Abstracts

Valproic acid is a commonly used anticonvulsant agent. Hyperammonemia with or without measurable hepatic abnormalities is a well-recognized side affect of chronic valproic acid treatment. Numerous evidences suggest that selenium may ameliorate some of the adverse metabolic consequences of valproic acid. There is no established treatment for valproic acid induced chronic hyperammonemia. For the past three years we have noted a strong co-relation between selenium deficiency and valproic acid therapy. We evaluated the long-term effect of selenium on valproate-induced hyperammonemia and seizure control. The medical records of twelve developmentally delayed adults, all with refractory epilepsy were reviewed retrospectively. Their average age was 38.25 years (ranging from 50 to 22 years). Six of the patients were female, and six were male. All patients had significantly elevated ammonia level with no explanation other than the effects of VPA. All patients had selenium deficiency according to their selenium blood level. All twelve patients received selenium supplement orally. The average length of Selenium therapy was 41.33 months (ranging from 53 to 23 months). The average daily dose was 119mg (ranging from 50 to 200mg). All patients remained on VPA during selenium therapy. The baseline and post-treatment Se and NH3 levels were measured. One patient was temporarily discontinued from our care and her selenium was stopped. Thereafter, both her seizure frequency and intensity increased. Her selenium supplement was resumed and she was not drop out of the observation. Before supplemental selenium, the mean selenium level was 88.48 mcg/L (ranged from 67 to 120.7 mcg/ml) and mean NH3 serum level was 84.6 umol/L (ranged from 57 to 102 umol/ml). After selenium treatment, serum Se level increased 31.14% (ranged from 103 to 161 mcg/ml) and NH3 level decreased 20.71% (ranged from 37 to 130 umol/ml). One patient[apos]s selenium was discontinued because she was temporarily transferred from our care. After the discontinuation, her seizure frequency increased 25% (from 1 per month to 1.25 per month); length increased 276% (from 245 sec. per month to 922 sec. per month). There was no other explanation found for those changes aside from the discontinuation of selenium supplementation; therefore, Dr. Murti resumed her selenium. The patient has not had any seizure, after the selenium supplement resumed till the time this report is written. Selenium supplement may help lower ammonia level in patients with valproate-induced hyperammonemia over long-term treatment. Selenium deficiency may lead to the lost of seizure control, even when the patient is remained on the same dose of valproic acid.