Abstracts

Rationale: Rationale: Vitamin D is a neurosteroidal hormone that serves as a vital regulator for neuroprotection and antiepileptic effects. It accomplishes this via neuro-immunomodulation and interplay with neurotransmitters which directly affects the brain. Vitamin D regulates nerve growth factor (NGF) and glial cell line derived neurotrophic factor (GDNF) suggesting it may be able to provide some protection against excitatory neurotransmitters such as glutamate. It also influences apoptsosis and cell cycle in the developing brain. Vitamin D deficiency causes abnormal brain development in children as it is associated with persistent alteration in neuronal systems. It may cause mild distortion in brain shape, increase lateral ventricle volumes and reduce brain differentiation. Antiepileptic drug (AED) use can increase the risk of vitamin D deficiency as it decreases the metabolism of Vitamin D and interferes with the re-adsorption process. This results in decreased bone quality, density, and may have significant influence with the neuronal issues such as decreasing cell proliferation and causing an increase in programmed cellular elimination. Review of literature regarding vitamin D deficiency with AED use refers to adult patients. There are few studies measuring the effect deficiency has on pediatric neurologic children. We present 25 pediatric patients with low Vitamin D levels associated with AED treatment. Methods: Method: Twenty five pediatric patients were selected who had low vitamin D levels on receiving AED treatment. Comparison included the effects of enzyme-inducing vs non-inducing AED's as well as single vs. multiple AED therapy. The length of time on AED's was also evaluated as well as race, age and seizure type. Results: Results: The two most frequently used AED's that caused a decrease in Vitamin D level were Keppra (7/25) and Lamictal (5/25). There was no influence due to age or weight. More Caucasians (16/25) than non Caucasians were affected and more males (16/25) than females. Non Enzyme inducing AED's (28) caused more of a decrease in levels than enzyme inducing AED's ((9). There was more of a decrease with single use of AED's (15/25) vs multiple AED's (7). The length of time on AED's was 1 mos. to 84 mos. with the average of 47 mos. The vitamin D 25-OHD levels ranged from 14ng/ml to 35ng/ml. The lowest level occurred on an 11yr old caucasian on 2 non-enzyme inducing AED's for 2 yrs with generalized seizures. Conclusions: Conclusion: AED use can increase the risk of vitamin D deficiency in the pediatric population resulting in decreased bone density and bone mass as well as potentially altering the neuronal systems and brain development. Vitamin D levels may need to be drawn after starting all children on AED's and more closely monitored than is currently recommended. Further studies are needed to assess which AED's may be more detrimental to neuronal health in order to obtain optimization of seizure control with normal neuronal network development in children with epilepsy.