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Clarence A. Broomfield - One of the best experts on this subject based on the ideXlab platform.

  • Hypothesis for Synergistic Toxicity of Organophosphorus Poisoning‐induced Cholinergic Crisis and Anaphylactoid Reactions
    Journal of applied toxicology : JAT, 1996
    Co-Authors: Fred M. Cowan, Tsung-ming Shih, David E. Lenz, J. M. Madsen, Clarence A. Broomfield
    Abstract:

    The neurotoxicity of organophosphorus (OP) compounds involves the inhibition of acetylcholinesterase (AChE), causing accumulation of acetylcholine (ACh) at synapses. However, Cholinergic Crisis may not be the sole mechanism of OP toxicity. Adverse drug reactions caused by synergistic toxicity between drugs with distinct pharmacological mechanisms are a common problem. Likewise, the multiple pharmacological activities of a single molecule might also contribute to either toxicity or efficacy. For example, certain OP compounds (e.g. soman) exhibit anti-AChE activity and also act as secretagogues by inducing mast cell degranulation with associated autacoid release and anaphylactoid reactions. Anaphylactoid shock can produce a lethal syndrome with symptoms of respiratory failure and circulatory collapse similar to the physiological sequelae observed for OP poisoning. Moreover, the major classes of drugs used as antidotes for OP intoxication can affect anaphylaxis. Acetylcholine can act as an agonist of autacoid release, and autacoids such as histamine can augment soman-induced bronchial spasm. In concert with the demonstrably critical role of Cholinergic Crisis in OP toxicity, the precepts of neuroimmunology indicate that secondary adverse reactions encompassing anaphylactoid reactions may complicate OP toxicity.

  • hypothesis for synergistic toxicity of organophosphorus poisoning induced Cholinergic Crisis and anaphylactoid reactions
    Journal of Applied Toxicology, 1996
    Co-Authors: Fred M. Cowan, Tsung-ming Shih, David E. Lenz, J. M. Madsen, Clarence A. Broomfield
    Abstract:

    The neurotoxicity of organophosphorus (OP) compounds involves the inhibition of acetylcholinesterase (AChE), causing accumulation of acetylcholine (ACh) at synapses. However, Cholinergic Crisis may not be the sole mechanism of OP toxicity. Adverse drug reactions caused by synergistic toxicity between drugs with distinct pharmacological mechanisms are a common problem. Likewise, the multiple pharmacological activities of a single molecule might also contribute to either toxicity or efficacy. For example, certain OP compounds (e.g. soman) exhibit anti-AChE activity and also act as secretagogues by inducing mast cell degranulation with associated autacoid release and anaphylactoid reactions. Anaphylactoid shock can produce a lethal syndrome with symptoms of respiratory failure and circulatory collapse similar to the physiological sequelae observed for OP poisoning. Moreover, the major classes of drugs used as antidotes for OP intoxication can affect anaphylaxis. Acetylcholine can act as an agonist of autacoid release, and autacoids such as histamine can augment soman-induced bronchial spasm. In concert with the demonstrably critical role of Cholinergic Crisis in OP toxicity, the precepts of neuroimmunology indicate that secondary adverse reactions encompassing anaphylactoid reactions may complicate OP toxicity.

Hideo Yasunaga - One of the best experts on this subject based on the ideXlab platform.

  • Cholinergic Crisis Caused by Cholinesterase Inhibitors: a Retrospective Nationwide Database Study
    Journal of Medical Toxicology, 2018
    Co-Authors: Hiroyuki Ohbe, Hiroki Matsui, Kiyohide Fushimi, Hideo Yasunaga
    Abstract:

    Introduction In contrast to information on the effects of organophosphate, pesticide, or environmental exposures, data on Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors are sparse. The present study aimed to describe the characteristics, demographics, and mortality of patients with Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors using a nationwide inpatient database in Japan. Methods We identified patients diagnosed with Cholinergic Crisis as a result of taking cholinesterase inhibitor medications in the Japanese Diagnosis Procedure Combination inpatient database from July 2010 to March 2016. We examined the patients’ characteristics, treatments, and mortality. Results A total of 235 patients with Cholinergic Crisis were identified during the 69-month study period. Forty-eight patients required mechanical ventilation (20.4%), and 15 patients died (6.4%) in hospital. The median lengths of hospital stay and intensive care unit stay were 15 days (interquartile range, 6–42) and 4 days (2–8), respectively. Approximately half of all hospitalized patients required catecholamines, atropine, or mechanical ventilation, while the other half did not require any of these treatments. Patients who required catecholamines, atropine, or mechanical ventilation were more likely to die and had longer hospital stays. Conclusions Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors is a rare but potentially life-threatening condition. Patients who require mechanical ventilation and catecholamines or atropine have a poorer prognosis.

  • Cholinergic Crisis Caused by Cholinesterase Inhibitors: a Retrospective Nationwide Database Study.
    Journal of medical toxicology : official journal of the American College of Medical Toxicology, 2018
    Co-Authors: Hiroyuki Ohbe, Hiroki Matsui, Kiyohide Fushimi, Hideo Yasunaga
    Abstract:

    In contrast to information on the effects of organophosphate, pesticide, or environmental exposures, data on Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors are sparse. The present study aimed to describe the characteristics, demographics, and mortality of patients with Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors using a nationwide inpatient database in Japan. We identified patients diagnosed with Cholinergic Crisis as a result of taking cholinesterase inhibitor medications in the Japanese Diagnosis Procedure Combination inpatient database from July 2010 to March 2016. We examined the patients’ characteristics, treatments, and mortality. A total of 235 patients with Cholinergic Crisis were identified during the 69-month study period. Forty-eight patients required mechanical ventilation (20.4%), and 15 patients died (6.4%) in hospital. The median lengths of hospital stay and intensive care unit stay were 15 days (interquartile range, 6–42) and 4 days (2–8), respectively. Approximately half of all hospitalized patients required catecholamines, atropine, or mechanical ventilation, while the other half did not require any of these treatments. Patients who required catecholamines, atropine, or mechanical ventilation were more likely to die and had longer hospital stays. Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors is a rare but potentially life-threatening condition. Patients who require mechanical ventilation and catecholamines or atropine have a poorer prognosis.

Fred M. Cowan - One of the best experts on this subject based on the ideXlab platform.

  • Hypothesis for Synergistic Toxicity of Organophosphorus Poisoning‐induced Cholinergic Crisis and Anaphylactoid Reactions
    Journal of applied toxicology : JAT, 1996
    Co-Authors: Fred M. Cowan, Tsung-ming Shih, David E. Lenz, J. M. Madsen, Clarence A. Broomfield
    Abstract:

    The neurotoxicity of organophosphorus (OP) compounds involves the inhibition of acetylcholinesterase (AChE), causing accumulation of acetylcholine (ACh) at synapses. However, Cholinergic Crisis may not be the sole mechanism of OP toxicity. Adverse drug reactions caused by synergistic toxicity between drugs with distinct pharmacological mechanisms are a common problem. Likewise, the multiple pharmacological activities of a single molecule might also contribute to either toxicity or efficacy. For example, certain OP compounds (e.g. soman) exhibit anti-AChE activity and also act as secretagogues by inducing mast cell degranulation with associated autacoid release and anaphylactoid reactions. Anaphylactoid shock can produce a lethal syndrome with symptoms of respiratory failure and circulatory collapse similar to the physiological sequelae observed for OP poisoning. Moreover, the major classes of drugs used as antidotes for OP intoxication can affect anaphylaxis. Acetylcholine can act as an agonist of autacoid release, and autacoids such as histamine can augment soman-induced bronchial spasm. In concert with the demonstrably critical role of Cholinergic Crisis in OP toxicity, the precepts of neuroimmunology indicate that secondary adverse reactions encompassing anaphylactoid reactions may complicate OP toxicity.

  • hypothesis for synergistic toxicity of organophosphorus poisoning induced Cholinergic Crisis and anaphylactoid reactions
    Journal of Applied Toxicology, 1996
    Co-Authors: Fred M. Cowan, Tsung-ming Shih, David E. Lenz, J. M. Madsen, Clarence A. Broomfield
    Abstract:

    The neurotoxicity of organophosphorus (OP) compounds involves the inhibition of acetylcholinesterase (AChE), causing accumulation of acetylcholine (ACh) at synapses. However, Cholinergic Crisis may not be the sole mechanism of OP toxicity. Adverse drug reactions caused by synergistic toxicity between drugs with distinct pharmacological mechanisms are a common problem. Likewise, the multiple pharmacological activities of a single molecule might also contribute to either toxicity or efficacy. For example, certain OP compounds (e.g. soman) exhibit anti-AChE activity and also act as secretagogues by inducing mast cell degranulation with associated autacoid release and anaphylactoid reactions. Anaphylactoid shock can produce a lethal syndrome with symptoms of respiratory failure and circulatory collapse similar to the physiological sequelae observed for OP poisoning. Moreover, the major classes of drugs used as antidotes for OP intoxication can affect anaphylaxis. Acetylcholine can act as an agonist of autacoid release, and autacoids such as histamine can augment soman-induced bronchial spasm. In concert with the demonstrably critical role of Cholinergic Crisis in OP toxicity, the precepts of neuroimmunology indicate that secondary adverse reactions encompassing anaphylactoid reactions may complicate OP toxicity.

Hiroyuki Ohbe - One of the best experts on this subject based on the ideXlab platform.

  • Cholinergic Crisis Caused by Cholinesterase Inhibitors: a Retrospective Nationwide Database Study
    Journal of Medical Toxicology, 2018
    Co-Authors: Hiroyuki Ohbe, Hiroki Matsui, Kiyohide Fushimi, Hideo Yasunaga
    Abstract:

    Introduction In contrast to information on the effects of organophosphate, pesticide, or environmental exposures, data on Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors are sparse. The present study aimed to describe the characteristics, demographics, and mortality of patients with Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors using a nationwide inpatient database in Japan. Methods We identified patients diagnosed with Cholinergic Crisis as a result of taking cholinesterase inhibitor medications in the Japanese Diagnosis Procedure Combination inpatient database from July 2010 to March 2016. We examined the patients’ characteristics, treatments, and mortality. Results A total of 235 patients with Cholinergic Crisis were identified during the 69-month study period. Forty-eight patients required mechanical ventilation (20.4%), and 15 patients died (6.4%) in hospital. The median lengths of hospital stay and intensive care unit stay were 15 days (interquartile range, 6–42) and 4 days (2–8), respectively. Approximately half of all hospitalized patients required catecholamines, atropine, or mechanical ventilation, while the other half did not require any of these treatments. Patients who required catecholamines, atropine, or mechanical ventilation were more likely to die and had longer hospital stays. Conclusions Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors is a rare but potentially life-threatening condition. Patients who require mechanical ventilation and catecholamines or atropine have a poorer prognosis.

  • Cholinergic Crisis Caused by Cholinesterase Inhibitors: a Retrospective Nationwide Database Study.
    Journal of medical toxicology : official journal of the American College of Medical Toxicology, 2018
    Co-Authors: Hiroyuki Ohbe, Hiroki Matsui, Kiyohide Fushimi, Hideo Yasunaga
    Abstract:

    In contrast to information on the effects of organophosphate, pesticide, or environmental exposures, data on Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors are sparse. The present study aimed to describe the characteristics, demographics, and mortality of patients with Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors using a nationwide inpatient database in Japan. We identified patients diagnosed with Cholinergic Crisis as a result of taking cholinesterase inhibitor medications in the Japanese Diagnosis Procedure Combination inpatient database from July 2010 to March 2016. We examined the patients’ characteristics, treatments, and mortality. A total of 235 patients with Cholinergic Crisis were identified during the 69-month study period. Forty-eight patients required mechanical ventilation (20.4%), and 15 patients died (6.4%) in hospital. The median lengths of hospital stay and intensive care unit stay were 15 days (interquartile range, 6–42) and 4 days (2–8), respectively. Approximately half of all hospitalized patients required catecholamines, atropine, or mechanical ventilation, while the other half did not require any of these treatments. Patients who required catecholamines, atropine, or mechanical ventilation were more likely to die and had longer hospital stays. Cholinergic Crisis caused by pharmaceutical cholinesterase inhibitors is a rare but potentially life-threatening condition. Patients who require mechanical ventilation and catecholamines or atropine have a poorer prognosis.

Tsung-ming Shih - One of the best experts on this subject based on the ideXlab platform.

  • Reactivation of Acetylcholinesterase Activity and Its Therapeutic Benefits in Nerve Agent Intoxication
    2010
    Co-Authors: Tsung-ming Shih, Donald M. Maxwell, Irwin Koplovitz, Robert K. Kan, John H. Mcdonough
    Abstract:

    Abstract : Organophosphorus chemical warfare nerve agents are potent inhibitors of the enzyme acetylcholinesterase (AChE). Inhibition of AChE at nerve terminals in peripheral tissues and the central nervous system (CNS) results in acetylcholine (ACh) overload and, depending on the extent of enzyme inhibition, Cholinergic Crisis. Current treatment strategies for nerve agent intoxication consist of using an oxime such as pyridine-2-aldoxime methylchloride (2-PAM) to reactivate the inhibited AChE and the antiCholinergic drug atropine sulfate to antagonize the effects of excess ACh at muscarinic Cholinergic receptors.

  • Hypothesis for Synergistic Toxicity of Organophosphorus Poisoning‐induced Cholinergic Crisis and Anaphylactoid Reactions
    Journal of applied toxicology : JAT, 1996
    Co-Authors: Fred M. Cowan, Tsung-ming Shih, David E. Lenz, J. M. Madsen, Clarence A. Broomfield
    Abstract:

    The neurotoxicity of organophosphorus (OP) compounds involves the inhibition of acetylcholinesterase (AChE), causing accumulation of acetylcholine (ACh) at synapses. However, Cholinergic Crisis may not be the sole mechanism of OP toxicity. Adverse drug reactions caused by synergistic toxicity between drugs with distinct pharmacological mechanisms are a common problem. Likewise, the multiple pharmacological activities of a single molecule might also contribute to either toxicity or efficacy. For example, certain OP compounds (e.g. soman) exhibit anti-AChE activity and also act as secretagogues by inducing mast cell degranulation with associated autacoid release and anaphylactoid reactions. Anaphylactoid shock can produce a lethal syndrome with symptoms of respiratory failure and circulatory collapse similar to the physiological sequelae observed for OP poisoning. Moreover, the major classes of drugs used as antidotes for OP intoxication can affect anaphylaxis. Acetylcholine can act as an agonist of autacoid release, and autacoids such as histamine can augment soman-induced bronchial spasm. In concert with the demonstrably critical role of Cholinergic Crisis in OP toxicity, the precepts of neuroimmunology indicate that secondary adverse reactions encompassing anaphylactoid reactions may complicate OP toxicity.

  • hypothesis for synergistic toxicity of organophosphorus poisoning induced Cholinergic Crisis and anaphylactoid reactions
    Journal of Applied Toxicology, 1996
    Co-Authors: Fred M. Cowan, Tsung-ming Shih, David E. Lenz, J. M. Madsen, Clarence A. Broomfield
    Abstract:

    The neurotoxicity of organophosphorus (OP) compounds involves the inhibition of acetylcholinesterase (AChE), causing accumulation of acetylcholine (ACh) at synapses. However, Cholinergic Crisis may not be the sole mechanism of OP toxicity. Adverse drug reactions caused by synergistic toxicity between drugs with distinct pharmacological mechanisms are a common problem. Likewise, the multiple pharmacological activities of a single molecule might also contribute to either toxicity or efficacy. For example, certain OP compounds (e.g. soman) exhibit anti-AChE activity and also act as secretagogues by inducing mast cell degranulation with associated autacoid release and anaphylactoid reactions. Anaphylactoid shock can produce a lethal syndrome with symptoms of respiratory failure and circulatory collapse similar to the physiological sequelae observed for OP poisoning. Moreover, the major classes of drugs used as antidotes for OP intoxication can affect anaphylaxis. Acetylcholine can act as an agonist of autacoid release, and autacoids such as histamine can augment soman-induced bronchial spasm. In concert with the demonstrably critical role of Cholinergic Crisis in OP toxicity, the precepts of neuroimmunology indicate that secondary adverse reactions encompassing anaphylactoid reactions may complicate OP toxicity.