Abstracts

Rationale: The Ketogenic Diet (KD) is a high fat low carbohydrate diet that effectively treats intractable epilepsy. Long term side effects of the KD have not been well studied. The purpose of this study was to measure the change in bone mineral content (BMC) in children with intractable epilepsy treated with the KD for 15 months. Methods: Prepubertal children ≥5 years in intractable epilepsy were eligible. A 4:1 KD ratio was maintained for 15 months. All children were supplemented with one multivitamin with minerals containing 200% DRI of vitamin D and calcium at recommended intake for age and gender. Whole body and spine BMC were measured using Dual Energy X-ray Absorptiometry. Z-scores were generated by comparing the children with intractable epilepsy to a cohort of 847 healthy children. Other measurements included demographics, anthropomtery, serum 25-hydroxy vitamin D, intact parathyroid hormone, electrolytes and dieatry intake. All measurements were performed at baseline, 3, 6, 12 and 15 months of KD therapy. Longitudinal mixed effects (LME) models were used to analyze change in BMC over time. The protocol was approved by CHOP Institutional Review Board. Results: 25 children (9 girls and 16 boys) with intractable epilepsy and a mean age of 7.3±1.9 years participated. At baseline, growth and bone health status were suboptimal as were serum vitamin D levels and dietary intake of calcium and vitamin D. Whole body and spine BMC-for-age both declined 0.6 Z-score per year and whole body and spine BMC-for-height declined 0.7 Z-score and 0.4 Z-score per year respectively. Height declined 0.5 Z-score per year. BMI Z-score, age, and ambulation status were positive predictors of BMC (P<0.0001), which declined sharply over 15 months of KD treatment. Gender, seizure types and frequency, number of AED, having cerebral palsy as a co-morbidity, dietary intake and serum nutrient levels (vitamin D and PTH) did not significantly contribute to the models. Conclusions: Bone health in children with intractable epilepsy was poor, particularly for younger non-ambulatory children with low BMI status. The KD resulted in progressive loss of BMC. The mechanism of which is unclear. Further studies are needed.