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Journal of Zhejiang University SCIENCE B

ISSN 1673-1581(Print), 1862-1783(Online), Monthly

2024 Vol.25 No.4 P.354-358

Seizure as the main presenting manifestation of three patients with acute glufosinate-ammonium poisoning

Ping WANG, Congying SONG, Xuan LU, Yuanqiang LU

Department of Emergency Medicine, the First Affiliated Hospital, School of Medicine, Zhejiang University,Hangzhou310003,China; Zhejiang Key Laboratory for Diagnosis and Treatment of Physic-chemical and Aging-related Injuries,Hangzhou310003,China; Department of Geriatric Medicine, the First Affiliated Hospital, School of Medicine, Zhejiang University,Hangzhou310003,China

luyuanqiang@zju.edu.cn

Abstract: Glufosinate-ammonium herbicides are the most widely used broad-spectrum, non-selective herbicides in the world. Glufosinate-ammonium is a structural analogue of glutamate (Glu) which can irreversibly inhibit the activity of glutamine synthetase (GS) and Glu decarboxylase in plants, thereby blocking the synthesis of glutamine (Gln) from Glu and ammonia (Hoerlein, 1994). This causes the plants to die because of the nitrogen metabolism disorder and subsequent intracellular accumulation of ammonia. In humans, the characteristic features of glufosinate-ammonium herbicide poisoning include gastrointestinal symptoms and neurotoxicity (Watanabe and Sano, 1998). Currently, there are no antidotes for glufosinate-ammonium herbicide poisoning, and thus supportive care is the key treatment.

Key words: Glufosinate-ammonium; Seizure; Herbicide intoxication; Head CT

Chinese Summary  <15> 三例以癫痫为主要表现的急性草铵膦中毒患者的病例报告

王萍1,2，宋聪颖1,2，陆璇2,3，陆远强1,2
1浙江大学医学院附属第一医院急诊科，中国杭州市，310003
2浙江省增龄与理化损伤性疾病诊治研究重点实验室，中国杭州市，310003
3浙江大学医学院附属第一医院老年科，中国杭州市，310003
摘要：草铵膦作为谷氨酸（Glu）的结构类似物，可以不可逆地抑制植物中谷氨酰胺合成酶（GS）和谷氨酸脱羧酶活性，从而阻止谷氨酰胺（Gln）生成，最终导致植物因氮代谢紊乱和细胞内氨积累而死亡。人误服草胺磷后也会出现相应的中毒症状，包括胃肠道症状和神经毒性。草铵膦作为最常见的致癫痫类除草剂，且无特定解毒剂，因此支持性治疗至关重要。在临床诊治过程中，如何及时有效识别草铵膦除草剂引起的神经毒性并提供适当治疗尤为关键。本文介绍了我院三名草铵膦中毒患者的主要症状，其中癫痫是主要的神经表现。随后，通过查阅相关文献，对草铵膦引发神经毒性的相关机制进行了总结，并讨论了神经毒性的预测和检测方法。

关键词组：草铵膦；癫痫；除草剂中毒；头部CT


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DOI:

10.1631/jzus.B2300469

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On-line Access:

2024-08-27

Received:

2023-10-17

Revision Accepted:

2024-05-08

Crosschecked:

2024-04-07

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