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.

Bone health in young women with epilepsy after one year of antiepileptic drug monotherapy

“…Of the few longitudinal studies, some revealed bone loss in children and adults as well as changes in indices of bone and mineral metabolism. [2][3][4][5] None have evaluated the effects of individual AEDs.…”

“…Of the few longitudinal studies, some revealed bone loss in children and adults as well as changes in indices of bone and mineral metabolism. [2][3][4][5] None have evaluated the effects of individual AEDs.We previously reported results of a cross-sectional study of bone mineral density (BMD) and indices of bone and mineral metabolism in premenopausal women with epilepsy taking Herein, we report our findings in women treated with one of four AEDs in monotherapy followed up for 1 year. Given the biochemical evidence of increased turnover at baseline in women receiving phenytoin, we hypothesized that there would be more bone loss in this group.…”

Molecular mechanisms responsible for the impact of antiepileptic therapy on bone mineral density of epileptic patients

“…Во многих работах показано, что терапия КБЗ вызы-вает снижение МПК в поясничном отделе позвоночника [29][30][31][32][33], шейке бедра [6,10,31,33], предплечье [33, 34] и пя-точной кости [35].…”

“…[38] у пациентов, принимающих КБЗ, показано увеличение уровня щелочной фосфатазы с изменением других марке-ров костного образования и резорбции, однако концентра-ция витамина D оставалась в пределах нормальных значе-ний. В двух других параллельных исследованиях продемон-стрировано отсутствие корреляции между уровнем витами-на D в сыворотке крови и снижением МПК при приеме КБЗ [10,30]. В работе А. Verrotti и соавт.…”

“…При оценке биохимиче-ских показателей костного метаболизма в большинстве ис-следований не выявлено статистически значимых различий в уровнях кальция [35,37,47]. Однако в других работах опи-сано значительное снижение концентрации кальция в сы-воротке крови [29,30].…”