{"title":"The features of toxic encephalopathy in a cohort of 129 patients with acute diquat poisoning.","authors":"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","doi":"10.1080/15563650.2026.2654539","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Diquat-induced toxic encephalopathy remains inadequately understood.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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; <i>P </i><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.</p><p><strong>Discussion: </strong>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.</p><p><strong>Conclusions: </strong>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%.</p>","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"755-768"},"PeriodicalIF":3.3000,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical toxicology (Philadelphia, Pa.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/15563650.2026.2654539","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/6/23 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
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%.