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Metabolic Bone Disease in Patients Receiving Long-Term Total Parenteral Nutrition

MOSHE SHIKE, M.D.; JOAN E. HARRISON, M.D.; WILLIAM C. STURTRIDGE, M.D., Ph.D.; CHERK S. TAM, M.D., Ph.D.; PETER E. BOBECHKO, M.D.; GLENVILLE JONES, Ph.D.; TIMOTHY M. MURRAY, M.D.; and KHURSHEED N. JEEJEEBHOY, M.B., B.S.; Ph.D.
[+] Article and Author Information

Grant support: by the Ontario Ministry of Health (Research Grant PR 228).

This paper was presented in part at the July 1979 meeting of the American Society for Clinical Nutrition and the Nutrition Society of Canada.

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


Toronto, Canada


© 1980 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1980;92(3):343-350. doi:10.7326/0003-4819-92-3-343
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We have prospectively investigated calcium and bone metabolism in 16 patients receiving total parenteral nutrition for periods ranging from 7 to 89 months. In 12 patients, bone biopsies at 6 to 73 months after the start of parenteral nutrition showed osteomalacia. Plasma 25-hydroxyvitamin D levels were normal in all patients. Seven persons developed hypercalcemia, and 10 had hypercalciuria with a negative calcium balance. Serum phosphorus was normal and plasma parathyroid hormone level, normal or decreased. Three patients with the severest form of the disease had vitamin D withdrawn from their solutions. Subsequently, urinary calcium decreased, and serum calcium became normal; two persons reverted to a positive calcium balance. Thus, patients receiving total parenteral nutrition may develop metabolic bone disease characterized by osteomalacia, hypercalcemia, hypercalciuria, and a negative calcium balance. This may be caused by both defective mineralization and increased bone resorption induced by vitamin D, its metabolites, or another unrecognized factor.

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