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Division of Hematology and Oncology (M.R.S., M.A.F.) and Endocrine Unit (J.S.F.), Department of Medicine, and the Biostatistics Center (H.L.), Massachusetts General Hospital, Boston, Massachusetts 02114
Address all correspondence and requests for reprints to: Dr. Matthew R. Smith, Massachusetts General Hospital, Cox 640, 100 Blossom Street, Boston, Massachusetts 02114. E-mail: smith.matthew{at}mgh.harvard.edu.
GnRH agonists decrease bone mineral density and increase fracture risk in men with prostate cancer. Raloxifene increases bone mineral density in postmenopausal women, but its efficacy in hypogonadal men is not known. In a 12-month open-label study, men with nonmetastatic prostate cancer (n = 48) who were receiving a GnRH agonist were assigned randomly to raloxifene (60 mg/d) or no raloxifene. Bone mineral densities of the posteroanterior lumbar spine and proximal femur were measured by dual energy x-ray absorptiometry. Mean (±SE) bone mineral density of the posteroanterior lumbar spine increased by 1.0 ± 0.9% in men treated with raloxifene and decreased by 1.0 ± 0.6% in men who did not receive raloxifene (P = 0.07). Bone mineral density of the total hip increased by 1.1 ± 0.4% in men treated with raloxifene and decreased by 2.6 ± 0.7% in men who did not receive raloxifene (P < 0.001). Similar between-group differences were observed in the femoral neck (P = 0.06) and trochanter (P < 0.001). In men receiving a GnRH agonist, raloxifene significantly increases bone mineral density of the hip and tends to increase bone mineral density of the spine.
This work was supported by the Prostate Cancer Foundation, by a National Institutes of Health Clinical Associate Physician Award (to M.R.S.), and by grants from the National Institutes of Health (to J.S.F.) (K24 DK02759) and the Mallinckrodt General Clinical Research Center (M01-RR-01066). The study sponsors played no role in the study design, in collection, analysis, and interpretation of data, or in writing of this report.
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