Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions

• Published in: Pediatrics international Vol. 43; no. 3; pp. 235 - 239
• Main Authors: Tütüncüoğlu, Sarenur, Kütükçüler, Necil, Kepe, Lütfü, Çoker, Canan, Berdeli, Afig, Tekgül, Hasan
• Format: Journal Article
• Language: English
• Published: Melbourne, Australia Blackwell Science Pty 01.06.2001
• Subjects: Cytokines - metabolism; febrile convulsions; Humans; Infant; interleukin-1α; interleukin-1β; prostaglandins; Prostaglandins - metabolism; Seizures, Febrile - metabolism; tumor necrosis factor-α; zinc; Zinc - metabolism
• ISSN: 1328-8067; 1442-200X
• DOI: 10.1046/j.1442-200x.2001.01389.x

Background : Some changes in the levels of proinflammatory cytokines, prostaglandins and zinc (Zn) in peripheral blood and cerebrospinal fluid (CSF) have been suggested to occur for the pathogenesis of febrile convulsions (FC). Methods : In order to test this hypothesis, the levels of tumor necrosis factor (TNF)‐α, interleukin (IL)‐1α, IL‐1β and prostaglandins (PGE2, PGF2α, PGD2) in the CSF and plasma and the levels of Zn in serum and CSF were investigated in children during the acute and late phases of FC. Results were compared with control subjects with meningismus. Results : During the acute phase of FC, children had significantly elevated plasma levels of IL‐1β, CSF levels of TNF‐α, plasma levels of PGE2, PGF2α and PGD2 and CSF levels of PGD2 (P<0.05). A positive correlation between the degree of fever and plasma IL‐1β levels was observed in both patients and controls. Three months after the acute phase of FC, plasma levels of IL‐1β had returned to levels seen in controls. Children with FC also had significantly decreased serum Zn levels during the acute phase (P<0.05). Hovewer, there was no significant difference between the groups with respect to CSF Zn levels (P>0.05). Conclusions : During the acute phase of FC, patients had significantly increased plasma IL‐1β and prostaglandin levels and decreased serum Zn levels. These changes may be responsible for FC pathogenesis.