May Long Term Oxcarbazepine Treatment Be Lead to Secondary Hyperparathyroidism?
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Background and Purpose The adverse effects of newer antiepileptic drugs are not well-known. This study assessed the impact of oxcarbazepine (OXC) treatment on bone turnover. Methods Forty-four children with idiopathic focal (and/or secondarily generalized) epilepsy who had been treated with OXC for more than 1 year were compared with 33 healthy, age- and sexmatched children. Serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone, osteocalcin, calcitonin, and 25-hydroxyvitamin D, and bone mineral density were measured to evaluate and compare bone mineralization between the two groups. Results The serum levels of calcium, osteocalcin, 25-hydroxyvitamin D, and bone mineral density did not differ significantly between the study and control groups. However, serum levels of parathyroid hormone, alkaline phosphatase, phosphorus, and calcitonin differed significantly between the two groups. Conclusions These findings suggest that OXC treatment leads to secondary hyperparathyroidism with high-turnover bone disease and/or impaired intestinal calcium absorption.
Abstract
Background and Purpose The adverse effects of newer antiepileptic drugs are not well-known. This study assessed the impact of oxcarbazepine (OXC) treatment on bone turnover. Methods Forty-four children with idiopathic focal (and/or secondarily generalized) epilepsy who had been treated with OXC for more than 1 year were compared with 33 healthy, age- and sexmatched children. Serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone, osteocalcin, calcitonin, and 25-hydroxyvitamin D, and bone mineral density were measured to evaluate and compare bone mineralization between the two groups. Results The serum levels of calcium, osteocalcin, 25-hydroxyvitamin D, and bone mineral density did not differ significantly between the study and control groups. However, serum levels of parathyroid hormone, alkaline phosphatase, phosphorus, and calcitonin differed significantly between the two groups. Conclusions These findings suggest that OXC treatment leads to secondary hyperparathyroidism with high-turnover bone disease and/or impaired intestinal calcium absorption.
참고문헌 (20)
- Dent CE, "Osteomalacia with long-term anticonvulsant therapy in epilepsy", Br Med J, 4, pp.69~72 (1970)
- Bogliun G, "Anticonvulsant drugs and bone metabolism", Acta Neurol Scand, 74, pp.284~288 (1986)
- Pack AM, "Adverse effects of antiepileptic drugs on bone structure: epidemiology, mechanisms and therapeutic implications", CNS Drugs, 15, pp.633~642 (2001)
- Coppola G, "Bone mineral density in children, adolescents, and young adults with epilepsy", Epilepsia, 50, pp.2140~2146 (2009)
- Babayigit A, "Adverse effects of antiepileptic drugs on bone mineral density", Pediatr Neurol, 35, pp.177~181 (2006)
- Verrotti A, "Increased bone turnover in prepubertal, pubertal, and postpubertal patients receiving carbamazepine", Epilepsia, 43, pp.1488~1492 (2002)
- Mintzer S, "Vitamin D levels and bone turnover in epilepsy patients taking carbamazepine or oxcarbazepine", Epilepsia, 47, pp.510~515 (2006)
- Berg AT, "Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE Commission on Classification and Terminology, 2005-2009", Epilepsia, 51, pp.676~685 (2010)
- Pack AM, "Epilepsy and bone health in adults", Epilepsy Behav, 5(2), pp.S24~S29 (2004)
- Pack AM, "Bone disease associated with antiepileptic drugs", Cleve Clin J Med, 71(2), pp.S42~S48 (2004)
- Crosley CJ, "Rickets associated with long-term anticonvulsant therapy in a pediatric outpatient population", Pediatrics, 56, pp.52~57 (1975)
- Schmitt BP, "Prevalence of hypocalcemia and elevated serum alkaline phosphatase in patients receiving chronic anticonvulsant therapy", J Fam Pract, 18, pp.873~877 (1984)
- Hahn TJ, "Interaction of diphenylhydantoin (phenytoin) and phenobarbital with hormonal mediation of fetal rat bone resorption in vitro", J Clin Invest, 62, pp.406~414 (1978)
- Weinstein RS, "Decreased serum ionized calcium and normal vitamin D metabolite levels with anticonvulsant drug treatment", J Clin Endocrinol Metab, 58, pp.1003~1009 (1984)
- Bouillon R, "The effect of anticonvulsant therapy on serum levels of 25-hydroxy-vitamin D, calcium, and parathyroid hormone", J Clin Endocrinol Metab, 41, pp.1130~1135 (1975)
- Välimäki MJ, "Bone mineral density measured by dual-energy x-ray absorptiometry and novel markers of bone formation and resorption in patients on antiepileptic drugs", J Bone Miner Res, 9, pp.631~637 (1994)
- Schoppet M, "Role for alkaline phosphatase as an inducer of vascular calcification in renal failure?", Kidney Int, 73, pp.989~991 (2008)
- Verrotti A, "Increased bone turnover in epileptic patients treated with carbamazepine", Ann Neurol, 47, pp.385~388 (2000)
- Koch HU, "Influence of diphenylhydantoin and phenobarbital on intestinal calcium transport in the rat", Epilepsia, 13, pp.829~834 (1972)
- Vernillo AT, "Phenytoin affects osteocalcin secretion from osteoblastic rat osteosarcoma 17", 2.8 cells in culture, 1990, pp.11, 309~312
