Vitamin D Boosts Alendronate Tail Effect on Bone Mineral Density in Postmenopausal Women with Osteoporosis

Vitamin D modulates bisphosphonate (BP) efficacy, but its contribution to bone mineral density (BMD) after BP discontinuation is not known. To address this topic, we performed a retrospective analysis of postmenopausal women exposed to alendronate (ALN) to treat osteoporosis who regularly continued the supplementation of cholecalciferol or calcifediol at recommended doses. In the ninety-six recruited women (age 61.1 +/- 6.9 years), ALN was administered for 31.2 +/- 20.6 months and then discontinued for 33.3 +/- 18.9 months. The modification of 25(OH)D serum levels over time was associated with a change of alkaline phosphatase (r = -0.22, p = 0.018) and C-terminal collagen type 1 telopeptide (r = -0.3, p = 0.06). Women in the tertile of the highest increase in 25(OH)D level showed a 5.7% BMD gain at lumbar spine, that was twice as great in comparison with participants with a lower 25(OH)D variation. At a multiple regression analysis, BMD change was associated with time since menopause (ss = 2.28, SE 0.44, p < 0.0001), FRAX score for major fracture (ss = -0.65, SE 0.29, p = 0.03), drug holiday duration (ss = -2.17, SE 0.27, p < 0.0001) and change of 25(OH)D levels (ss = 0.15, SE 0.03, p = 0.0007). After ALN discontinuation, improving the vitamin D status boosts the ALN tail effect on BMD.

Automated summary

Vitamin D supplementation can increase bone density in postmenopausal women, especially after discontinuation of alendronate. Changes in 25-hydroxyvitamin D levels are associated with changes in bone mineral density.