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A Plea for Monitoring and Treatment

Arch Neurol. 2001;58:1352-1353.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

APPROXIMATELY 30 years ago, the association between use of anticonvulsant drugs (also called antiepileptic drugs) and the development of skeletal bone lesions was described.¹ Accelerated catabolism of vitamin D was later demonstrated following phenobarbital treatment as a responsible mechanism for the low serum 25-hydroxyvitamin D concentrations in such patients.² It is now recognized that reduced 25-hydroxyvitamin D levels may result from the up-regulation of the hepatic cytochrome P₄₅₀ enzymes by anticonvulsant inducers, such as phenobarbital, phenytoin, and perhaps carbamazepine, or from the impairment of 25-hydroxylation of vitamin D.³

The resulting deficiency of vitamin D imposes the risk of skeletal fractures by increasing muscular weakness, accelerating bone loss, or impairing skeletal mineralization. Muscular weakness, which also occurs without associated skeletal findings of hypovitaminosis D,⁴ may increase the tendency to fall, and, in turn, heighten the risk of skeletal fracture. Subtle vitamin D deficiency results in compensatory secondary hyperparathyroidism and increased bone . . . [Full Text of this Article]

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