Association Between 25-hydroxyvitamin D Status and New Vertebral Fractures Post Percutaneous Vertebral Augmentation in Patients During Postmenopause: A Retrospective Case-control Study.

Abstract

Background: Serum 25-hydroxyvitamin D (25[OH]D) deficiency causes osteoporosis and increases muscle weakness, which worsens the risk of falls and osteoporotic vertebral fractures. However, the effect of a lower serum 25(OH)D level on new vertebral fractures, including osteoporotic vertebral refractures and cascade vertebral fractures post percutaneous vertebral augmentation in patients during postmenopause has not been reported.

Objectives: This study aimed to investigate the relationship between serum 25(OH)D and the risk of osteoporotic vertebral refractures and cascade vertebral fractures.

Study design: A retrospective case-control study.

Setting: This study took place at the Department of Spinal Surgery at a hospital affiliated with a medical university.

Methods: We retrospectively analyzed clinical data from patients during postmenopause aged >= 50 years who underwent percutaneous vertebral augmentation. The patients were categorized into a nonrefracture group, an osteoporotic vertebral refractures group, and a cascade vertebral fractures group. Univariate and multivariate logistic regression analysis models were employed to assess the effect of 25(OH)D on osteoporotic vertebral refractures and cascade vertebral fractures, while a receiver operating characteristic curve was used to evaluate its predictive value.

Results: A total of 528 patients were included in this study. Of these, 163 patients (30.9%) developed new vertebral fractures, with 124 (23.5%) classified as osteoporotic vertebral refractures and 39 (7.4%) as cascade vertebral fractures. The 25(OH)D levels were significantly lower in the new vertebral fracture group. Multivariate logistic regression analysis confirmed that an increase in 25(OH)D levels was protective against osteoporotic vertebral refractures occuring, including cascade vertebral fractures post percutaneous vertebral augmentation, even after adjusting for other potential confounding factors. A Pearson correlation analysis indicated a close relationship between vitamin D levels and L3 paraspinal muscle density and L3 bone mineral density in the enrolled patients with osteoporotic vertebral fractures (P < 0.05). A receiver operating characteristic curve analysis indicated an area under the curve of 0.751 for 25(OH)D levels in predicting the risk of osteoporotic vertebral refractures (cut-off value, 27.5 ng/mL; sensitivity, 62.74%; specificity, 72.60%; P = 0.001) and 0.831 for cascade vertebral fractures (cut-off value, 19.5 ng/mL, sensitivity, 56.41%; specificity, 97.53%; P = 0.001), respectively.

Limitations: This retrospective study was conducted at a single center with a limited number of patients during postmenopause who had prior percutaneous vertebral augmentation,  especially those that developed recurrent fractures.

Conclusions: A low serum 25(OH)D level is an independent risk factor for new vertebral fractures after percutaneous vertebral augmentation in patients during postmenopause. Appropriate active vitamin D supplementation following percutaneous vertebral augmentation surgery can effectively mitigate the risk of subsequent osteoporotic vertebral fractures.