Background: Following spinal cord injury (SCI) dramatic declines in sub-lesional bone mineral density (BMD) and deterioration of bone microarchitecture occur, and are associated with a high prevalence of fractures. Conventional risk factors for osteoporosis diagnosis in the non-SCI population put all individuals with SCI at a high risk of fracturing, however not all experience fractures. Vitamin D and parathyroid hormone (PTH) levels have been linked to skeletal health in the non-SCI population, and therefore may be a modifiable risk factor worth targeting to prevent bone loss post-SCI.
Objectives: To evaluate: 1) the prevalence of suboptimal vitamin D (Serum 25(OH)D <75nmol/L) status and identify the relationships between 25(OH)D and bone quality; and 2) the prevalence of secondary hyperparathyroidism (Serum intact PTH ≥ 7.0 pmol/L) and identify the relationships between serum PTH and bone quality, in males and females with chronic SCI.
Methods: Individuals were assessed via cross-sectional study design. Serum 25(OH)D was measured using a chemiluminescent immunoassay and serum intact PTH was measured using an electrochemiluminescent immunoassay. Bone quality parameters evaluated include: 1) DXA assessed distal femur and proximal tibia aBMD; and 2) pQCT assessed vBMD at the 4% tibia trabecular and 66% tibia cortical sites, and 66% tibia cortical thickness. Correlates of suboptimal vitamin D status were identified through univariate logistic regression analaysis. Pearson correlations were run to assess the relationships between the serum measures and the bone quality outcomes. Significance was p<0.05.
Results: Thirty-eight percent of the included 45 adult males and females with chronic SCI had suboptimal serum 25(OH)D levels. Additionally, those with vitamin D assessed in the winter months (OR=6.3, p=0.022), not taking calcium supplements (OR=7.1, p=0.038), not taking vitamin D supplements (OR=10.5, p=0.049), and of younger age (OR=0.92, p=0.038) were associated with suboptimal vitamin D levels. A weak, non-significant association was observed between PTH and serum 25(OH)D (r=-0.327, p=0.068) and there was a trend towards an inverse association between PTH and 66% tibia cortical thickness (r=-0.353, p=0.071).
Conclusions: Many individuals with chronic SCI have suboptimal serum 25(OH)D levels, particularly in the winter months. Disruption of the vitamin D-PTH axis may contribute to the bone loss seen in the chronic SCI population, particularly in cortical bone. Optimal serum 25(OH)D levels in the chronic SCI population may be higher than in the non-SCI population. This exploratory corrrelational study provides a framework for evaluation of relationships between 25(OH)D and bone quality in a larger cohort, adjusting for factors known to influence these outcomes in the SCI population.