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A Possible Role of Vitamin D in the Genesis of Parenteral-Nutrition-Induced Metabolic Bone Disease

MOSHE SHIKE, M.D.; WILLIAM C. STURTRIDGE, M.D., Ph.D.; CHERK S. TAM, M.B. B.S., Ph.D.; JOAN E. HARRISON, M.D.; GLENVILLE JONES, Ph.D.; TIMOTHY M. MURRAY, M.D.; H. HUSDAN, Ph.D.; JOCELYN WHITWELL, R.N., B.SC.N.; DOUGLAS R. WILSON, M.D.; and KHURSHEED N. JEEJEEBHOY, M.B.B.S., Ph.D.
[+] Article and Author Information

Grant support: grant PR 228, Province of Ontario Research Grant, and the Bone Mineralization Unit, University of Toronto.

Presented in part September 1980, at the International Conference on Calcium Regulating Hormones, Estes Park, Colorado.

▸Requests for reprints should be addressed to Moshe Shike, M.D.; Room 6352, Medical Sciences Building; University of Toronto; Toronto, Ontario, Canada M5S 1A8.


Toronto, Ontario, Canada


©1981 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1981;95(5):560-568. doi:10.7326/0003-4819-95-5-560
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Patients receiving long term parenteral nutrition may develop metabolic bone disease. In all 11 patients studied, histologic studies of bone showed excessive unmineralized bone tissue despite normal plasma 25-hydroxyvitamin D levels. Three patients also had bone pain and fractures and severe urinary loss of calcium and phosphate. Withdrawal of vitamin D from parenteral nutrition solutions was associated with improved histologic findings of bone in all patients, shown by a decrease in osteoid tissue and an increase in tetracycline uptake. In the three patients with symptoms, bone pain subsided, fractures healed, and urinary loss of calcium and phosphate decreased. Thus, vitamin D may be a factor in the genesis of parenteral nutrition-induced metabolic bone disease.

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