Oral Presentation ESA-SRB-AOTA 2019

A novel liver-targeted testosterone-therapy for the prevention of sarcopaenia in androgen deprived men with prostate cancer: a double-blind placebo-controlled study (#55)

Handoo Rhee 1 , Anojan Navaratham 1 , Irina Olienkova 1 , Deborah Gilroy 2 , Yolanda Scuderi 3 , Peter Heathcote 1 , Simon Wood 1 4 , Ken Ho 2 4 5
  1. Urology, Princess Alexandra Hospital, Brisbane, Queensland, Australia
  2. Endocrinology, Princess Alexandra Hospital, Brisbane, Queensland, Australia
  3. Pharmacy, Princess Alexandra Hospital, Brisbane, Queensland, Australia
  4. The University of Queensland, Brisbane, Queensland, Australia
  5. The Translation Research Institute, Brisbane, Queensland, Australia

Androgen deprivation therapy (ADT) causes sarcopaenia, increasing frailty and fracture risk in men with prostate cancer(PCa).  Liver-targeted testosterone treatment (LTTT) achieved through oral delivery of low dose testosterone stimulates protein anabolism without elevating peripheral androgen levels in hypogonadal men and postmenopausal women (1,2).

Aim

We investigated whether LTTT prevents sarcopaenia during ADT

Method

Forty nine men with PCa were recruited into a 6-month double-blind placebo-controlled study of 40mg/day of crystalline testosterone; 19 commencing and 30 on stable ADT for > 18 months. Testosterone and PSA levels, body composition (lean, fat and BMC), daily step count and grip strength were measured. Patients in whom PSA doubled or rose above 4 ng/mL were withdrawn.

Results

43 patients completed the study. Mean testosterone rose during LTTT but not placebo treatment (∆ +2.34±0.47 vs -0.67±0.41 nmol/L; p<0.01). Mean PSA level did not change significantly during LTTT or placebo treatment (+0.59±0.43 vs -0.05±0.37 ng/ml, p=0.27).  Blood urea fell during LTTT (∆ -0.41±0.41) but not placebo (∆ +0.05±0.35 mmol/L.). Lean mass (∆ +0.46±0.36 vs -0.37±0.32 kg; p=0.09) and BMC (∆ +0.01±0.02 vs -0.04±0.02 kg, p<0.03) increased compared to placebo. Neither mean daily step count nor grip strength changed significantly between treatments. Five of 6 patients withdrew from an increase in PSA levels, which returned to baseline. All five were on active treatment.

LTTT increased testosterone slightly but not PSA concentration among those completing the study. LTTT for six months induced beneficial biochemical and body compositional but not physical function effects. 10% withdrew from a reversible increase in PSA.

Conclusion

LTTT shows promise as simple therapy for preventing sarcopenia and bone loss during ADT in men with prostate Ca. Further studies are required to optimise the dose, safety and efficacy in PCa and to explore potential application in other catabolic states.

 

  1. 1. Birzniece V, Meinhardt UJ, Handelsman DJ, Ho KK. Testosterone stimulates extra-hepatic but not hepatic fat oxidation: comparison of oral and transdermal testosterone administration in hypopituitary men. Clin Endocrinol (Oxf). 2009;71(5):715-21. 2. Birzniece V, Umpleby MA, Poljak A, Handelsman DJ, Ho KK. Oral low-dose testosterone administration induces whole-body protein anabolism in postmenopausal women: a novel liver-targeted therapy. Eur J Endocrinol. 2013;169(3):321-7