LETTER
Osteomalacia and Phenytoin Therapy
A. M. Parfitt
15 April 1995 | Volume 122 Issue 8 | Page 632
TO THE EDITOR:
Contrary to the statement in a recent letter by Siddiqui [1], osteomalacia verified by iliac bone histologic findings after double tetracycline labeling is rare in patients treated with anticonvulsant agents who are normally active and adequately nourished [2-4]. In the only systematic studies of such patients, no case of osteomalacia was found [2, 3]. Far more common is increased bone turnover caused by secondary hyperparathyroidism, a condition that causes accelerated loss of cortical bone, particularly in the extremities [4]. This abnormality is referred to by French [5] as "osteoporosis," although vertebral fracture rates are not increased. An increase in serum alkaline phosphatase levels in a patient treated with anticonvulsant agents is an indication that serum 25-hydroxyvitamin D and parathyroid hormone levels should be measured. If the former is low or the latter high, treatment with vitamin D or one of its metabolites is needed for the duration of anticonvulsant therapy [4].
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Author and Article Information
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Henry Ford Hospital, Detroit, MI 48202-2689.
1. Siddiqui MA. Osteomalacia and phenytoin therapy (Letter). Ann Intern Med. 1994; 121:550.
2. Mosekilde L, Melsen F. Dynamic differences in trabecular bone remodeling between patients after jejuno-ileal bypass for obesity and epileptic patients receiving anticonvulsant therapy. Metab Bone Dis Rel Res. 1980; 2:77-82.
3. Weinstein RS, Bryce GF, Sappington LJ, King DW, Gallagher BB. Decreased serum ionized calcium and normal vitamin D metabolite levels with anticonvulsant drug treatment. J Clin Endocrinol Metab. 1984; 58:1003-9.
4. Parfitt AM. Osteomalacia and related disorders. In: Avioli LV, Krane SM, eds. Metabolic Bone Disease and Clinically Related Disorders. 2d ed. Philadelphia: W. B. Saunders; 1990:329-96.
5. French J. The long-term therapeutic management of epilepsy. Ann Intern Med. 1994; 120:411-22.
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