Abstracts

AED associated osteopathies may pose serious long-term consequences for patients with epilepsy. Although the pathophysiology is still uncertain, hypovitaminosis D presumably due to enzyme induction, remains a frequently cited potential mechanism. It has been suggested that optimal 25OH vitamin D (25OHD) levels [gt] 30 ng/ml may be optimal in all individuals. Typical vitamin D supplementation doses are 200-600 u/day. In patients with vitamin D deficiency, these doses are likely inadequate. The optimal vitamin D dose and formulation in patients receiving inducing AEDs is still unclear. The objective of this pilot study was to evaluate a high dose vitamin D regimen in a group of patients receiving an inducing AED who were determined to have suboptimal 25OHD serum levels. Patients receiving either CBZ or PHT were screened at the Madison VAMC Epilepsy Clinic. Those with 25OHD [lt] 30 ng/ml were given 50,000u vitamin D2 po q monthly. Measurements of 25OHD were repeated at 6 months. Determination of 25OHD was performed using the same chemiluminescent assay. Baseline assessment of bone mineral density at lumbar spine, proximal femur and distal forearm was also performed using DXA. 56 male patients were screened. At screening, mean 25-OHD concentrations = 24.7[plusmn] 9.6 ng/ml. N=30 had 25-OHD [lt] 30 ng/ml. Of those, 25 (mean age 76 yrs) agreed to participate in this study. N=17 were receiving PHT [amp] N=8 were taking CBZ. In this group, baseline 25-OHD = 20.3 [plusmn] 6.6 ng/ml. Following 6 months of vitamin D2 treatment, mean 25-OHD levels did not significantly change (21[plusmn] 5.7 ng/ml). At baseline, 40 % of patients were osteopenic and 24% were considered to have osteoporosis. Consistent with previous reports, reduced vitamin D and bone mineral density appears to be quite common in patients with epilepsy. These data further suggest that a regimen of 50,000u vitamin D2 given as a single, monthly oral supplement dose not significantly increase 25OHD serum concentrations in patients receiving enzyme inducing AEDs. There may be several explanations for these results and include marked enzyme induction, nonequivalence of vitamin D preparations (ergocalciferol [D2] vs cholecalciferol [D3]), or assay variability. While it has been previously assumed that vitamin D2 and D3 are equally effective, it has recently been suggested that vitamin D2 is less than 1/3 as potent as vitamin D3, and may have a shorter duration of action (Armas et al J Clin Endocrin [amp] Metab 89:5387-5391,2004). Finally, one recent report suggests that there may be substantial variability among various commercial assays for 25OHD. In summary, further prospective studies are clearly warranted to determine both the optimal vitamin D formulation and dosage regimen in this unique patient population.