Normally, the enzyme acetylcholinesterase quickly breaks down acetylcholine after it has delivered its message, but organophosphates inhibit acetylcholinesterase and, as a result, disrupt the transmission of nerve impulses at nerve endings. This is used at neuromuscular junctions, in the part of the nervous system that controls breathing and other automatic vital functions, and in parts of the central nervous system. One important neurotransmitter is acetylcholine. At the end of the neurons, these impulses are converted into chemical messages (neurotransmitters), which cross the gap between neurons and muscle cells (the neuromuscular junction) and bind to proteins (receptors) on the muscle cells that pass on the brain's message. The brain controls the body by sending electrical impulses along nerve cells (neurons) to the body's muscle cells. Organophosphates disrupt communication between the brain and the body in both insects and people. Independent data monitoring committee IQR,Įach year, about 200,000 people worldwide die from poisoning with organophosphorous insecticides, toxic chemicals that are widely used in agriculture, particularly in developing countries. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist. The South Asian Clinical Toxicology Research Collaboration is funded by a Wellcome Trust/National Health and Medical Research Council International Collaborative Research Grant 071669. This work was funded by grant 063560 from the Wellcome Trust's Tropical Interest Group to ME. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.įunding: ME is a Wellcome Trust Career Development Fellow. Received: DecemAccepted: Published: June 30, 2009Ĭopyright: © 2009 Eddleston et al. PLoS Med 6(6):Īcademic Editor: Mervyn Singer, University College London, United Kingdom (2009) Pralidoxime in Acute Organophosphorus Insecticide Poisoning-A Randomised Controlled Trial. To reduce confounding due to ingestion of different insecticides, we further analysed patients with confirmed chlorpyrifos or dimethoate poisoning alone, finding no evidence of benefit.Ĭitation: Eddleston M, Eyer P, Worek F, Juszczak E, Alder N, Mohamed F, et al. The need for intubation was similar in both groups (pralidoxime 26/121, placebo 24/114, adjusted HR 1.27 ). Incorporating the baseline amount of acetylcholinesterase already aged and plasma OP concentration into the analysis increased the HR for patients receiving pralidoxime compared to placebo, further decreasing the likelihood that pralidoxime is beneficial. Mortality was nonsignificantly higher in patients receiving pralidoxime: 30/121 (24.8%) receiving pralidoxime died, compared with 18/114 (15.8%) receiving placebo (adjusted hazard ratio 1.69, 95% confidence interval 0.88–3.26, p = 0.12). Pralidoxime produced substantial and moderate red cell acetylcholinesterase reactivation in patients poisoned by diethyl and dimethyl compounds, respectively. Two hundred thirty-five patients were randomised to receive pralidoxime (121) or saline placebo (114). We measured baseline markers of exposure and pharmacodynamic markers of response to aid interpretation of clinical outcomes. Mortality was the primary outcome secondary outcomes included intubation, duration of intubation, and time to death. We performed a double-blind randomised placebo-controlled trial of pralidoxime chloride (2 g loading dose over 20 min, followed by a constant infusion of 0.5 g/h for up to 7 d) versus saline in patients with organophosphorus insecticide self-poisoning.
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