Complete androgenic blockade used in the treatment of advanced prostatic carcinoma can be attained by administration of antiandrogens in orchidectomized patients or by combined therapy with LH-RH analogs and antiandrogens. The treatment, however, decreases the influence of both androgens end estrogens on bone tissue and may result in bone mass loss and increased propensity to fractures. The purpose of the study was to determine the influence of complete androgenic blockade on bone mass and

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... tal metabolism in men with advanced prostatic carcinoma and to assess whether 1α-OH vitamin D 3 (1α-OHD 3) together with calcium supplementation is able to prevent bone mass loss in men treated with complete androgenic blockade. 51 patients with advanced prostatic carcinoma, with skeletal metastases, aged 44-86, mean 68 ys were included into a 12-month prospective study. All patients were treated with orchidectomy followed by therapy with flutamide in a dose of 750 mg daily. 26 patients were additionally given 1α-OHD 3 in a dose of 0.5 µg/d and calcium carbonate in an initial dose of 1 g daily. It was found that the 12-month treatment with complete androgenic blockade resulted in a decrease in bone mineral density (BMD) by 8.1% in the lumbar spine, by 6.3% in the femoral neck and by 3.5% in the total skeleton. Therapy with 1α-OHD 3 and CaCO 3 caused complete inhibition of bone tissue loss in the lumbar spine and resulted in an increase in BMD by 2.2% in femoral neck and by 1.9% in the total skeleton. None of the examined patients experienced any skeletal fractures. In both groups of patients a prompt decrease in serum alkaline phosphatase activity-a marker of osteoblast activity and an increase in fasting urine calcium creatinine ratio indicating acceleration of bone resorption were found. Conclusions: in patients with advanced prostatic carcinoma treated with complete androgenic blockade acceleration of bone mass loss is observed; treatment with 1α-OHD 3 and CaCO 3 is able to prevent both trabecular and compact bone loss. (Pol J Endocrinol 2005; 3(56): 225-232)