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Oxidative stress in children receiving valproic acid

Aspasia Michoulas1, Vincent Tong, Xiao Wei Teng

  • 1Division of Neurology, Department of Pediatrics, and the Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada.

The Journal of Pediatrics
|November 11, 2006
PubMed

Insights

Valproic acid (VPA) treatment in children with epilepsy is linked to increased urinary 15-F2t-isoprostane (15-F2t-IsoP) levels, a marker of oxidative stress. This finding highlights a potential side effect of VPA therapy in pediatric patients.

Area of Science:

  • Pediatric Neurology
  • Biochemistry
  • Environmental Health

Background:

  • Epilepsy is a common neurological disorder in children.
  • Oxidative stress plays a role in various chronic conditions.
  • Valproic acid (VPA) is a widely used antiepileptic drug.

Purpose of the Study:

  • To investigate the effect of VPA on urinary 15-F2t-isoprostane (15-F2t-IsoP) levels in children.
  • To compare 15-F2t-IsoP levels in children treated with VPA, carbamazepine, or clobazam to healthy controls.

Main Methods:

  • Urine samples were collected from children with epilepsy on VPA, carbamazepine, or clobazam, and from age-matched controls.
  • Urinary 15-F2t-IsoP levels were quantified using enzyme-linked immunosorbent assay (ELISA).
  • Statistical analyses, including multiple linear regression, were employed to assess associations.

Main Results:

  • Children treated with VPA exhibited significantly higher urinary 15-F2t-IsoP levels compared to control, carbamazepine, and clobazam groups.
  • Younger age and exposure to second-hand smoke were predictors of elevated 15-F2t-IsoP in the control group.
  • Even without second-hand smoke exposure, VPA-treated children showed elevated 15-F2t-IsoP compared to other groups.

Conclusions:

  • VPA treatment in children is associated with increased urinary 15-F2t-IsoP levels.
  • This suggests that VPA may induce oxidative stress in pediatric patients.
  • Further research is warranted to understand the clinical implications of VPA-induced oxidative stress.
Abstract

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