The features of toxic encephalopathy in a cohort of 129 patients with acute diquat poisoning.

IF 3.3
Zejin Ou, Xin Li, Ying Li, Yunchao Chen, Ziyi Wang, Zhaohuan Luo, Zhenhong Long, Hao Zhou, Jianwu Dai, Tianqiong Wu, Tailing Liu, Zhiqian Yang, Chengye Sun, Yiwei Su, Linwei Tian, Yanmei Ruan, Zhi Wang
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Abstract

Introduction: Diquat-induced toxic encephalopathy remains inadequately understood.

Methods: Data on patients with acute diquat poisoning were retrospectively collected from May 2017 to May 2023. The diagnosis was confirmed qualitatively by ultra-high performance liquid chromatography quadrupole-time of flight mass spectrometry. A follow-up study was designed to explore the long-term health effects of diquat poisoning.

Results: A total of 129 patients with acute diquat poisoning were included in this study. Thirty-four patients died (27 of whom developed toxic encephalopathy) following a median dose of diquat (200 g/L) 190 mL (IQR:100-200 mL). Forty-five patients were diagnosed with toxic encephalopathy, mainly involving the brainstem, bilateral cerebellar peduncles, and basal ganglia. The development of toxic encephalopathy was associated with a significantly higher risk of death (odds ratio = 16.5; 95%CI: 6.2-43.8; P <0.001). Twenty-five of the 95 survivors were enrolled in a follow-up study. The main persistent features were peripheral nerve injuries in 20%, suspected peripheral nerve injuries in 40%, and reduced compound muscle action potential in 84%; chronic-phase encephalopathy occurred in 28%. Transcriptomic analysis revealed significant changes in the expression profiles of neuroregulatory factors, including inhibin-βA and sonic hedgehog.

Discussion: Toxic encephalopathy represented an important organ injury caused by acute diquat poisoning, which was strongly associated with an increased risk of death. Peripheral nerve injuries were also common at follow-up. Several limitations should be noted, including the lack of diquat concentrations, the small sample size, the short follow-up duration, and the single-center design.

Conclusions: Thirty-four of 129 (26.4%) patients died from diquat poisoning. Toxic encephalopathy was diagnosed in 45 of 129 (34.9%) patients, and its development was associated with a significantly higher risk of death. Follow-up revealed peripheral nerve injuries in 20% of patients, and chronic-phase encephalopathy in 28%.

129例急性地奎特中毒患者中毒性脑病的特点。
前言:地奎特引起的中毒性脑病仍然不充分了解。方法:回顾性收集2017年5月至2023年5月收治的急性地奎特中毒患者资料。采用超高效液相色谱-四极杆-飞行时间质谱法定性诊断。一项后续研究旨在探索双喹菊酯中毒对健康的长期影响。结果:本研究共纳入急性地奎特中毒患者129例。中位剂量地奎特(200 g/L) 190 mL (IQR:100-200 mL)后,34例患者死亡(其中27例发生中毒性脑病)。45例患者诊断为中毒性脑病,主要累及脑干、双侧小脑蒂和基底节区。中毒性脑病的发生与死亡风险显著增高相关(优势比= 16.5;95%CI: 6.2-43.8; P)讨论:中毒性脑病是急性地奎特中毒引起的重要器官损伤,与死亡风险增高密切相关。周围神经损伤在随访中也很常见。应该注意一些局限性,包括缺乏双喹酮浓度,样本量小,随访时间短,单中心设计。结论:129例患者中34例(26.4%)死于双喹酮中毒。129例患者中有45例(34.9%)被诊断为中毒性脑病,其发展与死亡风险显著升高相关。随访发现20%的患者有周围神经损伤,28%的患者有慢性脑病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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