Therapeutic Factors in Survival after Lethal Cholinesterase Inhibition by Phosphorus Insecticides

Freeman, Gustave; Epstein, Marvin A.

doi:10.1056/nejm195508182530702

Cited by 33 publications

(15 citation statements)

References 9 publications

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“…Laboratory data support qualitatively the conclusion of FREEMAN and EPSTEIN (1955) that early and vigorous use of atropine is a sine qua non in the successful treatment of anti-ChE poisoning. They demonstrate also that for every dose of an anti-ChE compound there is a maximally effective dosage of atropine; dosages of atropine above this level accomplish nothing additional therapeutically, although they may exercise effectiveness for longer periods of time than do maximally effective dosages.…”

Section: Optimal Conditions For Employment Of Antimuscarinic Drugssupporting

confidence: 67%

“…The conditions for optimal employment of atropine in cases of poisoning by organophosphorus compounds have been summarized by GROB and HARvEY (1953) and by FREEMAN and EPSTEIN (1955), and are discussed in detail in Chapter 22. Laboratory data support qualitatively the conclusion of FREEMAN and EPSTEIN (1955) that early and vigorous use of atropine is a sine qua non in the successful treatment of anti-ChE poisoning.…”

Section: Optimal Conditions For Employment Of Antimuscarinic Drugsmentioning

confidence: 98%

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Pharmacological Antagonists of the Anticholinesterase Agents

Wills¹

1963

Cholinesterases and Anticholinesterase Agents

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Section: Optimal Conditions For Employment Of Antimuscarinic Drugssupporting

confidence: 67%

Section: Optimal Conditions For Employment Of Antimuscarinic Drugsmentioning

confidence: 98%

Pharmacological Antagonists of the Anticholinesterase Agents

Wills¹

1963

Cholinesterases and Anticholinesterase Agents

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“…Treatment involves resuscitation, administration of the muscarinic antagonist atropine [13], and an oxime acetylcholinesterase reactivator [14], such as pralidoxime, and assisted ventilation as necessary [15]. The beneficial effects of atropine are clear [13],[16]. By contrast, the role of oximes is still the subject of much debate [17]–[19].…”

Section: Introductionmentioning

confidence: 99%

Pralidoxime in Acute Organophosphorus Insecticide Poisoning—A Randomised Controlled Trial

Eddleston

Eyer

Worek³

et al. 2009

PLoS Med

153

132

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“…Management (Eddleston et al , 2008a; Johnson et al , 2000) involves resuscitation and the administration of the muscarinic antagonist atropine (Heath and Meredith, 1992) and an oxime AChE reactivator such as pralidoxime (Eyer, 2003). The beneficial effects of atropine are clear (Freeman and Epstein, 1955; Heath and Meredith, 1992; Johnson et al , 2000). By contrast, the effect of pralidoxime remains unclear (Buckley et al , 2011).…”

Section: Introductionmentioning

confidence: 99%

Reactivation of Plasma Butyrylcholinesterase by Pralidoxime Chloride in Patients Poisoned by WHO Class II Toxicity Organophosphorus Insecticides

Konickx

Worek

Jayamanne

et al. 2013

Toxicological Sciences

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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 after pralidoxime administration to patients with laboratory-proven World Health Organization (WHO) class II OP insecticide poisoning. Patient data were derived from 2 studies, a cohort study (using a bolus treatment of 1g pralidoxime chloride) and a randomized controlled trial (RCT) (comparing 2g pralidoxime over 20min, followed by an infusion of 0.5g/h, with placebo). Two grams of pralidoxime variably reactivated BuChE in patients poisoned by 2 diethyl OP insecticides, chlorpyrifos and quinalphos; however, unlike acetylcholinesterase reactivation, this reactivation was not sustained. It did not reactivate BuChE inhibited by the dimethyl OPs dimethoate or fenthion. The 1-g dose produced no reactivation. Pralidoxime produced variable reactivation of BuChE in WHO class II OP-poisoned patients according to the pralidoxime dose administered, OP ingested, and individual patient. The use of BuChE assays for monitoring the effect of pralidoxime treatment is unlikely to be clinically useful.

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Therapeutic Factors in Survival after Lethal Cholinesterase Inhibition by Phosphorus Insecticides

Cited by 33 publications

References 9 publications

Pharmacological Antagonists of the Anticholinesterase Agents

Pharmacological Antagonists of the Anticholinesterase Agents

Pralidoxime in Acute Organophosphorus Insecticide Poisoning—A Randomised Controlled Trial

Reactivation of Plasma Butyrylcholinesterase by Pralidoxime Chloride in Patients Poisoned by WHO Class II Toxicity Organophosphorus Insecticides

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