Clinical toxicology (Philadelphia, Pa.) · 2026
The features of toxic encephalopathy in a cohort of 129 patients with acute diquat poisoning.
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Ou Zejin, Li Xin, Li Ying, Chen Yunchao, Wang Ziyi, Luo Zhaohuan, Long Zhenhong, Zhou Hao, Dai Jianwu, Wu Tianqiong, Liu Tailing, Yang Zhiqian, Sun Chengye, Su Yiwei, Tian Linwei, Ruan Yanmei, Wang Zhi
Аннотация
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%.
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%.