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A case report of severe pirimiphos-methyl intoxication: Clinical findings and cholinesterase status

A 63-year-old male was admitted to a district hospital after ingesting ethanol and pirimiphos-methyl (PM) with suicidal intentions. History included alcoholic cirrhosis with alcoholism, adiposity, diabetes with cerebral microangiopathy, chronic renal insufficiency, heparin-induced thrombocytopenia,...

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Autores principales: Zellner, Tobias, Rabe, Christian, von der Wellen-Pawlowski, Jens, Hansen, Dagmar, John, Harald, Worek, Franz, Eyer, Florian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9816423/
https://www.ncbi.nlm.nih.gov/pubmed/36618943
http://dx.doi.org/10.3389/fphar.2022.1102160
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author Zellner, Tobias
Rabe, Christian
von der Wellen-Pawlowski, Jens
Hansen, Dagmar
John, Harald
Worek, Franz
Eyer, Florian
author_facet Zellner, Tobias
Rabe, Christian
von der Wellen-Pawlowski, Jens
Hansen, Dagmar
John, Harald
Worek, Franz
Eyer, Florian
author_sort Zellner, Tobias
collection PubMed
description A 63-year-old male was admitted to a district hospital after ingesting ethanol and pirimiphos-methyl (PM) with suicidal intentions. History included alcoholic cirrhosis with alcoholism, adiposity, diabetes with cerebral microangiopathy, chronic renal insufficiency, heparin-induced thrombocytopenia, and status post necrotizing fasciitis. Emergency medical service reported an alert patient without signs of cholinergic crisis; activated charcoal and atropine were administered. Upon hospital arrival, he received fluid resuscitation, activated charcoal, and atropine. He was transferred to a toxicology unit the next day. On admission, he had no cholinergic signs (dry mucous membranes, warm skin, and mydriatic pupils) requiring small atropine doses (0.5 mg per hour). Four hours after admission, he developed bradycardia and respiratory distress, necessitating intubation. He received atropine by continuous infusion for 7 days (248 mg total) and obidoxime (bolus and continuous infusion). PM, pirimiphos-methyl-oxon (PMO), and phosphorylated tyrosine (Tyr) adducts derived from human serum albumin were analyzed in vivo. Cholinesterase status (acetylcholinesterase (AChE), butyrylcholinesterase (BChE), inhibitory activity of patient plasma and reactivatability, and phosphorylated BChE-derived nonapeptides) was measured in vivo. Obidoxime and atropine were monitored. PM and PMO were detectable, PM with maximum concentration ∼24 h post admission (p.a.) and PMO at ∼18 h p.a. Tyr adducts were detectable. AChE in vivo was suppressed on admission, increased continuously after starting obidoxime, and reached maximum activity after ∼30 h. AChE in vivo and reactivatability remained at the same level until the end of monitoring. BChE was already suppressed on admission; termination of the antidote treatment was possible after BChE had recovered to 1/5th of its normal value and extubation was possible after BChE had recovered to 2/5th. While a substantial part of BChE was already aged on admission, aging continued peaking at ∼24 h p.a. After initiating obidoxime treatment, plasma levels increased until obidoxime plasma levels reached a steady state. On admission, plasma atropine level was low; it increased with the start of the continuous infusion. Afterward, the level dropped to a steady state. The clinical course was characterized by bouts of pneumonia, necessitating re-intubation and prolonged ventilation, sepsis, delirium, and a peripheral neuropathy. After psychiatric evaluation, the patient was discharged to a neurological rehabilitation facility after 77 days of hospital care.
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spelling pubmed-98164232023-01-07 A case report of severe pirimiphos-methyl intoxication: Clinical findings and cholinesterase status Zellner, Tobias Rabe, Christian von der Wellen-Pawlowski, Jens Hansen, Dagmar John, Harald Worek, Franz Eyer, Florian Front Pharmacol Pharmacology A 63-year-old male was admitted to a district hospital after ingesting ethanol and pirimiphos-methyl (PM) with suicidal intentions. History included alcoholic cirrhosis with alcoholism, adiposity, diabetes with cerebral microangiopathy, chronic renal insufficiency, heparin-induced thrombocytopenia, and status post necrotizing fasciitis. Emergency medical service reported an alert patient without signs of cholinergic crisis; activated charcoal and atropine were administered. Upon hospital arrival, he received fluid resuscitation, activated charcoal, and atropine. He was transferred to a toxicology unit the next day. On admission, he had no cholinergic signs (dry mucous membranes, warm skin, and mydriatic pupils) requiring small atropine doses (0.5 mg per hour). Four hours after admission, he developed bradycardia and respiratory distress, necessitating intubation. He received atropine by continuous infusion for 7 days (248 mg total) and obidoxime (bolus and continuous infusion). PM, pirimiphos-methyl-oxon (PMO), and phosphorylated tyrosine (Tyr) adducts derived from human serum albumin were analyzed in vivo. Cholinesterase status (acetylcholinesterase (AChE), butyrylcholinesterase (BChE), inhibitory activity of patient plasma and reactivatability, and phosphorylated BChE-derived nonapeptides) was measured in vivo. Obidoxime and atropine were monitored. PM and PMO were detectable, PM with maximum concentration ∼24 h post admission (p.a.) and PMO at ∼18 h p.a. Tyr adducts were detectable. AChE in vivo was suppressed on admission, increased continuously after starting obidoxime, and reached maximum activity after ∼30 h. AChE in vivo and reactivatability remained at the same level until the end of monitoring. BChE was already suppressed on admission; termination of the antidote treatment was possible after BChE had recovered to 1/5th of its normal value and extubation was possible after BChE had recovered to 2/5th. While a substantial part of BChE was already aged on admission, aging continued peaking at ∼24 h p.a. After initiating obidoxime treatment, plasma levels increased until obidoxime plasma levels reached a steady state. On admission, plasma atropine level was low; it increased with the start of the continuous infusion. Afterward, the level dropped to a steady state. The clinical course was characterized by bouts of pneumonia, necessitating re-intubation and prolonged ventilation, sepsis, delirium, and a peripheral neuropathy. After psychiatric evaluation, the patient was discharged to a neurological rehabilitation facility after 77 days of hospital care. Frontiers Media S.A. 2022-12-23 /pmc/articles/PMC9816423/ /pubmed/36618943 http://dx.doi.org/10.3389/fphar.2022.1102160 Text en Copyright © 2022 Zellner, Rabe, Wellen-Pawlowski, Hansen, John, Worek and Eyer. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Zellner, Tobias
Rabe, Christian
von der Wellen-Pawlowski, Jens
Hansen, Dagmar
John, Harald
Worek, Franz
Eyer, Florian
A case report of severe pirimiphos-methyl intoxication: Clinical findings and cholinesterase status
title A case report of severe pirimiphos-methyl intoxication: Clinical findings and cholinesterase status
title_full A case report of severe pirimiphos-methyl intoxication: Clinical findings and cholinesterase status
title_fullStr A case report of severe pirimiphos-methyl intoxication: Clinical findings and cholinesterase status
title_full_unstemmed A case report of severe pirimiphos-methyl intoxication: Clinical findings and cholinesterase status
title_short A case report of severe pirimiphos-methyl intoxication: Clinical findings and cholinesterase status
title_sort case report of severe pirimiphos-methyl intoxication: clinical findings and cholinesterase status
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9816423/
https://www.ncbi.nlm.nih.gov/pubmed/36618943
http://dx.doi.org/10.3389/fphar.2022.1102160
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