Highlights
- •Inflammation is a contributing factor as well as consequence of seizure development in epilepsy
- •Prostaglandin E2 (PGE2), an inflammatory mediator, was elevated in the plasma of patients with epilepsy receiving no antiepileptic drug (AED) treatment (drug-free group)
- •Patients responding to valproate had lower plasma PGE2 levels compared to the non-responders as well as drug-free group
- •Alike the drug-free group, patients receiving phenytoin or carbamazepine had elevated plasma PGE2 levels
- •Altered PGE2 levels were independent of plasma arachidonic acid levels.
Abstract
Prostaglandin E2 (PGE2), a physiologically active lipid compound, is increased in several diseases characterized
by chronic inflammation. To determine its significance in epilepsy-associated inflammation
and response to antiepileptic drug (AED), we evaluated the plasma PGE2 (median, pg/ml) levels in drug-free patients with epilepsy (N = 34) and patients receiving AED monotherapy (N = 55) in addition to that in healthy controls (N = 34). When compared to controls, plasma PGE2 levels were significantly elevated in all drug-free patients independent of the type
of epilepsy (137.2 versus 475.7 pg/ml, p < 0.0001). Among the patients receiving AED monotherapy, only valproate responders
showed a significant decrease compared to both drug-free patients (232.1 versus 475.7 pg/ml,
p < 0.01) as well as valproate non-responders (232.1 versus 611.9 pg/ml, p < 0.0001). Both responders and non-responders on phenytoin or carbamazepine monotherapy
had elevated PGE2 levels similar to drug-free patients. In addition, no difference was observed in
plasma profiles of PGE2 precursor, arachidonic acid among the groups. Our work presents the clinical evidence
of the association between plasma PGE2 levels and valproate efficacy in patients with epilepsy.
Keywords
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Article info
Publication history
Published online: January 22, 2020
Accepted:
January 21,
2020
Received in revised form:
January 18,
2020
Received:
August 19,
2019
Identification
Copyright
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