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Journal of Clinical Endocrinology & Metabolism, Vol 44, 617-621, Copyright © 1977 by Endocrine Society
ARTICLES |
W Jubiz, MR Haussler, TA McCain and KG Tolman
Recent evidence has linked altered plasma vitamin D metabolite levels to the reported occurrence of hypocalcemia and other metabolic abnormalities in patients receiving anticonvulsant drugs. We have measured plasma levels of 25-hydroxyvitamin D (25-(OH)D) and 1,25- dihydroxyvitamin D (1,25-(OH)2D) in institutionalized patients on diphenylhydantoin (Dilantin) and/or phenobarbital therapy. Values were compared with those obtained in institutionalized patients receiving no drugs and with normal ambulatory subjects. Although plasma 25-(OH)D levels were lower in the patients on drugs, a deficiency of 1,25- (OH)2D, the tissue active metabolite of vitamin D, was not present. These results indicate that in patients taking anticonvulsant drugs, the serum calcium, phosphorus, alkaline phosphatase and parathyroid hormone (PTH) abnormalities are not caused by a defective formation of 1,25-(OH)2D.
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