Women with insufficient 25-hydroxyvitamin D without secondary hyperparathyroidism have altered bone turnover and greater incidence of vertebral fractures.

Abstract

The connection of 25-hydroxyvitamin D [25(OH)D] with bone metabolism is reported to occur indirectly through parathyroid hormone (PTH) activity. However, we hypothesized that 25(OH)D insufficiency raises the risk of bone fracture independent of PTH, since 25(OH)D insufficiency is not always accompanied by hyperparathyroidism. The aim of this study was to show a direct association between 25(OH)D, bone turnover markers, and fractures that was independent of PTH. We measured serum 25(OH)D in a group of 330 postmenopausal osteoporotic women who did not have secondary hyperparathyroidism. We analyzed the effects of 25(OH)D insufficiency [25(OH)D < 20 ng/mL] on the expression of several bone markers, including serum bone alkaline phosphatase (BAP), osteocalcin (OC), urinary N-terminal telopeptide of type-I collagen and free deoxypyridinoline (DPD), and inorganic phosphorus (IP), as well as on the prevalence of vertebral fractures. OC/BAP ratios and IP levels were significantly lower and DPD was significantly higher in 25(OH)D insufficient patients. These effects were independent of age, PTH, and estimated glomerular filtration rate (eGFR). 25(OH)D insufficiency, a low OC/BAP ratio, and low IP were related to the presence of prior vertebral fractures independent of PTH, bone mineral density (BMD), and eGFR. We propose that 25(OH)D insufficiency is associated with a low OC/BAP ratio and high DPD in postmenopausal osteoporosis patients without hyperparathyroidism. This pathological condition is associated with an increased incidence of prior vertebral fractures independent of PTH, BMD, and eGFR.