Year: 2025
Type: article
Abstract: 脓毒血症是由感染引发的宿主反应失调导致的致命性器官功能障碍，在儿童中具有高发病率和死亡率。由于儿童免疫系统发育不成熟，其病理机制和临床表现与成人存在显著差异，包括炎症反应失衡、免疫功能障碍及线粒体损伤等。全球数据显示，儿童脓毒血症年发病率为21例/10万人，新生儿群体尤为高危(2202例/10万活产)，死亡率呈U型年龄分布(4%~50%)。传统血培养技术因阳性率低、耗时长，难以满足早期诊断需求，而新型分子诊断技术(如Iridica Plex ID、SeptiFast)和生物传感技术(如适配体传感器)为快速精准诊断提供了新方向。此外，人工智能(如Stabl、NAVOY算法)和线粒体调控机制的研究为脓毒血症的个性化治疗和预后评估开辟了前景。未来需建立儿童专用诊疗体系，整合耐药基因监测、微创检测技术及免疫–代谢协同策略，以应对这一全球性健康挑战。 Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection, exhibiting high incidence and mortality in pediatric populations. Due to the immature development of children’s immune systems, its pathological mechanisms and clinical manifestations differ significantly from adults—characterized by imbalanced inflammatory responses, immune dysfunction, and mitochondrial injury. Global data indicate an annual pediatric sepsis incidence of 21 per 100,000 children, with neonates constituting a particularly high-risk group (2202 per 100,000 live births). Mortality follows a U-shaped age distribution (4%~50%). Conventional blood culture techniques, limited by low positivity rates and prolonged processing times, often fail to meet early diagnostic requirements. Emerging molecular diagnostics (e.g. Iridica Plex ID, SeptiFast) and biosensing technologies (e.g., aptamer-based sensors) offer new pathways for rapid and precise diagnosis. Furthermore, artificial intelligence applications (e.g., Stabl, NAVOY algorithms) and research into mitochondrial regulatory mechanisms present promising avenues for personalized treatment and prognostic evaluation. Future priorities include establishing pediatric-specific diagnostic and therapeutic frameworks that integrate antimicrobial resistance gene surveillance, minimally invasive detection technologies, and combined immunometabolic strategies to address this global health challenge.
Source: Advances in Clinical Medicine
Author: 峰 许
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
OpenAlex ID: W4412416851