Respiratory viruses and febrile response in children with febrile seizures: A cohort study and embedded case-control study. (January 2021)

• Record Type: Journal Article
• Authors: Hautala, Maria; Arvila, Jukka; Pokka, Tytti; Mikkonen, Kirsi; Koskela, Ulla; Helander, Heli; Glumoff, Virpi; Rantala, Heikki; Tapiainen, Terhi
• Is Part Of: Seizure. Volume 84(2021)
• Page Start: 69
• Page End: 77
• Publication Date: 2021-01
• Subjects: CI confidence interval -- CSF cerebrospinal fluid -- EBV Epstein–Barr virus -- ER emergency room -- FS febrile seizure -- HHV 6 - human herpes virus 6 -- hMPV human metapneumovirus -- IL interleukin -- i.v. intravenous -- PCR polymerase chain reaction -- RS virus respiratory syncytial virus -- SD standard deviation -- TNF tumor necrosis factor; febrile seizure -- Pathogenesis -- Respiratory virus -- Inflammatory response -- multiplex PCR; Epilepsy -- Periodicals; Epilepsy -- Periodicals; Seizures -- Periodicals; Épilepsie -- Périodiques; Electronic journals; Electronic journals; 616.853
• DOI: 10.1016/j.seizure.2020.11.007
• Languages: English
• ISSNs: 1059-1311

Abstract

Highlights: We studied respiratory viruses and host febrile response in febrile seizures (FS). Influenza, corona, parainfluenza, and enterovirus increased the risk for FS. In a virus matched setting, the febrile response of FS patients was stronger. These factors hold possible potential in the prevention of FS. Abstract: Objective: There are limited data on the pathogen-related and host-related factors in the pathogenesis of febrile seizures (FS). We designed a controlled study to compare the role of different respiratory viruses and febrile response in FS. Methods: In a prospective cohort study of 1899 pediatric emergency room patients aged 6 months-6 years with a positive respiratory virus multiplex PCR, we identified 225 patients with FSs. We first compared the distribution of respiratory viruses in age-stratified patients with FSs with that in other patients. In an embedded case-control study, we compared the febrile response in patients with FSs with that in the controls matched for age, season and the same respiratory virus. Results: The relative risk for FS was the highest for coronavirus OC43, 229E, and NL63 infections [RR: 3.2, 95 % confidence interval (CI): 1.4–7.2) and influenza A and B [RR: 2.5, 95 % CI: 1.4–4.7] as compared to those with other respiratory viral infections. The patients with FSs had a stronger febrile response of 39.2 ° C (difference: 0.8 ° C, 95 % CI: 0.5–1.2) later during hospitalization after acute care than the controls matched for the same respiratory virus. Conclusions: Influenza and coronaviruses caused relatively more FS-related emergency room visits than other respiratory viruses. Furthermore, the febrile response was stronger in the patients with FSs than in the controls matched for the same respiratory virus. The results suggest that the pathomechanism of FSs includes modifiable pathogen-related and host-related factors with possible potential in the prevention of FSs.