title: Cross-sectional study of bone turnover during bicalutamide monotherapy for prostate cancer.
abstract: OBJECTIVE
  Monotherapy with bicalutamide increases serum concentrations of testosterone and estradiol. Because estrogens play an important role in male bone metabolism, bicalutamide monotherapy may have fewer adverse effects on bone than androgen-deprivation therapy with a gonadotropin-releasing hormone agonist.
  
  
  METHODS
  In a cross-sectional study, we compared gonadal steroid levels and biochemical markers of bone turnover among three groups of men with prostate cancer: hormone-naive men, men treated with a gonadotropin-releasing hormone agonist, and men receiving bicalutamide monotherapy. Men with bone metastases or metabolic bone disease were excluded. Fifty-five eligible subjects were included in the analyses.
  
  
  RESULTS
  Serum testosterone and estradiol concentrations were lower in men treated with a gonadotropin-releasing hormone agonist than in hormone-naive men or men receiving bicalutamide monotherapy (P <0.001 for each comparison). Serum testosterone and estradiol concentrations were higher in men receiving bicalutamide monotherapy than in the hormone-naive men (P <0.001). The mean serum urinary excretion of deoxypyridinoline, urinary excretion of N-telopeptide, and serum osteocalcin were significantly higher in men treated with a gonadotropin-releasing hormone agonist than in the other groups (P <0.05 for each comparison). In contrast, biochemical markers of bone turnover were similar for hormone-naive men and men receiving bicalutamide monotherapy (P >0.05 for each comparison).
  
  
  CONCLUSIONS
  Biochemical markers of bone turnover are elevated in men receiving gonadotropin-releasing hormone agonist treatment but not in men receiving bicalutamide monotherapy. These observations suggest that bicalutamide monotherapy may maintain bone mineral density and prevent fractures.
authors.affiliation: Division of Hematology Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA.
authors.forename: Matthew R
authors.initials: MR
authors.lastname: Smith
authors.forename: Mary Anne
authors.initials: MA
authors.lastname: Fallon
authors.forename: Melissa J
authors.initials: MJ
authors.lastname: Goode
mesh_terms: D000726:Androgen Antagonists / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D000813:Anilides / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D018931:Antineoplastic Agents, Hormonal / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D015415:Biomarkers; D015519:Bone Density / Q000187:drug effects; D001862:Bone Resorption / Q000139:chemically induced / Q000378:metabolism; D001842:Bone and Bones / Q000187:drug effects* / Q000378:metabolism*; D003430:Cross-Sectional Studies; D004958:Estradiol / Q000097:blood; D050723:Fractures, Bone / Q000209:etiology / Q000517:prevention & control; D007987:Gonadotropin-Releasing Hormone / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D008297:Male; D009570:Nitriles; D010006:Osteoblasts / Q000187:drug effects; D015675:Osteocalcin / Q000097:blood; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism; D010024:Osteoporosis / Q000139:chemically induced / Q000150:complications; D011471:Prostatic Neoplasms / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D013739:Testosterone / Q000097:blood; D014105:Tosyl Compounds
chemical_list: D000726:Androgen Antagonists; D000813:Anilides; D018931:Antineoplastic Agents, Hormonal; D015415:Biomarkers; D009570:Nitriles; D014105:Tosyl Compounds; D015675:Osteocalcin; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D004958:Estradiol; C053541:bicalutamide