부산대학교 도서관

Background. Both a decrease in bone formation and the skeletal consequences of secondary hyperparathyroidism have been implied in the pathogenesis of age-related femoral neck osteoporosis. However, studies using biochemical indices of bone remodeling in hip fracture patients have yielded conflicting results. Similarly, secondary hyperparathyroidism has not been a consistent finding in this population. Some of these inconsistencies might reflect differences in the assays used as well as in the timing of the sampling. Moreover, measurements were mostly performed in a limited number of patients. In this regard, the aim of the present study was to analyze potential alterations in bone metabolism in a large population of elderly hip fracture patients. Methods. Circulating concentrations of 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25[(OH).sub.2][D.sub.3]], intact parathyroid hormone (PTH), and calcitonin were measured in 117 elderly women (within a few hours after sustaining a fracture of the proximal femur) and in 117 healthy age-matched controls. In addition, serum osteocalcin and urinary excretion of (deoxy)pyridinoline were determined as markers of bone formation and resorption, respectively. Results. Serum levels of 25(OH)D and 1,25[(OH).sub.2][D.sub.3] were decreased in hip fracture patients. When correcting for differences in serum vitamin D binding protein, serum 25(OH)D was still significantly lower in patients than in controls, whereas serum 1,25[(OH).sub.2][D.sub.3] was not. Moreover, 25(OH)D deficiency in hip fracture patients was associated with an increase in circulating PTH and urinary excretion of (deoxy)pyridinoline. Serum osteocalcin, on the other hand, was significantly decreased in fracture patients. There was no statistically significant difference in calcitonin. Conclusion. These data suggest that there is reduced bone formation and increased bone resorption in patients with hip fracture. Although limited by its cross-sectional design, the present study emphasizes the role of secondary hyperparathyroidism-induced bone resorption in the pathogenesis of age-related osteoporosis, mainly due to a lack of 25(OH)D.