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Longitudinal Study of Bone Turnover after Acute Spinal Cord Injury¹

Departments of Chemical Pathology (D.R., W.L., G.W., B.M., P.E.H.) and Medicine (R.C.C.) and the Spinal Injuries Unit (J.W.), Princess Alexandra Hospital, Woolloongabba, Queensland 4102; and Sullivan and Nicolaides Laboratories (R.F.), Taringa, Queensland 4068, Australia

Address all correspondence and requests for reprints to: Dr. David Roberts, Department of Chemical Pathology, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Queensland 4102, Australia. E-mail: davidr{at}australiamail.com

Increased bone turnover is a sequel of spinal cord injury (SCI) and predisposes to a number of clinically relevant complications, including osteoporosis and fractures. There are limited data available regarding the changes in modern markers of bone metabolism after SCI. We report a 6-month longitudinal follow-up of biochemical markers of bone metabolism (free and total deoxypyridinoline, total pyridinoline, N-telopeptide, osteocalcin, and total alkaline phosphatase) and bone mineral densitometry in 30 subjects with acute SCI. Markers of bone formation showed only a minor rise, remaining within the reference range. In contrast, markers of bone resorption showed a significant rise after acute SCI, peaking around weeks 10–16, with values up to 10 times the upper limit of normal. Paired bone mineral densities (n = 11; on the average, determined 14 weeks apart) showed no change at the hip, lumbar spine, or radius, but demonstrated a decrement in the entire lower limbs. Changes in biochemical markers of bone formation and resorption were comparable in patients with quadriplegia and paraplegia, except for a greater increase in quadriplegics in pyridinoline, expressed as a percentage of baseline. In conclusion, a marked increase in bone resorption and modest changes in bone formation occur after SCI, and possibly increased bone resorption occurs in quadriplegia.

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