Abstracts

Rationale: Selenium deficiency induced by divalproex may cause a progressive encephalopathy. Iron overload can exacerbate lipid peroxidation. Daily ingestion of iron in antiepileptic drugs may exacerbate the risk of iron overload in patients at hemochromatosis, further increasing the risk of progressive encephalopathy. Methods: We report our observation in a child with hemochromatosis who developed iron overload after 9 years of exposure to iron oxide excipient in divalproex and subsequently exposure to iron oxide excipient in levetiracetam (LEV). Results: Before diagnosis of iron overload seizure frequency was high (several daily seizures). Divalproex was discontinued.and replaced by LEV. No improvement in seizure frequency was seen. A few months later, the child was first observed to have a total iron of 35,28mmol/L, TIBC of 12 mcg/dL and saturation of 94%. After phlebotomy total iron declined while transferrin saturation remained high. Seizure frequency decreased, averaging 1 seizure per month without any subsequent change in antiepileptic therapy. This 18 year-old heterozygous hemochromatosis patient has not required any additional phlebotomy and seizure control is still improved. Conclusions: Iron overload due to exipient iron oxide in divalproex may contribute to seizure worsening in children with hemochromatosis.