***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND Treatment with a gonadotropin-releasing hormone agonist decreases bone mineral density and increases the risk of fracture in men with prostate cancer . We conducted a controlled study of the prevention of osteoporosis in men undergoing treatment with a gonadotropin-releasing hormone agonist .  METHODS In a 48-week , open-label study , we r and omly assigned 47 men with advanced or recurrent prostate cancer and no bone metastases to receive either leuprolide alone or leuprolide and pamidronate ( 60 mg intravenously every 12 weeks ) . Bone mineral density of the lumbar spine and the proximal femur was measured by dual-energy x-ray absorptiometry . Trabecular bone mineral density of the lumbar spine was measured by quantitative computed tomography . Forty-one men completed the study . RESULTS In men treated with leuprolide alone , the mean ( + /-SE ) bone mineral density decreased by 3.3+/-0.7 percent in the lumbar spine , 2.1+/-0.6 percent in the trochanter , and 1.8+/-0.4 percent in the total hip , and the mean trabecular bone mineral density of the lumbar spine decreased by 8.5+/-1.8 percent ( P<0.001 for each comparison with the base-line value ) . In contrast , the mean bone mineral density did not change significantly at any skeletal site in men treated with both leuprolide and pamidronate . There were significant differences between the two groups in the mean changes in bone mineral density at 48 weeks in the lumbar spine ( P<0.001 ) , trochanter ( P = 0.003 ) , total hip ( P=0.005 ) , and trabecular bone of the lumbar spine ( P=0.02 ) . CONCLUSIONS Pamidronate prevents bone loss in the hip and lumbar spine in men receiving treatment for prostate cancer with a gonadotropin-releasing hormone agonist Bone mineral density ( BMD ) and bone mineral content ( BMC ) were measured in the femoral neck area , trochanteric area and Wards triangle , and in the distal radius of the left forearm before and after 1 year of endocrine treatment in 27 patients with prostatic cancer . Eleven of the patients were treated with orchidectomy and 16 with combined oral and intramuscular estrogens . The patients were free from metastases during the entire observation period . In the orchidectomized patients , BMD and BMC of the distal radius decreased significantly following treatment , whereas no changes were observed in the estrogen-treated patients . These preliminary results demonstrate that estrogens may protect bone in male subjects also and may merit further investigations on larger groups of patients PURPOSE And rogen deprivation therapy is associated with fracture risk in men with prostate cancer . We assessed the effects of toremifene , a selective estrogen receptor modulator , on fracture incidence in men receiving and rogen deprivation therapy  during a 2-year period . MATERIAL S AND METHODS In this double-blind , placebo controlled phase III study 646 men receiving and rogen deprivation therapy for prostate cancer were assigned to toremifene ( 80 mg by mouth daily ) and 638 were assigned to placebo . Subjects were followed for 2 years . The primary study end point was new vertebral fractures . Secondary end points included fragility fractures , bone mineral density and lipid changes . RESULTS The 2-year incidence of new vertebral fractures was 4.9 % in the placebo group vs 2.5 % in the toremifene group , a significant relative risk reduction of 50 % ( 95 % CI -1.5 to 75.0 , p = 0.05 ) . Toremifene significantly increased bone mineral density at the lumbar spine , hip and femoral neck vs placebo ( p < 0.0001 for all comparisons ) . There was a concomitant decrease in markers of bone turnover ( p < 0.05 for all comparisons ) . Toremifene also significantly improved lipid profiles . Venous thromboembolic events occurred more frequently with toremifene than placebo with 7 subjects ( 1.1 % ) in the placebo group experiencing a venous thromboembolic event vs 17 ( 2.6 % ) in the toremifene group . Other adverse events were similar between the groups . CONCLUSIONS Toremifene significantly decreased the incidence of new vertebral fractures in men receiving and rogen deprivation therapy for prostate cancer . It also significantly improved bone mineral density , bone turnover markers and serum lipid profiles PURPOSE Gonadotropin-releasing hormone ( GnRH ) agonists decrease bone mineral density ( BMD ) and increase fracture risk in men with prostate cancer . Annual zoledronic acid increases BMD in postmenopausal women , but its efficacy in hypogonadal men is not known . PATIENTS AND METHODS In a 12-month study , 40 men with nonmetastatic prostate cancer who were receiving a GnRH agonist and had T scores more than -2.5 were r and omly assigned to zoledronic acid ( 4 mg intravenously on day 1 only ) or placebo .  BMD of the posteroanterior lumbar spine and proximal femur were measured by dual-energy x-ray absorptiometry . RESULTS Mean ( + /- SE ) BMD of the posteroanterior lumbar spine decreased by 3.1 % + /- 1.0 % in men assigned to placebo and increased by 4.0 % + /- 1.0 % in men assigned to zoledronic acid ( P < .001 ) . BMD of the total hip decreased by 1.9 % + /- 0.7 % in men assigned to placebo and increased by 0.7 % + /- 0.5 % in men assigned to zoledronic acid ( P = .004 ) . Similar between-group differences were observed for the femoral neck and trochanter . Serum N-telopeptide , a marker of osteoclast activity , decreased significantly after zoledronic acid treatment . CONCLUSION In men receiving a GnRH agonist  , a single treatment with zoledronic acid significantly increased BMD and durably suppressed serum N-telopeptide levels for 12 months . Annual zoledronic acid may be a convenient and effective strategy to prevent bone loss in hypogonadal men To report a r and omized , placebo‐controlled study of treatment with zoledronic acid every 3 months in patients with hormone‐sensitive prostate cancer , both with and without bone metastases , to assess the effect on bone mineral density ( BMD ) and markers of bone turnover PURPOSE And rogen deprivation therapy for prostate cancer is associated with osteoporosis and increased fracture risk . Previous studies of zoledronic acid demonstrated bone loss prevention in patients initiating and rogen deprivation therapy .  There are limited data on patients on prolonged and rogen deprivation therapy or in Veterans Affairs patients with multiple risk factors for osteoporosis . METHODS We r and omized 93 patients with M0 prostate cancer in this placebo controlled trial in the Veterans Affairs health care system . Preplanned strata included 50 patients on and rogen deprivation therapy for less than 1 year ( stratum 1 ) and 43 on and rogen deprivation therapy for greater than 1 year ( stratum 2 ) . In each stratum patients were r and omized to 4 mg zoledronic acid intravenously every 3 months for 4 treatments or intravenous placebo . The primary end point was the percent change in bone mineral density at the lumbar spine at 12 months . RESULTS Age , race , body mass index and osteoporosis risk factors were similar for the 2 treatments . Most patients were former smokers , had moderate alcohol intake , were not on calcium/vitamin D supplements and were relatively sedentary at baseline . In stratum 1 spine bone mineral density increased 5.95 % in the zoledronic acid arm and decreased 3.23 % in the placebo arm ( p = 0.0044 ) . In stratum 2 spine bone mineral density increased 6.08 % in the zoledronic acid arm and only increased 1.57 % in the placebo arm ( p = 0.0005 ) . Treatment was well tolerated with minimal impact on renal function . CONCLUSIONS Zoledronic acid improved bone mineral density in patients with M0 prostate cancer on and rogen deprivation therapy for 1 year or less , or greater than 1 year . This finding indicates that bisphosphonate therapy remains effective when initiated later in the course of and rogen deprivation therapy and is efficacious in Veterans Affairs patients with multiple risk factors for osteoporosis UNLABELLED Today , and rogen deprivation therapy is a cornerstone of treatment for advanced prostate cancer , although it presents important complications such as osteoporosis .  Neridronate , a relatively new bisphosphonate , is able to prevent bone loss in patients with prostate cancer during and rogen ablation . INTRODUCTION And rogen-deprivation therapy ( ADT ) is a cornerstone of treatment for advanced prostate cancer . This therapy has iatrogenic complications , such as osteoporosis . The aim of our study was to evaluate the efficacy of neridronate , a relatively new bisphosphonate , to prevent bone loss during and rogen ablation . MATERIAL S AND METHODS Forty-eight osteoporotic patients with prostate cancer , treated with 3-month depot triptorelina  , were enrolled and r and omly assigned to two different treatment groups : group A ( n = 24 ) was treated with a daily calcium and cholecalciferol supplement ( 500 mg of elemental calcium and 400 IU cholecalciferol ) , and group B ( n = 24 ) received in addition to the same daily calcium and cholecalciferol supplement , 25 mg of neridronate given intramuscularly every month . All patients also received bicalutamide for 4 weeks . Lumbar and femoral BMD was evaluated by DXA at baseline and after 1 year of therapy ; moreover , deoxypyridinoline ( DPD ) and bone alkaline phosphatase ( BALP ) were determined at the beginning , midway through , and at the end of the study . RESULTS After 6 and 12 months , whereas patients treated only with calcium and cholecalciferol ( group A ) showed a marked bone loss , with increased levels of DPD and BALP compared with baseline values , patients treated also with neridronate ( group B ) had substantially unchanged levels of these markers . After 1 year of treatment , lumbar and total hip BMD decreased significantly in patients treated only with calcium and cholecalciferol ( group A ) , whereas it did not change significantly at any skeletal site in patients treated also with neridronate ( group B ) . No relevant side effects were recorded during our study . CONCLUSIONS Neridronate is an effective treatment in preventing bone loss in the hip and lumbar spine in men receiving ADT for prostate cancer Objectives : Long-term results of radiotherapy in locally advanced prostate cancer are poor due to local and distant failures . Since prostate cancer is hormone dependent , tumor and rogen deprivation may enhance tumor eradication . Methods : Three r and omized phase III trials , RTOG and EORTC are reported : they assess and rogen suppression by using a luteinizing hormone-releasing hormone analogue ( LH-RHa ) with or without and rogen blockade before and during , or during and after external irradiation . Results : A gain in disease-free , local relapse-free and metastasis-free survival has been obtained ( p < 0.001 ) . Only the EORTC 22863 trial has reported a significant improvement in overall survival ( p = 0.001 ) with an LH-RHa started the first day of radiotherapy and administered every 4 weeks over 3 years . In the RTOG 85 - 10 trial , and LH-RHa , initiated in the last week of radiation therapy and continued until relapse , increased overall survival only in patients with poorly differentiated tumor with a Gleason score of 8–10 ( p = 0.03 ) . Conclusion : And rogen suppression prior to and during radiation improves disease-free survival ;  adjuvant hormonal therapy with an LH-RHa during and after radiation improves overall survival OBJECTIVE And rogen-deprivation therapy ( ADT ) is the usual treatment for locally advanced or metastatic prostate cancer . Osteoporosis is a common complication of ADT . The aim of our study was to evaluate the efficacy of neridronate , a relatively new bisphosphonate to prevent bone loss during and rogen ablation . METHODS Sixty patients with prostate cancer and osteoporosis were enrolled and r and omly assigned to 2 different treatment regimes : group A ( 30 patients ) treated with maximum and rogenic blockage ( MAB ) , and group B ( 30 patients )  treated with bicalutamide 150 mg . Each group was divided in 2 subgroups A1-A2 and B1-B2 . All patients received calcium and cholecalciferol supplements ( 500 mg of elemental calcium and 400 IU cholecalciferol ) daily . The A2 and B2 subgroups were also treated with neridronate ( 25 mg intramuscular monthly ) . Lumbar and femoral bone mineral density ( BMD ) was evaluated by dualenergy X-ray absorptiometry ( DXA ) , both at baseline and after one year of treatment . Deoxypyridinoline ( DPD ) and bone-alkaline phosph 
    Output:
    
However , there was no significant reduction in fractures .
Currently , our meta- analysis suggested that oral and intravenous bisphosphonates caused a rapid increase in spine and hip or femoral BMD in non-metastatic prostate cancer patients receiving and rogen-deprivation therapy .
Fever and gastrointestinal symptoms were common with the use of bisphosphonates .
These short-term trials ( maximum of 12 months ) did not show fracture reduction .