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Decreased serum 24,25-dihydroxy vitamin D concentrations in children receiving chronic anticonvulsant therapy
Insights
Anticonvulsant drugs like phenobarbitone and phenytoin may cause osteomalacia by lowering serum 24,25-dihydroxy vitamin D (24,25(OH)2D) levels. This deficiency, not affecting 25-hydroxy vitamin D (25-OHD), is linked to bone issues in children and adolescents.
Area of Science:
- Endocrinology
- Pediatric Medicine
- Pharmacology
Background:
- Anticonvulsant drugs are widely used for long-term treatment.
- Potential side effects of these drugs on bone metabolism are a concern.
- Vitamin D metabolites play a crucial role in bone health.
Purpose of the Study:
- To investigate the impact of long-term phenobarbitone or phenytoin treatment on vitamin D metabolite levels in children and adolescents.
- To explore the relationship between altered vitamin D metabolite concentrations and bone health in patients on anticonvulsants.
Main Methods:
- Serum concentrations of 24,25-dihydroxy vitamin D (24,25(OH)2D) and 25-hydroxy vitamin D (25-OHD) were measured.
- Measurements were taken in 31 children and adolescents on long-term anticonvulsant therapy and in a control group.
- Radiological assessment for osteopenia was performed in some patients.
Main Results:
- Patients on phenobarbitone or phenytoin showed significantly depressed serum 24,25(OH)2D concentrations compared to controls.
- Serum 25-OHD concentrations were similar between patients and controls.
- Four patients with osteopenia exhibited very low 24,25(OH)2D levels and low 24,25(OH)2D:25-OHD ratios.
Conclusions:
- 24,25(OH)2D deficiency may contribute to the pathogenesis of osteomalacia in patients treated with anticonvulsant drugs.
- These findings provide indirect evidence for the importance of 24,25(OH)2D in maintaining normal bone structure.
- Monitoring 24,25(OH)2D levels could be relevant in children and adolescents on long-term anticonvulsant therapy.
Abstract:
Serum 24,25-dihydroxy vitamin D (24,25(OH)2D) and 25-hydroxy vitamin D (25-OHD) concentrations and the ratio between the two were measured in 31 Israeli children and adolescents receiving long-term treatment with phenobarbitone or phenytoin and in controls. 24,25 (OH)2D concentrations were significantly depressed in the patients, although the 25-OHD concentrations were similar to those in the healthy controls. In four patients with radiological evidence of osteopenia very low serum 24,25(OH)2D concentrations and serum 24,25(OH)2D: 25-OHD ratios were recorded. The findings suggest that 24,25(OH)2D deficiency may play an important part in the pathogenesis of osteomalacia in patients treated with anticonvulsant drugs and provide further indirect evidence that 24,25(OH)2D is important for normal bone structure.