The Absence of Efficacy of Zoledronic Acid to Prevent Bone Loss at the Knee, but not the Hip, in Persons with Acute Spinal Cord Injury

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 281-290-Comparative Effectiveness/Health Outcomes/Quality Improvement/Patient or Provider Education/Endocrine Emergencies
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-286
William A Bauman*1, Christopher M Cirnigliaro1, Michael F LaFountaine1, Leighann C Martinez2, Pierre K Asselin1 and Steven C Kirshblum2
1James J. Peters VA Medical Center, Bronx, NY, 2Kessler Institute for Rehabilitation, West Orange, NJ
Background: During the initial years after acute spinal cord injury (SCI), the rate of bone loss causes an absolute depletion of the sublesional skeleton, particularly at the knee, a region that often falls below the fracture threshold. In persons with SCI, fractures occur with minimal trauma and lead to secondary morbidity. This study determined the efficacy of a single dose of zoledronic acid to prevent BMD loss at the hip and knee at 6 and 12 months after acute SCI.  Methods: A prospective, open-label, controlled drug intervention trial was performed on 14 patients with acute SCI: 7 subjects (6 of 7 were motor complete nonambulatory) received IV zoledronic acid (5 mg) at baseline and 7 subjects (all motor complete) served as controls and received no intervention. Areal BMD was performed at baseline, 6, and 12 months by dual energy x-ray absorptiometry (DXA; GE LUNAR Prodigy Advance) at the hip (e.g., total hip and femoral neck) and knee (e.g., distal femur and proximal tibia). Results: Compared to the treatment group, at 6 months the control group at the total hip lost significantly greater absolute (difference from baseline: -0.035 ± .029 g/cm2 vs. -0.142 g/cm2 ± 0.056, p = 0.0008) and percent of BMD (-3.0% ± 2.0 vs. -13.9% ± 5.1, respectively, p < 0.001).  At 12 months, BMD at the total hip continued to decline, albeit at a significantly slower rate and magnitude in the treatment group than in the control group for both absolute (difference from baseline: -0.079 ± .035 g/cm2 vs. -0.206 g/cm2 ± 0.010, p = 0.008) and percent of BMD  (-7.2% ± 3.4 vs. -20.1% ± 9.8, respectively, p < 0.01). BMD was not attenuated in the treatment group compared to controls at the distal femur and proximal tibia at the 6 month (-8.2% ± 3.1 vs.-2.7% ± 5.0, respectively, p < 0.05; and -9.6% ± 6.3 vs.-4.8% ± 6.8, respectively, p = NS) and 12 month (-16.8% ± 5.7 vs.-8.4% ± 7.2, respectively, p < 0.05; and -18.1% ± 10.2 vs.-7.9% ± 12.3, respectively, p = NS). Conclusions:  Zoledronic acid significantly reduced the loss of BMD at the hip in persons with acute SCI for at least the first 12 months after paralysis. In contrast, zoledronic acid failed to preserve BMD at the knee, and the knee is appreciated to be the region that is most susceptible to fragility fracture in the SCI population. Treatment with bisphosphonates at time of acute SCI appears to have differential treatment efficacy on regions in which trabecular (knee) or cortical bone (hip) predominate.

Nothing to Disclose: WAB, CMC, MFL, LCM, PKA, SCK

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Sources of Research Support: Veterans Affairs Rehabilitation Research and Development National Center of Excellence for the Medical Consequences of Spinal Cord Injury (#B9212-C)