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Complications of the ketogenic diet
K Ballaban-Gil1, C Callahan, C O'Dell
1Comprehensive Epilepsy Management Center, and Department of Neurology, Albert Einstein College of Medicine, Bronx, New York 10467-2490, USA.
Insights
The ketogenic diet, used for pediatric epilepsy, can cause serious adverse events in 10% of children. Careful monitoring is essential, especially when the diet is combined with valproate (VPA).
Area of Science:
- Pediatric Neurology
- Metabolic Disorders
Background:
- The ketogenic diet is a well-established therapy for pediatric epilepsy, used for over 70 years.
- While generally safe, serious complications associated with the diet are rarely reported.
Observation:
- This study prospectively monitored 52 children with epilepsy treated with the classic ketogenic diet over 22 months.
- Adverse events were carefully documented to assess diet-related complications.
Findings:
- Five children (10%) experienced serious adverse events (AE) including hypoproteinemia, lipemia, hemolytic anemia, Fanconi's renal tubular acidosis, and elevated liver function tests.
- Notably, 80% of children with AE were also treated with valproate (VPA), suggesting a potential interaction.
Implications:
- Clinicians must be aware of the potential for serious adverse events when prescribing the ketogenic diet for pediatric epilepsy.
- The possible interaction between the ketogenic diet and valproate (VPA) requires careful consideration and monitoring.
Purpose:
The ketogenic diet has been successfully used in treatment of pediatric epilepsy for >70 years. Few serious complications caused by the diet have been reported. We report complications that have been experienced by children receiving the ketogenic diet.
Methods:
In a 22-month period, we treated 52 children with the classic ketogenic diet and monitored them in a prospective manner.
Results:
Five children (10%) experienced serious adverse events (AE) after initiation of the diet. Four patients (80%) were treated with valproate (VPA) in addition to the diet, as compared with 25 (53%) of the other 47 children. Two patients developed severe hypoproteinemia within 4 weeks of initiation of the diet, and 1 of them also developed lipemia and hemolytic anemia. A third child developed Fanconi's renal tubular acidosis within 1 month of diet initiation. Two other children manifested marked increases in liver function tests, 1 during the initiation phase and the other 13 months later.
Conclusions:
Clinicians who wish to use the ketogenic diet must be aware of the potential of serious AE and possible interactions of the diet with VPA.