title: Bone mineral density in Japanese prostate cancer patients under androgen-deprivation therapy.
abstract: Androgen-deprivation therapy (ADT) of patients with prostate cancer (PCa) is known to reduce bone mineral density (BMD). However, the most studies examined Caucasian or black patients and the effects of ADT on the bone metabolism of East Asians are unclear. Therefore, we performed a cross-sectional study to elucidate the influence of ADT on bone metabolism in Japanese patients. In total, 101 native Japanese patients with PCa were enrolled. They consisted of 58 ADT-treated and 43 hormone-naive patients. The BMD in the lumbar spine, total hip, and femoral neck was measured by dual energy X-ray absorptiometry and expressed in s.d. units relative to young adult men (T-score) or age-matched men (Z-score). Serum levels of bone metabolism markers were also measured. The BMDs at the three sites revealed that 2.3% (1/43) and 8.6% (5/58) of the hormone-naive and ADT-treated PCa patients had osteoporosis respectively, but this difference failed to achieve statistical significance (P=0.294). The two groups also did not differ significantly in their Z-scores of the three sites, and univariate and multivariate analyses indicated that ADT was not a significant risk factor for decreased BMD. In addition, a significant correlation between the duration of ADT and BMD was not observed for all three sites measured. However, the ADT-treated patients had significantly higher serum levels of N-terminal telopeptide of type I collagen (NTx) than the hormone-naive patients (P=0.017). To our knowledge, this is the first study to demonstrate the low prevalence of osteoporosis in both ADT-treated and hormone-naive Japanese PCa patients. Moreover, ADT did not significantly increase the prevalence of osteoporosis in this Japanese population.
authors.affiliation: Department of Urology, Akita University School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Takeshi
authors.initials: T
authors.lastname: Yuasa
authors.forename: Norihiko
authors.initials: N
authors.lastname: Tsuchiya
authors.forename: Shinya
authors.initials: S
authors.lastname: Maita
authors.forename: Teruaki
authors.initials: T
authors.lastname: Kumazawa
authors.forename: Takamitsu
authors.initials: T
authors.lastname: Inoue
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Saito
authors.forename: Zhiyong
authors.initials: Z
authors.lastname: Ma
authors.forename: Takashi
authors.initials: T
authors.lastname: Obara
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tsuruta
authors.forename: Shigeru
authors.initials: S
authors.lastname: Satoh
authors.forename: Tomonori
authors.initials: T
authors.lastname: Habuchi
mesh_terms: D015502:Absorptiometry, Photon; D000368:Aged; D000726:Androgen Antagonists / Q000627:therapeutic use*; D044466:Asian People; D015519:Bone Density / Q000187:drug effects*; D001851:Bone Diseases, Metabolic / Q000097:blood / Q000209:etiology; D001859:Bone Neoplasms / Q000097:blood / Q000188:drug therapy* / Q000556:secondary; D024042:Collagen Type I / Q000097:blood; D003430:Cross-Sectional Studies; D005272:Femur Neck / Q000378:metabolism; D006615:Hip / Q000502:physiology; D006801:Humans; D008159:Lumbar Vertebrae / Q000378:metabolism; D008297:Male; D010024:Osteoporosis / Q000097:blood / Q000209:etiology; D010455:Peptides / Q000097:blood; D017430:Prostate-Specific Antigen / Q000097:blood; D011471:Prostatic Neoplasms / Q000097:blood / Q000188:drug therapy* / Q000473:pathology
chemical_list: D000726:Androgen Antagonists; D024042:Collagen Type I; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; D017430:Prostate-Specific Antigen