Abstracts

Rationale: RATIONALE: The energy composition of the classic ketogenic diet (KD) consists mainly of fat calories. Although the exact mechanism is unknown, the KD can be used to manage seizures in patients with epilepsy. Non-fasting serum glucose levels during KD therapy have been observed to be lower than with a regular diet. In the presence of limited glucose, ketones provide an alternative energy source. Ketone levels can be measured in serum as betahydroxybutyrate (BHB). We sought to examine the relationship between BHB and glucose levels following initiation of the KD. Methods: METHODS: We reviewed laboratory data of children who received 4:1 KD as primary treatment of epilepsy from 2000 to 2004. Non-fasting glucose levels were drawn prior to and at 1, 3 and 6 months after initiation of KD therapy. BHB levels were determined at 1, 3 and 6 months following the initiation of therapy. Seizure control was evaluated based on parental reports. Results: RESULTS: Of the 40 patient charts that were reviewed, 19 contained sufficient data for analysis. The mean glucose level prior to KD initiation was 94mg%. The average (non-fasting) glucose levels at 1, 3 and 6 months on the KD were 68mg%, 67mg% and 68mg%, respectively. The mean BHB levels at 1, 3 and 6 months were 5.1mmol/L, 5.4mmol/L and 6.1mmol/L, respectively. Complete seizure control following initiation of the KD was achieved in 4/19 (21%) children. Mean non-fasting glucose levels prior to and at 1, 3 and 6 months after KD therapy in this cohort were 90mg%, 65mg%, 73mg% and 68mg%, respectively. BHB levels in seizure free patients on the KD were 5.6mmol/L, 6.5mmol/L and 6.4mmol/L at 1, 3 and 6 months, respectively. Improvement in seizure control (50-99%) on KD was noted in 12/19 (63%). Mean non-fasting glucose levels prior to and at 1, 3 and 6 months after KD therapy in this cohort were 88mg%, 67mg%, 68mg% and 68mg%, respectively. BHB levels in seizure improved patients on KD were 4.9mmol/L, 5.6mmol/L and 5.9mmol/L at 1, 3 and 6 months, respectively. Less than 50% improvement in seizure control with KD therapy was noted in 3/19 (16%). Average non-fasting glucose levels prior to and at 1 and 3 months after KD therapy in this cohort was 83mg%, 74mg%, and 66mg%, respectively. BHB levels in this cohort were 4.7mmol/L and 5.7mmol/L at 1 and 3 months, respectively. Conclusions: CONCLUSIONS: Following initiation of KD therapy for management of epilepsy we observed an inverse relationship between non-fasting serum glucose and BHB levels. Successful management of epilepsy with KD does not appear to correlate with either serum glucose or BHB titers.