ABSTRACT
OBJECTIVES@#To assess the vitamin D status in postmenopausal women with osteoporotic fractures, determine its concentration by fracture site at the clinical setting, and compare the proportion of vitamin D deficiency with that reported in literature.@*METHODS@#The prospective study included 317 postmenopausal women with osteoporotic fractures who were treated consecutively from 2016 to 2018. After obtaining informed consent for participation in the seamless treatment of osteoporosis against fractures study, which is our initiative to prevent secondary osteoporotic fractures, we registered the patients, examined bone mineral density (BMD) at the unfractured femoral neck and lumbar spine, serum 25-hydroxyvitamin D (25(OH)D) concentration, blood chemistry, and bone turnover markers.@*RESULTS@#The mean age of the patients was 80.7 years. Moreover, 78% of patients of all fractures had 25(OH)D concentration < 20 ng/mL, whereas 12% of patients had 25(OH)D concentration ≥ 30 ng/mL 25(OH)D concentration in hip fractures was significantly lower than that in vertebral or distal radius fractures (P < 0.05). Multiple regression analysis revealed that 25(OH)D concentration is significantly associated with femoral neck BMD (β = 0.16; 95% confidence interval [CI], 0.78–12.17, P = 0.03) and serum albumin concentration (β = 0.21; 95% CI, 0.62–2.96, P < 0.001) in patients with 25(OH)D concentration < 30 ng/mL.@*CONCLUSIONS@#The results of this study show that the proportion of postmenopausal women with osteoporotic fractures who had vitamin D deficiency was higher than the proportion in previous reports that examined general postmenopausal women (35.2%–52.0%).
ABSTRACT
OBJECTIVES: The purpose of this study was to investigate the influences of interruption and reinitiation of monthly minodronate therapy on the bone mineral density (BMD) and bone metabolism markers in postmenopausal women with osteoporosis. METHODS: Study patients were included if they had been administered monthly minodronate therapy for ≥6 months, interrupted the therapy, and reinitiated the therapy for ≥12 months. The BMD and bone metabolism markers were assessed at 4 time points: initiation, interruption, reinitiation and 1 year after reinitiation of therapy. RESULTS: A total of 23 patients were enrolled. The mean monthly minodronate treatment period was 23.8 ± 12.9 months following a mean interruption period of 11.9 ± 5.4 months. Once increased by monthly minodronate treatment for 2 years on average, the BMD of lumbar spine and radius did not significantly decrease even after an interruption for 1 year on average. However, the BMD of the femoral neck did decrease after interruption. The BMD of the lumbar spine and radius increased further after 1 year of monthly minodronate retreatment. The BMD of the femoral neck did not change. Once decreased after the treatment for an average of 2 years followed by an interruption for 1 year, bone metabolism markers increased gradually but did not recover to baseline levels. A potent suppressive effect on bone resorption was noted. The change rate was greater for the bone formation marker procollagen 1 N-terminal propeptide. CONCLUSIONS: Monthly minodronate treatment increases BMD and reduces bone metabolism markers. The effect lessens after treatment interruptions, and can be restored by retreatment.