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有机磷中毒所致中间综合征中的突触后神经肌肉功能障碍

Postsynaptic neuromuscular dysfunction in organophosphate induced intermediate syndrome.

作者信息

De Wilde V, Vogelaers D, Colardyn F, Vanderstraeten G, Van den Neucker K, De Bleecker J, De Reuck J, Van den Heede M

机构信息

Department of Intensive Care, University Hospital, Ghent, Belgium.

出版信息

Klin Wochenschr. 1991 Feb 26;69(4):177-83. doi: 10.1007/BF01665865.

DOI:10.1007/BF01665865
PMID:1645823
Abstract

A 65-year-old Caucasian female developed an intermediate syndrome seven days after an acute cholinergic crisis, caused by the ingestion of fenthion. Cholinesterase activity in the blood, plasma and red cells was monitored daily by the method according to Nenner and serial serum fenthion levels were measured by capillary gas chromatography. Electromyographic studies showed fade on tetanic stimulation by means of surface electrodes at 20 Hz of the left M. abductor digiti quinti at day 7, which could no longer be observed at day 19. Fade on low-frequency stimulation and post-tetanic facilitation were both absent. A biopsy of the N. suralis was normal. A biopsy of the M. tibialis anterior revealed a limited rhabdomyolysis with a very weak staining for cholinesterase. It is hypothesized that the pathophysiologic process underlying the syndrome is the result of a time-confined phenomenon, which includes both changes in the postsynaptic structures by a desensitization process and a gradually restoring ratio of acetylcholine to acetylcholinesterase. This hypothesis is suggested by the similarity in the EMG-findings of this patient and those in myasthenia gravis, which is known to be characterized by a postsynaptic transmission defect.

摘要

一名65岁的白种女性在因摄入倍硫磷引发急性胆碱能危象七天后出现中间综合征。采用Nenner法每日监测血液、血浆和红细胞中的胆碱酯酶活性,并通过毛细管气相色谱法测定血清倍硫磷的系列水平。肌电图研究显示,在第7天,通过表面电极以20Hz频率对左侧小指展肌进行强直刺激时出现衰减,而在第19天不再观察到这种情况。低频刺激时的衰减和强直后易化均未出现。腓肠神经活检正常。胫前肌活检显示有局限性横纹肌溶解,胆碱酯酶染色非常弱。据推测,该综合征潜在的病理生理过程是一种时间受限现象的结果,这一现象包括突触后结构因脱敏过程而发生的变化以及乙酰胆碱与乙酰胆碱酯酶比例的逐渐恢复。该患者与重症肌无力患者的肌电图表现相似,提示了这一假说,而重症肌无力已知以突触后传递缺陷为特征。

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Postsynaptic neuromuscular dysfunction in organophosphate induced intermediate syndrome.有机磷中毒所致中间综合征中的突触后神经肌肉功能障碍
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PLoS One. 2018 Sep 27;13(9):e0203596. doi: 10.1371/journal.pone.0203596. eCollection 2018.
2
Serum creatine phosphokinase: a probable marker of severity in organophosphorus poisoning.血清肌酸磷酸激酶:有机磷中毒严重程度的一个可能标志物。
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Muscular strength and vibration thresholds during two years after acute poisoning with organophosphate insecticides.

本文引用的文献

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Severe and prolonged poisoning by fenthion. Significance of the determination of the anticholinesterase capacity of plasma.
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Insecticides affecting acetylcholine receptor interactions.影响乙酰胆碱受体相互作用的杀虫剂。
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[Simultaneous determination of acetylcholinesterase (EC 3.1.1.77) activity in whole blood, plasma and erythrocytes with the automatic titrator].[使用自动滴定仪同时测定全血、血浆和红细胞中的乙酰胆碱酯酶(EC 3.1.1.77)活性]
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Neurological manifestations of organophosphorous insecticide poisoning.有机磷杀虫剂中毒的神经学表现。
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Electrophysiological studies in acute organophosphate poisoning.急性有机磷中毒的电生理研究
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Organophosphate poisoning.有机磷中毒
Ann Emerg Med. 1987 Feb;16(2):193-202. doi: 10.1016/s0196-0644(87)80015-x.
10
Neurotoxic effects of organophosphorus insecticides. An intermediate syndrome.有机磷杀虫剂的神经毒性作用。中间综合征。
N Engl J Med. 1987 Mar 26;316(13):761-3. doi: 10.1056/NEJM198703263161301.