Abstracts

Rationale: Bone mineral density (BMD) loss is a known complication in patients with epilepsy. Etiologies include but are not limited to the effect of anti-epileptic drugs (AEDs) on Vitamin D levels through the induction of hepatic enzymes. No clear guidelines to call for prevention of bone loss associated with AED’s exist, especially in children and adolescents with epilepsy. Study Objective: (1) To compare 25-hydroxy vitamin D (25-OHD) levels between patients on different classes of AEDs in pediatric patients on chronic epilepsy treatment. (2) To determine certain patient characteristics that may predict a low vitamin D level state. Methods: Retrospective chart review was performed on pediatric epilepsy patients treated with AEDs for at least 6 months with available 25-OHD levels, recruited from the outpatient neurology clinic of The Women and Children’s Hospital of Buffalo (WCHOB). Non-ambulatory patients and patients with known diseases that may interfere with bone homeostasis were excluded. 25-OHD levels were defined as insufficient <32 ng/ml and deficient <20ng/ml. Controls (pediatric patients without epilepsy) were recruited from the endocrinology clinic at WCHOB. AED therapy was classified based on P450 activity into enzyme-inducing (Phenytoin, Phenobarbital, Carbamazepine, Oxacarbazepine, Primidone) and non enzyme-inducing (Sodium Valproate, Lamotrigine, or Levetiracetam). Results: Analyses were based on a sample size of 63 patients; 47 (74.6%) had epilepsy (cases) and 16(25.4%) without epilepsy (controls). The mean (standard deviation) for 25-OHD levels was 18.3(10.4) and 26.1(6.3) in the case and control groups respectively, this difference was statistically significant (p=.008). 25-OHD levels predicted the case-control status, patients with higher 25-OHD levels were less likely to be in the epilepsy group (OR=.91; 95%CI =.85-.98, p =.01). The 25-OHD mean differences between AED types were significant between enzyme inducing and non-enzyme inducing AEDs (p =.000). There was a statistically significant main effect for the enzyme activity status of current AED (p-value 0.02) with a strong effect size (partial eta squared = 0.293). A main effect for race was statistically significant (p=.000; partial eta squared = 0.410). The interaction term effect between enzyme activity and Race showed a trend however it did not reach statistical significance (p = 0.079). Caucasian patients on non-enzyme inducing AEDs had the highest means 25-OHD (mean 33.4 SD 10.2) compared to African-American patients with mean 13.1 (6.6). African-American patients had the lowest 25-OHD levels with minimal effect of enzyme activity AEDs on the levels. Conclusions: Vitamin D levels are lower in children with epilepsy than controls. Enzyme-inducing AEDs may have a role. African-American patients are at greatest risk for low 25-OHD levels.