Background Prostate cancer is the most common male malignancy. Due to its condition of androgen-dependent cancer, the androgenic inhibition by LHRH agonists and/or testosterone receptors blockage are a basic treatment pillar. The loss of bone mass and the increased fracture risk are secondary effects of the anti-androgen therapy. On the other hand, prostate cancer incidence increases with age, so the affected population has a baseline high fracture risk.

Objectives To analyze the bone turnover, osteoporosis prevalence and fracture risk in prostate cancer patients with and without anti-androgen therapy.

Methods We included 45 prostate cancer patients from H.U.P La Fe that were visited consecutively by the rheumatologist to evaluate associated bone disease. Analytical parameters included were calcium, phosphorous, alkaline phosphatase, 25 OH vitamin D, PTH, P1NP and βCTX. Lower back and hipbone densitometry was performed in all patients. The fracture risk estimation was by the FRAX scoring system. A mixed linear regression model and a segmented regression model, as well as the Wilcoxon test, were used for statistical analysis.

Results Patients mean age was 74 years (48-89). An osteoporosis prevalence of 18% and osteopenia prevalence of 40% was found in the densitometric analysis. Hipbone fracture risk evaluated by FRAX is higher than 3% in 10 patients (3 with densitometric osteoporosis and 7 with densitometric osteopenia. No results of patients having fracture risk evaluated by FRAX higher than 10% were found.

78% of the total number of patients was treated with LHRH agonists and 51% with bicalutamide (testosterone receptors blockers). LHRH agonist treatment interval showed a median of 3 months. Vitamin D values lower than 30ng/mL were observed in 73% of patients, and values lower than 15ng/mL were observed in 24% of patients. There was an inverse relationship between vitamin D and P1NP levels (P=0.0101). Moreover, there was an inverse relationship between P1NP and bCTX levels, and hipbone t-score (P=0.007 femoral neck and P=0.023 hipbone, and P=0.003 femoral neck and P=0.008 hipbone, respectively). Patients treated with LHRH agonists showed high P1NP levels (40.4ng/mL vs 29.4ng/mL; P=0.046) and bCTX levels (0.7ng/mL vs 0.3ng/mL; P=0.0006).

Conclusions In our patients is remarkably the high prevalence of hypovitaminosis D (73%). LHRH agonist treatment increased bone turnover biomarker levels. The increase of these biomarkers is related to a hipbone mass decrease. FRAX score could help to identify high fracture risk patients with low bone density (osteopenia).

Disclosure of Interest None declared