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Sodium valproate -- induced skeletal myopathy.
1Department of Pediatrics, Bhabha Atomic Research Centre Hospital, Anushaktinagar, Mumbai, India.
Indian Journal of Pediatrics
|April 7, 2005
Summary
Long-term sodium valproate therapy can cause carnitine deficiency, leading to skeletal myopathy in children. Supplementation with L-carnitine reversed these effects, improving muscle weakness.
Area of Science:
- Neurology
- Clinical Pharmacology
- Biochemistry
Background:
- Sodium valproate is a widely used antiepileptic drug.
- Neurocysticercosis is a parasitic infection of the brain causing epilepsy.
- Long-term use of sodium valproate has been associated with various side effects.
Observation:
- A four-year-old boy with epilepsy secondary to neurocysticercosis developed limb girdle weakness.
- Electromyography (EMG) confirmed a myopathic process.
- Low plasma carnitine levels were detected, suggesting drug-induced carnitine deficiency.
Findings:
- Sodium valproate therapy was identified as the likely cause of carnitine deficiency.
- Discontinuation of sodium valproate and initiation of L-carnitine supplementation led to significant clinical improvement.
- Plasma carnitine levels normalized after L-carnitine supplementation.
Implications:
- This case highlights a potential adverse effect of long-term sodium valproate treatment.
- Monitoring carnitine levels may be warranted in patients on long-term sodium valproate.
- L-carnitine supplementation can be an effective treatment for drug-induced carnitine deficiency and myopathy.