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Published on: May 10, 2024
Valproate-induced eosinophilia in children with epilepsy: role of interleukin-5
Alexandros C Makis1, Meropi Tzoufi, Maria D Kateri
1Department of Child Health, University Hospital of Ioannina, Ionnina, Greece. me00350@cc.uoi.gr
Insights
Sodium valproate therapy in children with epilepsy is linked to elevated Interleukin-5 (IL-5) levels, potentially causing eosinophilia. This increase in IL-5 may also contribute to valproate's effectiveness as an antiepileptic treatment.
Area of Science:
- Neuroscience
- Immunology
Background:
- Interleukin-5 (IL-5) plays a role in both eosinophil development and neural processes.
- Epilepsy treatment often involves medications that can have immune-related side effects.
Purpose of the Study:
- To investigate the relationship between serum Interleukin-5 (IL-5) levels and sodium valproate monotherapy in children with epilepsy.
- To compare IL-5 levels in children on valproate with those on carbamazepine and healthy controls.
Main Methods:
- Serum IL-5 levels were quantified using enzyme-linked immunosorbent assay (ELISA).
- The study included 68 children with epilepsy on valproate, 14 on carbamazepine, and 60 healthy controls.
- Eosinophil counts and clinical response to valproate were also assessed.
Main Results:
- Children on valproate showed significantly higher IL-5 levels compared to carbamazepine users and controls.
- Eosinophilia was present in 35.3% of valproate users, with higher IL-5 levels observed in this subgroup.
- Elevated IL-5 levels were also noted in valproate users without eosinophilia, and a majority of valproate responders exhibited high IL-5 levels.
Conclusions:
- Sodium valproate may induce eosinophilia by stimulating IL-5 production.
- Elevated IL-5 levels in valproate users, even without eosinophilia, suggest a potential role in the drug's antiepileptic mechanism.
Abstract:
Interleukin-5 contributes both in eosinophilopoiesis and neural development. Serum interleukin-5 levels were measured with enzyme-linked immunosorbent assay technique in 68 children with epilepsy receiving sodium valproate monotherapy and compared with the levels of 60 healthy controls and 14 children with epilepsy receiving carbamazepine. Eosinophilia was observed in 35.3% of children receiving valproate. Interleukin-5 in valproate users was significantly higher compared with children receiving carbamazepine and controls. Valproate users who exhibited eosinophilia had higher interleukin-5 levels compared with those without eosinophilia. However, the interleukin-5 level was also elevated, although to a lesser degree, in children without eosinophilia. The majority of valproate responders had high interleukin-5 levels. A positive correlation between interleukin-5 levels and the eosinophil count was also noted. We postulate that valproate contributes to the pathogenesis of eosinophilia, probably inducing interleukin-5 production. The finding that serum interleukin-5 was significantly elevated in valproate responders and even in valproate users without eosinophilia suggests that the increase in interleukin-5 might represent one of valproate's antiepileptic mechanisms.
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