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Clin Chim Acta. 2006 Jun;368(1-2):48-52. Epub 2006 Feb 9.

Bone resorption markers in vitamin D insufficiency.

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Department of Clinical Biochemistry, Institute of Medical and Veterinary Science, Frome Road, Adelaide, South Australia 5000, Australia.


Severe vitamin D deficiency (serum 25 hydroxyvitamin D (25(OH)D) below 12.5 nmol/L) causes rickets and osteomalacia, but there is good evidence that lesser degrees of hypovitaminosis D (vitamin D insufficiency) have deleterious effects on bone and other organs. Evidence of impaired mineralization, suggestive of vitamin D insufficiency, has been found in bone biopsies of hip fracture patients in the UK, and several studies around the world have shown a rise in serum parathyroid hormone (PTH) as 25(OH)D levels fall below 50 nmol/L. Fifty-seven percent of hospital inpatients in a Boston study had vitamin D insufficiency and their serum 25(OH)D showed an inverse relationship to their serum alkaline phosphatase (ALP) levels. Thirty-five percent of outpatients had vitamin D insufficiency in an Adelaide study, where ALP and urine hydroxyproline and pyridinium cross-links were all inversely related to serum 25(OH)D. The increased bone resorption of vitamin D insufficiency is important on two counts. Firstly, increased bone resorption may lead to increased bone loss and osteoporosis and, secondly, increased turnover appears to increase fracture risk in its own right. A consensus is developing that serum 25(OH)D levels should be maintained at 50 nmol/L or greater in the elderly to minimize the occurrence of fractures. In addition, it appears that optimal levels of bone resorption markers in this population are at or just below the mean level for premenopausal women.

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