发热性癫痫儿童的风险因素概述

Imane Abbari, Widad Gueddari, A. Bousfiha
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摘要

简介热性惊厥(FS)是儿童最常见的神经系统疾病。主要由发热引起,对中枢神经系统(CNS)无任何损害。目的:本综述深入探讨了FS发生的风险因素,尤其是炎症反应和遗传易感性:使用关键词 "发热性癫痫发作"、"炎症反应"、"促炎细胞因子"、"抗炎细胞因子 "在 PubMed 上进行了搜索。搜索策略包括荟萃分析、前瞻性病例对照研究、临床试验、观察性研究和综述:热性惊厥的发病高峰期为 18 个月,通常发生在 6 个月至 5 岁之间。各种遗传、炎症和环境因素(包括病毒和疫苗)都会诱发发热惊厥。发热性惊厥家族史阳性会增加发生 FS 的风险,在兄弟姐妹中(20%),在父母一方中(33%)。炎症反应基因的参与,包括细胞因子基因 IL1B、IL1R、IL6 和 IL4。根据这些研究结果,FS 与促炎和抗炎细胞因子的级联激活有关,而这些细胞因子在炎症调节中的失衡在 FS 的发病中起到了一定的作用:结论:目前的知识表明,遗传易感性和炎症反应失调是 FS 的成因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
An overview of risk factors in children with febrile seizures
Introduction: Febrile seizures (FS) are the most common neurologic disorder seen in children. Caused mainly by fever without any damage to the central nervous system (CNS). The associations of several factors, which we can find in the inflammatory response and genetic predisposition, are involved in the occurrence of FS. Aim: This review provides insight into risk factors, particularly the involvement of the inflammatory response and genetic susceptibility in the occurrence of FS. Methods: A PubMed search was performed using the keywords « febrile seizures », « inflammatory response », « Pro-inflammatory cytokines », «And anti-inflammatory cytokines ». The search strategy included meta-analyses, prospective case-control studies, clinical trials, observational studies, and reviews. Results: Febrile seizures with a peak incidence of 18 months usually occur between 6 months and 5 years. A variety of genetic, inflammatory, and environmental factors, including viruses and vaccines, trigger FS. A positive family history of febrile seizures increases the risk for FS occurrence with (20%) in siblings and (33%) in one parent. The involvement of inflammatory response genes, including the cytokine genes IL1B, IL1R, IL6, and IL4. According to these findings, FS is associated with the activation of a cascade of pro- and anti-inflammatory cytokines and the unbalance between these cytokines in the inflammation regulation plays a role in the development of FS. Conclusion: Current knowledge suggests that genetic susceptibility and inflammatory response dysregulation contribute to FS's genesis.
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