title: Effect of chemotherapy on skeletal health in male survivors from testicular cancer and lymphoma.
abstract: OBJECTIVE
  There are concerns over the late effects of cancer therapy, including accelerated bone loss leading to increased risk of osteoporosis. Treatment-related bone loss is well recognized in breast and prostate cancer, due to overt hypogonadism, but there has been little evaluation of the skeletal effects of chemotherapy alone in adults. This study assesses the extent of bone loss due to previous chemotherapy in men.
  
  
  METHODS
  The bone mineral density (BMD) of men who had received previously chemotherapy with curative intent for lymphoma or testicular cancers was compared with that of an age-matched population of men from a cancer control population that had not received chemotherapy. BMD was measured by dual-energy X-ray scanning. Additionally, measurement of sex hormones and the bone turnover markers N-telopeptide fragment of type I collagen and bone-specific alkaline phosphatase were done. All statistical tests were two sided.
  
  
  RESULTS
  One hundred fifteen chemotherapy-treated patients and 102 cancer controls were recruited. There was no statistical difference in BMD between the chemotherapy and control groups at either spine or hip and the mean BMD values in both groups were no lower than that of a reference population. There were no significant differences in estradiol, luteinizing hormone, and testosterone, but follicle-stimulating hormone values were significantly higher in the chemotherapy group (P=0.011). The mean values of NH2-terminal telopeptide fragment of type I collagen and bone-specific alkaline phosphatase were within the reference ranges.
  
  
  CONCLUSIONS
  The absence of accelerated bone loss following chemotherapy is reassuring and suggests that standard dose cytotoxic chemotherapy has no lasting clinically important direct effects on bone metabolism.
authors.affiliation: Academic Unit of Clinical Oncology, Weston Park Hospital, University of Sheffield, UK. J.E.Brown@leeds.ac.uk
authors.forename: Janet E
authors.initials: JE
authors.lastname: Brown
authors.forename: Sue P
authors.initials: SP
authors.lastname: Ellis
authors.forename: Paul
authors.initials: P
authors.lastname: Silcocks
authors.forename: Aubrey
authors.initials: A
authors.lastname: Blumsohn
authors.forename: Sandra A
authors.initials: SA
authors.lastname: Gutcher
authors.forename: Clare
authors.initials: C
authors.lastname: Radstone
authors.forename: Barry W
authors.initials: BW
authors.lastname: Hancock
authors.forename: Matthew Q
authors.initials: MQ
authors.lastname: Hatton
authors.forename: Robert E
authors.initials: RE
authors.lastname: Coleman
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D000367:Age Factors; D000469:Alkaline Phosphatase / Q000097:blood / Q000187:drug effects; D000970:Antineoplastic Agents / Q000009:adverse effects*; D015519:Bone Density / Q000187:drug effects*; D001842:Bone and Bones / Q000187:drug effects*; D024042:Collagen Type I / Q000097:blood / Q000187:drug effects; D004958:Estradiol / Q000097:blood; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D007986:Luteinizing Hormone / Q000097:blood / Q000187:drug effects; D008223:Lymphoma / Q000188:drug therapy; D008297:Male; D010024:Osteoporosis / Q000139:chemically induced / Q000453:epidemiology; D010455:Peptides / Q000097:blood / Q000187:drug effects; D017741:Survivors; D013736:Testicular Neoplasms / Q000188:drug therapy; D013739:Testosterone / Q000097:blood
chemical_list: D000970:Antineoplastic Agents; D024042:Collagen Type I; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; D013739:Testosterone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D000469:Alkaline Phosphatase