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J Am Geriatr Soc. 2001 Jul;49(7):877-83.

Serum and urine markers of bone metabolism during the year after hip fracture.

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Department of Orthopaedic Surgery, The Union Memorial Hospital, Baltimore, Maryland, USA.



As part of a larger study to describe indices of recovery during the year after hip fracture, the current prospective study investigated longitudinal changes in serum and urine markers of bone metabolism for the year after hip fracture and related them to bone mineral density (BMD).


A representative subset of participants provided serum and urine samples and had bone density measured at 3, 10, 60, 180, and 365 days postfracture.


Two Baltimore hospitals.


The subjects were 205 community-dwelling, white women age 65 and older with fresh proximal femur fractures.


Samples were assayed for specific bone-related proteins and bone turnover markers, including serum osteocalcin (OC), procollagen type 1 carboxy-terminal extension peptide (PICP), bone-specific alkaline phosphatase (BAP), and urinary deoxypyridinoline (DPD) cross-links. Selected hormonal regulators of bone metabolism, including parathyroid hormone (PTH), calcitonin (CT), 1,25-dihydroxy vitamin D(3) (1,25 (OH)(2)D), and estrone (E(1)) were measured from serum samples. Repeated measures analyses were used to evaluate postfracture changes in each of the markers.


BAP, OC, and PICP were most active during the early postfracture period (3-60 days). BAP and OC remained elevated at 365 days compared with 3 days. DPD rose 48% from 3 days to 60 days, but this difference was not statistically significant. PTH and 1,25 (OH)(2)D increased steadily and significantly from 3 to 365 days. E(1) was highest at baseline and decreased at each time point, whereas CT showed no significant changes. When subjects were stratified into high-, medium-, and low-BMD groups based on their measurement at 3 days, both osteoclastic and osteoblastic markers in the low-BMD group displayed exaggerated and different patterns over time compared with the other groups.


Currently, the standard treatment of care for hip fractures still results in high morbidity and mortality and failure to regain prefracture quality of life. Gaining an understanding of bone cell activity in these patients after hip fracture, derived by measuring markers longitudinally during recovery, provides a baseline by which to measure the effectiveness of new interventions to improve recovery from hip fracture.

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