Hae:

Oulun yliopiston väitöskirjat

Viral etiology and cytokine responses of infections leading to febrile seizures

ISBN-10:	978-952-62-4265-1
Kieli:	englanti
Kustantaja:	Oulun yliopisto
Laitos:	Faculty of Medicine
Painosvuosi:	2024
Sidosasu:	pehmeäkantinen
Sijainti:	Print Tietotalo
Sivumäärä:	140
Tekijät:	Hautala, Maria

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The exact pathomechanism of febrile seizures (FSs) is unknown but it is thought to involve host-related and pathogen-related factors. Most of the episodes occur during respiratory viral infections. Virus-induced cytokine release is thought to play a central role in the pathomechanism, because cytokines can induce hyperexcitability which can lead to seizures. In a cohort study of 1899 pediatric emergency room (ER) patients from January 2013 to September 2017, we compared the distribution of respiratory viruses in children with FSs, divided in age-stratified groups with that in other ER patients. We found that coronaviruses OC43, 229E and NL63 and influenza A and B caused relatively more FS-related ER-visits than other respiratory viruses. In an embedded case-control study, we found that the febrile response in children with FSs remained stronger during inpatient care than that in the age- and respiratory virus-matched controls. In our controlled follow-up study, we compared the levels of 12 serum cytokines following the patients’ first FSs, during febrile episodes without FSs, following recurrent FSs and during healthy periods, as well as between children with FSs and control group. 251 children with first FSs participated in the study, of which 17 children with recurrent FSs completed the study protocol. Serum cytokine interleukin-1 receptor antagonist (IL-1RA) was higher in children with FSs following the first FSs than during febrile episodes without FSs and healthy periods in the same individuals. IL-1RA was also higher in patients with FSs following first and recurrent FSs compared with febrile controls. There was no difference in the IL-1RA between the febrile episodes without FSs and febrile controls. Finally, we studied serum cytokine high mobility group box 1 (HMGB1) in a controlled follow-up study with 122 children with FSs, including 18 children who had recurrent seizures and completed the study protocol. HMGB1 was lower in children with recurrent FSs following first FSs compared with febrile control children matched by age and sex. We did not find any other differences between the groups nor different types of FSs. In our update of a previous meta-analysis of HMGB1 the differences were only significant in studies conducted in East Asian populations. The pathomechanism of FSs involves modifiable pathogen-related and host-related factors.

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