Bone Mineral Status in Pediatric Outpatients on Antiepileptic Drug Monotherapy

Abstract

Drug-induced osteopenia has been reported in institutionalized children on chronic antiepileptic drug therapy. The aim of this study was to assess longitudinally bone mineral status in pediatric outpatients on antiepileptic drug monotherapy. The study group consisted of 30 ambulatory children on a normal diet: 15 on valproic acid, 11 on carbamazepine, and 4 on phenobarbital monotherapy. Bone mineral density, serum active vitamin D (1,25-dihydroxyvitamin D), and certain biochemical markers of bone formation (calcium, phosphorus, alkaline phosphatase, intact parathyroid hormone, osteocalcin, calcitonin, and urinary calcium to serum creatinine and urinary phosphorus to serum creatinine ratios) were studied at the beginning of antiepileptic drug monotherapy and at the end of 2 years of treatment. Age- and sex-specific Z-scores of bone mineral density were measured at anterior-posterior L2—L4 by dual-energy x-ray absorptiometry. Drug-induced osteopenia was defined in only two patients (one on carbamazepine and the other on phenobarbital monotherapy), with Z-scores of bone mineral density less than —1.5. Serum levels of active vitamin D and biochemical markers were not significantly correlated with the Z-scores of bone mineral density. We detected a frequency of antiepileptic drug—induced osteopenia of 6.7% in pediatric outpatients after 2 years of monotherapy. However, osteopenia was not attributed to a defect in serum active vitamin D production owing to hyperparathyroidism in children on antiepileptic drug monotherapy. ( J Child Neurol2006;21:411—414; DOI 10.2310/7010.2006.00066).