From Febrile Seizures to Epilepsy: IL-1β (-511) and IL-10 (-1082) Gene Polymorphisms


Creative Commons License

Akan A., Açık S., Nur B. G., HASPOLAT Ş.

Journal of Pediatric Research, cilt.13, sa.2, ss.116-121, 2026 (ESCI, Scopus, TRDizin)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 13 Sayı: 2
  • Basım Tarihi: 2026
  • Doi Numarası: 10.4274/jpr.galenos.2026.38455
  • Dergi Adı: Journal of Pediatric Research
  • Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.116-121
  • Anahtar Kelimeler: Febrile seizures, genetic polymorphism, interleukin-1 beta, interleukin-10
  • Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
  • Sağlık Bilimleri Üniversitesi Adresli: Evet

Özet

Aim: The etiology of febrile seizures (FS) is multifactorial, including genetic, immunological, and inflammatory components. The primary objective of this research was to assess the relationship between IL-1β (-511) and IL-10 (-1082) gene polymorphisms and the likelihood of recurrent FS and subsequent epilepsy in pediatric patients. Materials and Methods: In this study, we retrospectively reviewed data from 44 patients diagnosed with FS. We employed restriction fragment length polymorphism-polymerase chain reaction (PCR) and amplification refractory mutation system-PCR techniques in order to detect genetic variations in the IL-1β (-511) and IL-10 (-1082) loci. The study population underwent long-term follow-up for an average of 13±5 years to evaluate the correlations between these polymorphisms and clinical prognoses, specifically FS recurrence and the onset of epilepsy. Results: In the IL-1β (-511) region, no significant association was found between G/A, A/A, or G/G polymorphisms and FS recurrence (p=0.131) or epilepsy development (p=0.407). Likewise, the G allele at the IL-10 (-1082) position showed no meaningful correlation with epilepsy risk (p=0.378). However, the presence of the A allele at the locus in question was found to be significantly associated with the development of epilepsy (p=0.002). Carriers of the A allele exhibited a 10.8-fold increased risk of epilepsy compared to non-carriers (odds ratio=10.8; 95% confidence interval: 2.04-57). Conclusion: Our data indicate that the IL-10 (-1082) A allele serves as a significant predictor for epilepsy susceptibility after FS. These results highlight the potential role of cytokine gene variations, especially IL-10, in determining the long-term neurological prognosis of children with FS.