Reactivation of Plasma Butyrylcholinesterase by Pralidoxime Chloride in Patients Poisoned by WHO Class II Toxicity Organophosphorus Insecticides
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چکیده
منابع مشابه
Reactivation of Plasma Butyrylcholinesterase by Pralidoxime Chloride in Patients Poisoned by WHO Class II Toxicity Organophosphorus Insecticides
Some clinicians assess the efficacy of pralidoxime in organophosphorus (OP) poisoned patients by measuring reactivation of butyrylcholinesterase (BuChE). However, the degree of BuChE inhibition varies by OP insecticide, and it is unclear how well oximes reactivate BuChE in vivo. We aimed to assess the usefulness of BuChE activity to monitor pralidoxime treatment by studying its reactivation aft...
متن کاملPlasma butyrylcholinesterase as a marker of clinical outcome in diethyl organophosphorus insecticide poisoned patients treated with pralidoxime.
We are grateful for Lucyk and colleagues’ interest in our work on the value of plasma butyrylcholinesterase (BuChE) as a marker of pralidoxime effect. We note their interest in the association between early BuChE reactivation and clinical outcome. Most importantly, the original randomized controlled trial (RCT; Eddleston et al., 2009) assessed the effectiveness of pralidoxime in patients proven...
متن کاملButyrylcholinesterase level in poisoned patients by phosphide compounds
Background: Metal phosphides are widely used as a rodenticide and insecticide and poisoning with these substances has a very high mortality. The aim of this study was to evaluate the butyrylcholinesterase (BuCh) level in poisoning with metal phosphides. Methods: In this case series study, 60 poisoned patients with zinc phosphide (ZnP) and aluminum phosphide (ALP) who was admitted to poisoning ...
متن کاملRed blood cell acetylcholinesterase and plasma butyrylcholinesterase status: important indicators for the treatment of patients poisoned by organophosphorus compounds.
Inhibition of acetylcholinesterase (AChE) is regarded as the primary toxic mechanism of organophosphorus compounds (OP). Therapeutic strategies are directed to antagonise overstimulation of muscarinic receptors with atropine and to reactivate inhibited AChE with oximes. Reactivation is crucial within the neuromuscular synapse, where atropine is ineffective, since peripheral neuromuscular block ...
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ژورنال
عنوان ژورنال: Toxicological Sciences
سال: 2014
ISSN: 1096-6080,1096-0929
DOI: 10.1093/toxsci/kft337