title: Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia.
abstract: OBJECTIVE
  Treatment for childhood leukaemia induces many risk factors for development of decreased bone mineral density (BMD). Physical activity is also known to affect BMD. The aim was to study BMD and markers of bone turnover in a well-defined group of survivors of acute lymphoblastic leukaemia (ALL) who had all reached final height as well as peak bone mass, taking both previous treatment and physical activity into consideration.
  
  
  METHODS
  All patients treated for ALL before the onset of puberty in the region of western Sweden, between 1973 and 1985, in first remission were included. Thirty-five out of forty-seven patients aged 20-32 years participated. Nineteen patients had received cranial radiotherapy, and the median follow-up time was 20 years.
  
  
  METHODS
  BMD was assessed using dual-energy X-ray absorptiometry (DEXA). Serum concentrations of markers of bone turnover were analysed. Physical performance was measured using a performance exercise capacity stress test.
  
  
  RESULTS
  BMD was slightly reduced in lumbar spine (-0.4 SD), but not in femoral neck or total body. BMD in femoral neck was correlated to physical performance and dose of corticosteroid, but no correlation was found with spontaneous growth hormone (GH) secretion. Markers of bone turnover were also correlated to physical performance, but not to GH secretion.
  
  
  CONCLUSIONS
  Physical fitness seems to be the most important factor in developing and preserving normal bone mineral density in ALL patients. We propose that lifestyle education promoting physical activity is encouraged from an early point in time for these patients.
authors.affiliation: Department of Paediatrics, Division of Haematology and Oncology, Sahlgrenska Academy of Göteborg University, Göteborg, Sweden. marianne.jarfelt@vgregion.se
authors.forename: M
authors.initials: M
authors.lastname: Jarfelt
authors.forename: H
authors.initials: H
authors.lastname: Fors
authors.forename: B
authors.initials: B
authors.lastname: Lannering
authors.forename: R
authors.initials: R
authors.lastname: Bjarnason
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D015519:Bone Density / Q000502:physiology*; D016723:Bone Remodeling / Q000502:physiology*; D024042:Collagen Type I; D005260:Female; D006801:Humans; D008297:Male; D009043:Motor Activity / Q000502:physiology; D015675:Osteocalcin / Q000097:blood; D010024:Osteoporosis / Q000097:blood / Q000209:etiology* / Q000378:metabolism; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000097:blood / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D011347:Procollagen / Q000097:blood; D018709:Statistics, Nonparametric
chemical_list: D024042:Collagen Type I; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C042813:procollagen type I carboxy terminal peptide; D015675:Osteocalcin; D000469:Alkaline Phosphatase