LETTER
Osteomalacia and Phenytoin Therapy
Mumtaz A. Siddiqui, MD
1 October 1994 | Volume 121 Issue 7 | Page 550
TO THE EDITOR:
In her review article [1], Dr. French mentions osteoporosis that is treatable with vitamin D as a long-term consequence of phenytoin therapy. In fact, osteomalacia with hypocalcemia and elevated alkaline phosphatase levels is far more common. This condition is attributed to both altered metabolism of vitamin D and the inhibition of intestinal absorption of Ca++ [2]. Phenytoin also increases the metabolism of vitamin K and reduces the concentration of vitamin K-dependent proteins that are important for normal Ca++ metabolism [3]. This may explain why osteomalacia is not always ameliorated by the administration of vitamin D. Phenytoin may block the effect of the parathyroid hormone on bone, inducing a type of pseudohypoparathyroidism [4], with resulting bone and teeth changes.
1. French J. The long-term therapeutic management of epilepsy. Ann Intern Med. 1994; 120:411-22.
2. Goodman LS, Gilman AG. The Pharmacological Basis of Therapeutics. 8th ed. New York: Macmillan; 1990:442.
3. Keith DA, Gundberg GM, Japour A, Aronoff J, Alvarez N, Gallop PM. Vitamin K dependent proteins and anticonvulsant medication. Clin Pharmacol Ther. 1983; 34:529-32.
4. Harris M, Goldhaber P. Root abnormality in epileptics and the inhibition of parathroid hormone-induced bone resorption by diphenylhydantoin in tissue culture. Arch Oral Biol. 1974; 19:981.
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