1%) but no increase in serious cardiac, prostate or other adverse events.

The study said the testosterone induced increases in cortical bone, which comprises 80% of the human skeleton, suggest that treatment might affect fracture risk.

“This is the first RCT to address the effects of testosterone treatment on bone microarchitecture, however the implications for fracture outcomes require further studies.”

“Of note, from a clinical perspective, our findings are clearly not meant to endorse testosterone treatment to improve skeletal health in men without pathological hypogonadism and with a normal serum testosterone.”

The study, published in the Journal of Clinical Endocrinology and Metabolism, was led by Dr Mark Fui with senior investigator Professor Mathis Grossmann from Austin Health.