title: Early treatment with zoledronic acid prevents bone loss at the hip following acute spinal cord injury.
abstract: Osteoporosis after spinal cord injury is common. Reductions in bone density are rapid and fracture rates are higher after injury. Early treatment with 4 mg zoledronic acid significantly reduced bone loss at the hip compared to untreated individuals in the first year. Treatment appeared safe and well tolerated.
  
  
  BACKGROUND
  Bone mineral density (BMD) is lost rapidly following spinal cord injury (SCI), predominantly in the lower limbs. Bone turnover markers suggest an early increase in resorption.
  
  
  METHODS
  A randomised, open-label study of 14 patients with acute SCI randomised to receive 4 mg IV zoledronic acid or standard treatment. BMD was measured by dual-X-ray absorptiometry at the lumbar spine and hip (femoral neck, total and trochanter) at baseline, 3, 6 and 12 months. Bone turnover markers (serum C-terminal telopeptide and Procollagen I N-terminal peptide and urinary N-terminal telopeptide/Cr ratio) were also measured.
  
  
  RESULTS
  After 12 months, there was a significant difference in BMD between the groups at the total hip (12.4%, p = 0.005), trochanter (13.4%, p = 0.028) and lumbar spine (2.7%, p = 0.033). However, the difference between groups at the femoral neck was not significant (4.8%, p = 0.741). In the treated group, bone resorption was reduced and remained reduced up to 12 months. Other than flu-like symptoms immediately after the infusion, no adverse events were observed.
  
  
  CONCLUSIONS
  IV zoledronic acid is an effective and well-tolerated treatment to prevent bone mineral density loss at the total hip and trochanter for up to 12 months following SCI.
authors.affiliation: Metabolic Unit, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore, HA7 4LP, UK. jbubbear@doctors.org.uk
authors.forename: J S
authors.initials: JS
authors.lastname: Bubbear
authors.forename: A
authors.initials: A
authors.lastname: Gall
authors.forename: F R I
authors.initials: FR
authors.lastname: Middleton
authors.forename: M
authors.initials: M
authors.lastname: Ferguson-Pell
authors.forename: R
authors.initials: R
authors.lastname: Swaminathan
authors.forename: R W
authors.initials: RW
authors.lastname: Keen
mesh_terms: D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D015519:Bone Density / Q000187:drug effects; D050071:Bone Density Conservation Agents / Q000008:administration & dosage* / Q000627:therapeutic use; D001862:Bone Resorption / Q000209:etiology / Q000517:prevention & control; D001842:Bone and Bones / Q000378:metabolism; D004164:Diphosphonates / Q000008:administration & dosage* / Q000627:therapeutic use; D004334:Drug Administration Schedule; D005260:Female; D005500:Follow-Up Studies; D006621:Hip Joint / Q000503:physiopathology; D006801:Humans; D007093:Imidazoles / Q000008:administration & dosage* / Q000627:therapeutic use; D008159:Lumbar Vertebrae / Q000503:physiopathology; D008297:Male; D010024:Osteoporosis / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D013119:Spinal Cord Injuries / Q000150:complications* / Q000503:physiopathology; D055815:Young Adult; D000077211:Zoledronic Acid
chemical_list: D015415:Biomarkers; D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D007093:Imidazoles; D000077211:Zoledronic Acid