Oral Presentation ESA-SRB 2023 in conjunction with ENSA

Preventing osteoporosis in spinal cord injury (POPSCI) trial: early zoledronic acid infusion in acute spinal cord injury (#102)

Shejil Kumar 1 2 3 , Jean Doyle 1 , Maria-Liza Nery 1 , Roxana Heriseanu 4 , Gerard Weber 4 , Lianne Nier 4 5 , Roderick Clifton-Bligh 1 6 7 , Christian Girgis 1 3 6
  1. Endocrinology Department, Royal North Shore Hospital, Sydney
  2. Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia
  3. Endocrinology Department, Westmead Hospital, Sydney
  4. Department of Rehabilitation Medicine, Royal Rehab Hospital, Sydney
  5. Department of Rehabilitation Medicine, Royal North Shore Hospital, Sydney
  6. Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia
  7. Cancer Genetics Laboratory, Kolling Institute of Medical Research, Sydney

Background: Traumatic spinal cord injury (SCI) is a significant cause of disability, exacerbated by accelerated bone loss and increased fracture risk predominantly around the knee. Few studies have explored efficacy of IV zoledronic acid (ZOL) in patients with SCI with limited follow-up <24-months.

Methods: We conducted a prospective study investigating use of early ZOL after acute SCI. The study included two cohorts; an ‘intervention’ cohort (n = 11) admitted to Royal North Shore or Royal Rehab Hospitals, Sydney between 2018-2022 who sustained traumatic SCI in the past 8-12 weeks and received a single dose of 4mg ZOL after baseline studies, and a ‘historical control’ cohort (n = 9) who sustained traumatic SCI within the last 1-5 years and received standard care. All participants underwent baseline and 6-monthly bloods (including bone turnover markers (CTx and P1NP)) and 12-monthly DXA BMD scans of lumbar spine, left hip and knee.

Results: Baseline comparisons between both cohorts are summarised in Table 1. The ‘intervention’ cohort had higher baseline CTx, P1NP and sclerostin concentrations consistent with higher bone turnover in acute SCI. ‘Historical controls’ had lower baseline left hip and femoral metaphyseal BMD consistent with longer exposure to skeletal unloading. Majority experienced an acute phase reaction after ZOL (9/11 – 82%). In the ‘intervention’ cohort, CTx and P1NP fell by mean 50% at 12-months and plateaued to 36-months. Left hip BMD fell gradually by mean 13% by 36-months. Left femoral metaphyseal BMD declined by mean 22% respectively at 12-months and plateaued to 36-months. No fractures occurred.

Conclusions: Early ZOL prevented a rise in bone turnover markers in acute SCI however patients still experienced rapid decline in distal femoral BMD. Further studies assessing knee BMD response to antiresorptives and longer follow-up in SCI cohorts are required to optimise fracture risk reduction.

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