Related Experiment Video
Updated: Aug 6, 2026

Scanning Skeletal Remains for Bone Mineral Density in Forensic Contexts
Published on: January 29, 2018
Bone mineral status in pediatric outpatients on antiepileptic drug monotherapy
Hasan Tekgul1, Gul Serdaroglu, Afig Huseyinov
1Department of Pediatrics, Division of Pediatric Neurology, Ege University Medical Faculty, Izmer, Turkey. htekgul@med.ege.edu.tr
Insights
Antiepileptic drug monotherapy in children rarely caused osteopenia over two years. Bone mineral density was not linked to vitamin D levels, suggesting other factors may be involved in drug-induced bone loss.
Area of Science:
- Pediatric Endocrinology
- Pharmacology
- Bone Metabolism
Background:
- Drug-induced osteopenia is a concern in children on long-term antiepileptic drugs.
- Previous studies focused on institutionalized children, necessitating research on ambulatory outpatients.
Purpose of the Study:
- To longitudinally assess bone mineral status in pediatric outpatients receiving antiepileptic drug monotherapy.
- To investigate the relationship between bone mineral density and serum active vitamin D levels.
Main Methods:
- A 2-year longitudinal study of 30 ambulatory pediatric outpatients on valproic acid, carbamazepine, or phenobarbital monotherapy.
- Bone mineral density (BMD) measured using dual-energy x-ray absorptiometry (DXA).
- Assessed serum levels of active vitamin D and biochemical bone markers.
Main Results:
- A low frequency (6.7%) of osteopenia (BMD Z-scores < -1.5) was observed in two patients (one on carbamazepine, one on phenobarbital).
- No significant correlation was found between serum active vitamin D levels or biochemical markers and BMD Z-scores.
- Osteopenia was not attributed to impaired active vitamin D production or hyperparathyroidism.
Conclusions:
- Antiepileptic drug monotherapy in ambulatory pediatric outpatients has a low risk of inducing osteopenia over two years.
- The development of osteopenia in this context is not clearly linked to vitamin D deficiency or altered bone turnover markers.
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.
Related Concept Videos
Pharmacokinetics in Pediatric Patients: Drug Distribution
Pharmacokinetics in Pediatric Patients: Overview and Drug Absorption
Pharmacokinetics in Pediatric Patients: Drug Excretion
Antiepileptic Drugs: Potassium Channel Activators
Ezogabine has gained approval as an adjunctive treatment...
Pharmacokinetics in Pediatric Patients: Drug Metabolism
Antiepileptic Drugs: Calcium Channel Blockers
Calcium channel blockers exert their antiepileptic effects by targeting T-type calcium channels, which are integral to transmitting nerve signals in the central nervous system. These channels allow the passage of calcium ions, which are vital for neuronal communication. By inhibiting T-type calcium channels, calcium channel blockers effectively reduce the release of neurotransmitters and...
