title: Treatment with zoledronic acid ameliorates negative geometric changes in the proximal femur following acute spinal cord injury.
abstract: Acute spinal cord injury is associated with rapid bone loss and an increased risk of fracture. In this double-blind, randomized, placebo-controlled trial, 17 patients were followed for 1 year after administration of either 4 or 5 mg of zoledronic acid or placebo. Bone mineral density (BMD) and structural analyses of the proximal femur were performed using the hip structural analysis program at entry, 6 months, and 12 months. The 17 subjects completed 12 months of observation, nine receiving placebo and eight zoledronic acid. The placebo group showed a decrease in BMD, cross-sectional area, and section modulus and an increase in buckling ratio at each proximal femur site at 6 and 12 months. Six months after zoledronic acid, BMD, cross-sectional area, and section modulus increased at the femoral neck and intertrochanteric regions and buckling ratio decreased consistent with improved bone stability. However, at 12 months, the femoral narrow-neck values declined to baseline. In contrast to placebo, the intertrochanteric region and femur shaft were maintained at or near baseline through 12 months in the zoledronic acid-treated group. Urine N-telopeptide excretion was increased at baseline and declined in both the placebo and treatment groups during the 12 months of observation. We conclude that a single administration of zoledronic acid will ameliorate bone loss and maintain parameters of bone strength at the three proximal femur sites for 6 months and at the femur intertrochanteric and shaft sites for 12 months.
authors.affiliation: Department of Physical Medicine and Rehabilitation, Kennedy Krieger Institute, 707 North Broadway, Baltimore, MD 21205, USA. shapiroj@kennedykrieger.org
authors.forename: J
authors.initials: J
authors.lastname: Shapiro
authors.forename: B
authors.initials: B
authors.lastname: Smith
authors.forename: T
authors.initials: T
authors.lastname: Beck
authors.forename: P
authors.initials: P
authors.lastname: Ballard
authors.forename: M
authors.initials: M
authors.lastname: Dapthary
authors.forename: K
authors.initials: K
authors.lastname: BrintzenhofeSzoc
authors.forename: J
authors.initials: J
authors.lastname: Caminis
mesh_terms: D000293:Adolescent; D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D015415:Biomarkers / Q000097:blood; D015519:Bone Density / Q000187:drug effects; D050071:Bone Density Conservation Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001862:Bone Resorption / Q000209:etiology / Q000517:prevention & control*; D002118:Calcium / Q000097:blood; D004164:Diphosphonates / Q000009:adverse effects / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D005260:Female; D005269:Femur / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D005272:Femur Neck / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007093:Imidazoles / Q000009:adverse effects / Q000627:therapeutic use*; D008297:Male; D013119:Spinal Cord Injuries / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D000077211:Zoledronic Acid
chemical_list: D015415:Biomarkers; D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D007093:Imidazoles; D000077211:Zoledronic Acid; D000469:Alkaline Phosphatase; D002118:Calcium